ABSTRACT
BACKGROUND: Pressure injuries are associated with skin temperature changes, but little is known about skin temperature characteristics of the Kennedy Lesion (KL). PURPOSE: The purpose of this study was to describe early skin temperature changes in KLs using long-wave infrared thermography. METHODS: KLs were identified from chart review in 10 ICU patients. Skin assessments were performed within 24 hours of new skin discoloration. Temperature measurements were performed using a long-wave infrared thermography imaging system. Relative Temperature Differential (RTD) between the discolored area and a selected control point was calculated. RTDs of > +1.2 degrees C and < -1.2 degrees C were considered abnormal. Demographic data and observable characteristics of the KL were collected when available. Descriptive statistics (Mean plus/minus SD; % ) were used. RESULTS: The major finding of this study was that there were no early skin temperature differences between the KLs and surrounding skin. CONCLUSION: The early stage of the KL may be limited to microvascular injury which results in a normal skin temperature. More studies are needed to verify this finding and to ascertain whether KL skin temperature changes over time. The study also supports the bedside use of thermography in skin temperature assessment.
Subject(s)
Pressure Ulcer , Skin Temperature , Humans , Ulcer , Body Temperature , Skin , Pressure Ulcer/diagnosisABSTRACT
A deep-tissue pressure injury (DTPI) is a serious type of pressure injury that begins in tissue over bony prominences and can lead to the development of hospital-acquired pressure injuries (HAPIs). Using a commercially available thermal imaging system, study authors documented a total of 12 thermal anomalies in 9 of 114 patients at the time of admission to one of the study institution's ICUs over a 2-month period. An intensive, proven wound prevention protocol was immediately implemented for each of these patients. Of these 12 anomalies, 2 ultimately manifested as visually identifiable DTPIs. This represented a 60% reduction in the authors' institution's historical DTPIs/HAPI rate. Because these DTPIs were documented as present on admission using the thermal imaging tool, researchers avoided a revenue loss associated with nonreimbursed costs of care and also estimated financial benefits associated with litigation expenses known to be generated with HAPIs.Using thermal imaging to document DTPIs when patients present has the potential to significantly reduce expenses associated with pressure injury litigation. The clinical and financial benefits of early documentation of skin surface thermal anomalies in anatomical areas of interest are significant.
Subject(s)
Diagnostic Imaging/methods , Infrared Rays , Intensive Care Units , Pressure Ulcer/diagnostic imaging , Pressure Ulcer/prevention & control , Cohort Studies , Early Diagnosis , Female , Humans , Male , Patient Admission , Retrospective Studies , Sensitivity and Specificity , Severity of Illness IndexABSTRACT
The severe diabetic nephropathy that develops in the hypertensive transgenic (mRen-2)27 rat with streptozotocin (STZ) diabetes has previously been considered angiotensin II-dependent. Because metabolic pathways are also activated in the diabetic kidney, the present study aimed to determine whether renoprotection could be afforded with inhibitors of advanced glycation end products (AGEs), ALT-946, and aminoguanidine (AG). At 6 weeks of age, nondiabetic control and STZ diabetic Ren-2 rats were randomized to receive vehicle, ALT-946 (1 g/l), or AG (1 g/l) and were studied for 12 weeks. Systolic blood pressure was unchanged with diabetes, ALT-946, or AG. Both kidney weight and glomerular filtration rate were increased with diabetes and unchanged with ALT-946 or AG. ALT-946 and AG equally ameliorated glomerulosclerosis and medullary pathology; however, ALT-946 did reduce cortical tubular degeneration to a greater extent than AG. Albumin excretion rate, which was elevated with diabetes, was reduced with ALT-946 but not AG. AGE immunolabeling was increased in glomeruli and reduced with ALT-946 and AG. These findings indicate that even in the context of renal injury presumed to be primarily blood pressure- and/or angiotensin II-dependent, approaches that interfere with metabolic pathways such as inhibitors of AGE formation can confer renal protection in experimental diabetes.
