Role of Patient Specifics on Mechanical Risk and Load Relief During Support of Bony Prominences

Wound Healing Society 2015 update on guidelines for pressure ulcers.

Experimental and theoretical analyses of compression induced muscle damage : aetiological factors in pressure ulcers

The aim of this systematic review was to examine the associations and relationship between commonly cited risk factors and the pathology of pressure ulcer (PU) development. Using systematic review methodology, original research studies, prospective design and human studies written in English were included. The search was conducted in March 2018, using Ovid, Ovid EMBASE and CINAHL databases. Data were extracted using a pre-designed extraction tool and all included studies were quality appraised using the evidence-based librarianship critical appraisal. A total of 382 records were identified, of which five met the inclusion criteria. The studies were conducted between 1994 and 2017. Most studies were conducted in hospital and geriatric wards. The mean sample size was 96±145.7 participants. Ischaemia, recovery of blood flow and pathological impact of pressure and shear was mainly found as the cited risk factor and PU aetiology. This review systematically analysed five papers exploring the relationship between risk factors for PU development and aetiology. It identified many risk factors and underlying pathological mechanisms that interact in the development of PU including ischaemia, stress, recovery of blood flow, tissue hypoxia and the pathological impact of pressure and shear. There are several pathways in which these pathological mechanisms contribute to PU development and identifying these could establish potential ways of preventing or treating the development of PU for patients.

The etiology of pressure ulcers: Skin deep or muscle bound?

Incidence of pressure ulcers as primary outcomes in clinical trials: A comment on

Healing of severe pressure injuries (PIs) in patients with multiple comorbidities requires a multifaceted and interdisciplinary approach and includes the use of support surfaces. Published clinical data guiding support surface selection are very limited. Long-term acute care hospitals frequently treat medically complex patients, many with severe PIs. To compare healing rates in patients with severe PIs on air-fluidized therapy (AFT) or fluid immersion system (FIS) support surfaces. After obtaining informed consent, patients with a stage 3 or 4 PI were randomized to receive either AFT or FIS in addition to the standard protocol of care. Baseline and weekly wound measurements were obatined using a 3-dimensional camera measurement tool. The required sample size was calculated to be 60. After the study had started, the long-term acute care hospital admission criteria changed, severely limiting the number of patients who met the study inclusion criteria. Only 4 patients with a stage 4 PI completed the study. Of those, 2 were on an AFT and 2 were on an FIS surface. All wounds reduced in size; 0.12 and 0.57 cm²/day for patients on AFT and 0.68 and 1.34 cm²/day for patients on FIS. All but 1 wound had a reduction in wound volume ranging from -0.2 and 0.97 cm³ to 1.78 and 4.18 cm³/day for patients on AFT and FIS, respectively. Obtaining much-needed evidence to guide support surface selections for patients with severe PIs is challenging and requires multicenter studies.

Review objective The objective of this review is to establish whether using the Braden subscale mobility assessment is comparable to using the full Braden assessment scale. The specific review questions to be addressed are: 1. What preventive pressure ulcer nursing interventions are initiated based on assessment of mobility impairment alone or in comparison with the full Braden risk assessment scale? 2. What is the effect of using mobility assessment alone on incidence of hospital acquired pressure ulcers? Inclusion criteria Types of participants This review will consider studies that include adult patients, 18 years and older, in acute care setting who are at risk of developing pressure ulcers. At risk patients are those identified using Braden risk assessment scale as ‘at risk’, ‘moderate risk’, ‘high risk; and ‘very high risk’ for developing pressure ulcer6, 9 or the sub scale for impaired mobility as ‘completely immobile’, ‘very limited’ and ‘slightly limited’. Studies involving children only and studies conducted in the emergency department only or in the operating room only will be excluded from the review as they are not consistent with the review objective. Types of intervention(s)/Phenomena of interest This review will consider studies that include pressure ulcer risk identified using assessment of the subscale mobility impairment compared with full Braden scale assessment where available. Types of outcomes This review will consider the following primary outcome measures: • Whether patients in either study arm are more or less likely to receive appropriate preventative interventions, including, but not limited to protective mattresses, creams and skin barriers, vitamin supplements, patient positioning etc • Incidence of hospital acquired pressure ulcers Secondary outcome measures: • Reliability of mobility assessment ± Braden assessment • Frequency of assessment

Does Pressure Cause Pressure Ulcers? An Inquiry Into the Etiology of Pressure Ulcers

Until the last two decades, research on the aetiology of pressure ulcers was primarily based on animal models, using rabbits, pigs, rats and dogs. Although these studies have been very valuable, there are ethical as well as conceptual reasons to look for alternative models. Sophisticated non-invasive techniques like Magnetic Resonance Imaging (MRI) and Ultrasound as well as advanced theoretical modelling have offered opportunities for studies with human volunteers. This chapter describes the activities in the laboratories of the authors in the last 15 years which have focused on the aetiology of pressure ulcers. This includes in vitro studies on single cells and on artificial skeletal muscle tissues. These investigations have provided considerable insight into aspects of deformation damage and the role of ischemia in pressure ulcer development. The results appeared consistent with animal studies and human studies.

Compression and hypoxia in an engineered skeletal muscle model

Etiology and Incidence of Pressure Ulcers in Surgical Patients

An Integrative Review of Pressure Relief in Surgical Patients

That changes of local skin temperature and relative humidity may play a part in predisposing people to pressure ulcer development has long been recognized but perhaps overlooked due to the strong focus upon pressure redistribution. Around 2010 interest has grown in the microclimate and its management within pressure ulcer prevention. There is limited data upon which to base firm conclusions around whether modifying the microclimate influences pressure ulcer development. There is growing data that local skin cooling may reduce the hyperaemic response following unloading while altering some aspects of cytokine production. However these potentially beneficial effects of skin cooling may reduce the patient’s experience and quality of life. Skin-mattress relative humidity may be higher among patients who later develop superficial sacral pressure ulcers compared with other patients who do not develop these injuries. However interpretation of this data is compounded by the wide intra- and inter- individual differences in microclimate parameters. There is a growing need for increased communication between textile and pressure ulcer researchers if progress is to be made in elucidating the role (if any) of the microclimate in pressure ulcer prevention.

A new concept: ‘Relative position between the external force and the bony prominence’ explains location-specific occurrence of superficial injury over an undermining lesion

Pressure ulcer (PU) prevention is crucial for critically ill patients in the intensive care unit, but etiologic factors leading to their development have not yet been completely elucidated. This study explores the relationships among etiologic factors, interventional nursing care, and morphological characteristics of PUs in intensive care unit patients. We used a qualitative exploratory method to link morphological characteristics of specific PUs to etiologic factors. Details of individual PUs were described by sketching the PU photograph and categorized to characterize the morphology of PUs. After identification of characteristics, the development process was evaluated by in-depth review of medical records. The morphological characteristics of 30 PUs were organized into 4 categories. This process revealed a type of PU not previously described, which we labeled "leaf-type." These PUs were located on the lower sacrum, rhombic-oval in shape, and characterized by purpura and PU wrinkles. Possible etiologic factors for the specific PUs were divided into 4 categories: (1) the occurrence of PU risk episodes, (2) failure of the peripheral circulation, (3) periods of critical immobility, and (4) position change techniques inducing skin deformation. PU can be categorized into 4 morphological types, including a new category of leaf-shaped PU. We found that frequently repeated position changes such as lateral tilt and repeated head elevation caused deformation of the sacral skin that may play a role in PU development.