We report a case of diabetic ketoacidosis (DKA) complicated by acute myocarditis, which was confirmed by cardiac biopsy. A 26-year-old man was hospitalized with severe DKA. On admission, nonspecific ST-T change was noted on the electrocardiogram (ECG). The patient's levels of creatine phosphokinase (CPK) and glutamic oxaloacetic transaminase were slightly elevated, but he did not complain of chest discomfort or symptoms of heart disease. On the first day after admission, ST-T elevation was noted on ECG during treatment of DKA. By cardiac angiography and cardiac biopsy, coronary heart disease was ruled out and postmyocarditic change was histologically confirmed. An episode of upper respiratory viral infection before the onset of acute diabetes suggested that the patient suffered from viral-induced myocarditis and consequent development of IDDM. This possibility was confirmed by the clinical course of ECG change, with elevated CPK and lactate dehydrogenase and a slightly elevated antibody titer for echovirus.
Introduction: Depth assessment is important for severe pressure ulcers (PUs); however, a device for the metric measurement of wounds, including depth, is lacking in clinical settings. Recent technological advancements have enabled the evaluation of the depth of wounds, and three-dimensional measurements are now available. The aim of this study was to test the utility of a newly developed three-dimensional wound measurement device in the clinical setting. Methods: We recruited three patients, each with a PU, who were being treated by a PU team at a university hospital. We measured the length, width, area, and maximal depth of the ulcers by using the device and with the conventional method. The ulcer volume was measured only with the device. The difference in measurement results of the device before and after debridement was compared in the first patient. The difference in measurement results between the conventional method and the device was compared in the second patient. Correlation coefficients between the conventional method and the device obtained from longitudinal data were calculated in the third patient. Results: The changes in measurements between before and after debridement were easily detected by the device in the first patient. Although the maximal depth was different, the length, width, and area were consistent between the conventional method and the device in the second patient. The correlation coefficients of the length, width, and area between the conventional method and the device were 0.35, 0.48, and 0.59, respectively, in the third patient whose PU exhibited a vague wound edge. Conclusion: Although two-dimensional measurements were comparable between the conventional method and the device, there were some challenges to performing three-dimensional measurement more precisely. A further study is needed to determine the specific characteristics of wounds that result in poor measurement accuracy.
Incontinence‐associated dermatitis (IAD) is caused by prolonged exposure to urine/liquid stool. It is a common and often painful skin condition in older incontinent adults because of poor prevention. Patients with urinary infections are at risk of developing IAD, and to guide the development of novel prevention strategies, we aimed to develop an animal model of IAD by urine and bacteria. First, contralateral sites on the dorsal skin of Sprague–Dawley rats were compromised by sodium lauryl sulphate (SLS), simulating frequent cleansing with soap/water. Filter discs were then placed inside ring‐shaped chambers on foam dressings, inoculated with or without Pseudomonas aeruginosa, covered with agarose gels immersed in cultured filtrated urine, and secured in place with an occlusive dressing for 3 days. Untreated and SLS‐compromised sites served as controls. The IAD was developed at bacteria‐inoculated sites, characterised by severe IAD‐like redness that persisted for up to 3 days post‐exposure and higher disruption of the skin barrier function compared with non‐inoculated sites. Pathological changes included epidermal thickening, partial skin loss, inflammatory cell infiltration, accumulation of red blood cells, and invasion of bacteria into the epidermis. This novel, clinically relevant IAD rat model can serve for future prevention developments.
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