In Vitro Characterization of Pressure Redistribution Among Commercially Available Wound Dressings.

OBJECTIVE: Recent clinical evidence has suggested that certain wound dressings may play a significant role in protocols to prevent or reduce pressure injury (PI) in patients at risk by modifying the pressure, friction, and shear forces that can contribute to PI. The aim of this study was to investigate the pressure reduction properties of commercially available wound dressings in vitro. METHODS: Using a standardized protocol (1.7 kg, 7.5-cm sphere), testing was performed in a controlled environment by the same clinician using a pressure mapping device (XSENSOR LX205; XSENSOR Technology Corporation, Calgary, Alberta, Canada) to measure and compare the pressure mitigation properties in a variety of wound dressings. RESULTS: A total of 13 different commercially available dressings were tested in triplicate for changes in pressure redistribution as compared with the control. One dressing demonstrated the greatest reduction of pressure forces (OxyBand PR; 50.33 ± 1.45 mm Hg) compared with the control (302.7 ± 0.33 mm Hg) and the greatest surface area of all the study dressings tested. There was a negative correlation (R2 = 0.73) between the average pressure distribution of a wound dressing and its contact area. Further, the peak pressure for OxyBand PR (P ≤ .05) was significantly different from all other tested dressings. CONCLUSIONS: One dressing (OxyBand PR) provided superior pressure redistribution and significantly reduced peak pressure in this study when compared with currently available standard foam and silicone dressings that are marketed for the purpose of PI prevention.

Myoglobin and troponin concentrations are increased in early stage deep tissue injury.

Pressure-induced deep tissue injury is a form of pressure ulcer which is difficult to detect and diagnose at an early stage, before the wound has severely progressed and becomes visible at the skin surface. At the present time, no such detection technique is available. To test the hypothesis that muscle damage biomarkers can be indicative of the development of deep tissue injury after sustained mechanical loading, an indentation test was performed for 2 h on the tibialis anterior muscle of rats. Myoglobin and troponin were analysed in blood plasma and urine over a period of 5 days. The damage as detected by the biomarkers was compared to damage as observed with T2 MRI to validate the response. We found that myoglobin and troponin levels in blood increased due to the damage. Myoglobin was also increased in urine. The amount of damage observed with MRI immediately after loading had a strong correlation with the maximal biomarker levels: troponin in blood rs = 0.94; myoglobin in blood rs = 0.75; and myoglobin in urine rs = 0.57. This study suggests that muscle damage markers measured in blood and urine could serve as early diagnosis for pressure induced deep tissue injury.

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

OBJECTIVE: To 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. DESIGN: Retrospective; secondary analysis of existing data. SETTING: Acute hospitalization and inpatient rehabilitation sites at a university medical center. PARTICIPANTS: Individuals 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). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Plasma 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. RESULTS: An 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. CONCLUSIONS: Altered 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.

Urine glycyl-L-proline increase and skin trophicity.

Glycyl-L-proline (gly-pro) is an end product of collagen metabolism that is further cleaved by prolidase (EC 3.4.13.9); the resulting proline molecules are recycled into collagen or other proteins. We postulated a relationship between defective gly-pro hydrolysis, increased collagen degradation and skin destruction. This relationship was tested using HPLC to measure the gly-pro in urine. 24 hour urine samples were collected from 27 old people (86 +/- 6 years old), of whom 15 were suffering from skin pressure sores of the sacrum or calcaneus. The urine from patients with pressure sores contained significantly more gly-pro than the urine from the control. A cut-off at 7 mumol/mmol creatinine gave the test a positive predictive value of 70%. Collagen breakdown was also increased as indicated by the increase of hydroxyproline (hyp) in the urine. But this breakdown seemed to stop at the gly-pro step.

Prospective study of pressure ulcer risk in spinal cord injury patients.

Sixty men with spinal cord injury who had developed pressure ulcers in the past but whose skin was intact when they joined the study were followed for 2 years, or until a pressure ulcer developed. Forty of the men were contacted every 4-6 weeks to answer questions about their skin care practices and to provide a 24 hour urine sample. The others were only contacted at the beginning and the end of the study to answer a questionnaire and to provide a urine sample. Changes in skin collagen metabolism were monitored by measuring urinary excretion of a metabolite, glucosyl-galactosyl hydroxylysine (glu-gal Hyl), corrected for creatinine excretion. Sustained increases in levels of glu-gal Hyl excretion were detected at least 2 months and as much as 5 months in advance of overt clinical signs of ulcer development. Increased excretion of glu-gal Hyl was significantly associated (p < 0.05) with the development of a pressure ulcer. An increase in the urinary excretion of glu-gal Hyl is an indication of increased degradation of skin collagen. Body mass index (weight/height2) of 33% of subjects with pressure ulcers, and 12% of those without, was at least one standard deviation below the mean of all subjects. Thirty-six percent of those who smoked developed ulcers, while only 26% of the nonsmokers did.(ABSTRACT TRUNCATED AT 250 WORDS)

Collagen metabolite excretion as a predictor of bone- and skin-related complications in spinal cord injury.

Immediately after the trauma, spinal cord injury patients have an increased rate of collagen synthesis and an even greater increase of collagen degradation. Collagen lost from bone is implicated in the etiology of osteoporosis and heterotopic ossification, and collagen lost from skin might lead to a propensity to develop pressure ulcers. The urinary excretion of two collagen metabolites has been monitored and their fluctuation related to the onset of skin or bone complications in these patients. One metabolite, glucosyl-galactosyl hydroxylysine, is more abundant in skin collagen; the other, galactosyl hydroxylysine, is more abundant in bone collagen. The excretion of both metabolites increases after injury, reaching a peak between three and six months after injury, and declines gradually, reaching control values about a year after injury. If a skin pressure ulcer develops, the urinary excretion of the diglycoside remains elevated instead of gradually decreasing. Similarly, if osteoporosis or heterotopic ossification is diagnosed, the monoglycoside excretion does not return to control values until the bone turnover stabilizes. Monitoring of the urinary excretion of both glycosides might prove helpful in prompting early examination to establish the presence of emerging skin and bone complications. Thus, aggressive preventive therapy could be given sooner.