A review of deep tissue injury development, detection, and prevention: shear savvy.

Pressure ulcer prevention strategies include the prevention, and early recognition, of deep tissue injury (DTI), which can evolve into a Stage III or Stage IV pressure ulcer. In addition to their role in pressure-induced ischemia, shearing forces are believed to contribute substantially to the risk of DTI. Because the visual manifestation of a DTI may not occur until many hours after tissues were damaged, research to explore methods for early detection is on-going. For example, rhabdomyolysis is a common complication of deep tissue damage; its detection via blood chemistry and urinalysis is explored as a possible diagnostic tool of early DTI in anatomical areas where muscle is present. Substances released from injured muscle cells have a predictable time frame for detection in blood and urine, possibly enabling the clinician to estimate the time of the tissue death. Several small case studies suggest the potential validity and reliability of ultrasoun for visualizing soft tissue damage also deserve further research. While recommendations to reduce mechanical pressure and shearing damage in high-risk patients remain unchanged, their implementation is not always practical, feasible, or congruent with the overall plan of patient care. Early detection of existing tissue damage will help clinicians implement appropriate care plans that also may prevent further damage. Research to evaluate the validity, reliability, sensitivity, and specificity of diagnostic studies to detect pressure-related tissue death is warranted.

Using temperature of pressure-related intact discolored areas of skin to detect deep tissue injury: an observational, retrospective, correlational study.

Pressure-related intact discolored areas of skin (PRIDAS) are generally described as an area of nonblanching erythema (Stage I pressure ulcer) or deep tissue injury (DTI), but the validity of these definitions has not been tested. Preclinical studies and forensic observations have shown that skin temperature may help identify nonviable tissue. To investigate the effect of temperature difference between a PRIDAS and its adjacent intact skin and the subsequent development of skin necrosis, an observational, retrospective, correlational study was conducted. Data from all acute care hospital patients with an observed PRIDAS who received a skin integrity consult, including a skin temperature measurement of a PRIDAS site, were abstracted to ascertain if PRIDAS temperature correlated with the development of skin necrosis after 7 to 14 days and to examine the effect of additional patient variables on the progression or resolution of a PRIDAS. Skin temperatures were measured using a commercial, hand-held, infrared thermography camera, and the presence or absence of capillary refill was documented. Among the 85 patients studied, the difference between PRIDAS temperature and adjacent skin ranged from -3.2 ̊ C. to +3.0 ̊C. Of the 55 PRIDAS with a lower temperature at baseline than adjacent skin ("cool", average -1.2 ̊ C), 29 progressed to necrosis, compared to one of 30 PRIDAS with a higher temperature than adjacent skin ("warm", average + 1.2 ̊ C) (P <0.001). After adjusting for patient age, skin color, and PRIDAS site, the cool PRIDAS were 31.8 times more likely to progress to necrosis than the warm PRIDAS. Combining the presence/absence of capillary refill and PRIDAS temperature, 0% of 26 patients with signs of blanching and a warm PRIDAS versus 65% of 26 patients with a nonblanching and cool PRIDAS developed skin necrosis (P <0.001, Fisher exact test for the difference between the two combined values). Research examining the delayed appearance of DTI and large, multicenter, prospective validation studies are warranted. The current National Pressure Ulcer Advisory Panel definition of a Stage I pressure ulcer needs to be amended to reflect the strong relationship to DTI development.

Gentian violet 1% solution in the treatment of wounds in the geriatric patient: a retrospective study.

To review the use of gentian violet 1% (GV) in a long-term care facility for the treatment of small, open wounds and extremity eschars of all sizes and thickness. The records of all the patients receiving topical GV therapy over a period of 1 year, from May 19, 2007 - May 19, 2008 were reviewed. The total sample was 70 patients (38 male, 32 female), average age 65.9 y.o., with 111 wounds (41 patients had >1 wound). The types of wounds were divided into 3 categories: 1) Split-thickness scabs (N = 37) limited to the epithelium, 2) full-thickness eschars and wounds with no depth <1 cm (N = 50), and 3) full-thickness eschars >1 cm located on the lower extremity (average 3.3 cm in diameter [N = 24]). All the wounds had been treated the same: topical application of GV to the wounds daily. None of the patients had any documented adverse events to the GV. Out of the 111 wounds, 103 healed completely. All wounds remained negative for cellulitis. 1) GV is a viable alternative topical agent for healing small, superficial wounds, ineffective scabs, and both small and large pressure ulcer eschars on lower extremities of geriatric patients, 2) there was very little evidence of scarring with the use of GV.

Applying observations from forensic science to understanding the development of pressure ulcers.

Autopsies and pathology findings can enhance understanding of processes that occur while a person is still alive. Hence, wound care clinicians from all disciplines can learn about pressure-related injury from necrosis research performed on decedents by forensic pathologists. The current system of pressure ulcer staging and assessment is unidimensional and contains many gaps, leading to variations and errors in the way pressure damage to tissues is classified and described. To provide a foundation for the development of a theoretical temporal framework, deep tissue injury research results, expert observations, and interpretations of clinical events from within the disciplines of wound care and forensic science - as well as research and observations documented in the vascular, plastic reconstructive, and general surgery literature - were reviewed. The results suggest that many similarities exist between forensic descriptions of tissue necrosis post mortem and pressure-related necrosis, that deep tissue injury can be detected within 24 hours of occurrence, and that the time between visible signs of deep tissue injury and their occurrence can be estimated, providing the foundation for a temporal framework. While research to validate this temporal framework for pressure-related deep tissue injury is needed, clinicians can start applying these observations to help understand the circumstances surrounding the development of, and factors contributing to, the development of deep tissue injury. Clarification of timelines and improved understanding of deep tissue injury risk factors are needed.