Time of Onset to Changes in Skin Condition During Exposure to Synthetic Urine

Abstract

PURPOSE: The purpose of this study was to evaluate the impact of incontinence on epithelial-moisture barrier function and the subsequent risk for incontinence-associated dermatitis by exposing healthy volunteers to a premium incontinence pad wet with synthetic urine. DESIGN: Prospective, single-group study. PARTICIPANTS AND SETTING: Thirty women 65 years or older participated in the study. Participants had healthy skin of the buttocks, perineal, and perigenital areas and were not incontinent of urine or stool. The study was conducted at a contracted clinical research facility in Southeastern United States. METHODS: Four hundred milliliters of synthetic urine was distributed across the width of a premium incontinence pad with wicking technology containing a superabsorbent polymer core. Participants laid supine for a total of 4 hours, with the wet pad under the buttocks. Skin assessments were conducted at baseline prior to contact with the wet pad, at 15 minutes, 30 minutes, and 1, 2, and 4 hours after exposure to the synthetic urine. Outcome measures were skin moisture content, cutaneous pH, transepidermal water loss (TEWL), mean coefficient of friction values (static and dynamic), and tolerability evaluations (expert clinical grader–assessed erythema and participant-assessed discomfort). RESULTS: Mean moisture content of the skin increased from 46.19 ± 22.1 to 1845.28 ± 542.7 micro-Siemens (μS) after just 15 minutes of exposure and was significantly increased at all time points compared to baseline (P < .001). Cutaneous pH increased from 5.67 ± 0.5 to 6.25 ± 0.1 after 15 minutes; pH was higher at all time points compared to baseline (P < .001). Passive transfer of water through the stratum corneum (TEWL) showed an increase from 9.02 ± 2.2 g/m2/h at baseline to 16.83 ± 5.2 g/m2/h at 4 hours (P < .001). There was a significant increase from baseline to 4 hours in mean coefficient of static friction (0.32 ± 0.01 vs 0.47 ± 0.03; P < .00001) as well as mean coefficient of dynamic friction (0.29 ± 0.01 vs 0.42 ± 0.02; P < .00001). There was a significant increase in erythema and an increase in participant-assessed discomfort at all time points (P < .005). CONCLUSIONS: Our findings suggest that impairment of the skin's epithelial-moisture barrier function associated with inflammation and development of incontinence-associated dermatitis begins rapidly after an incontinence event, even with the use of a premium pad with wicking technology. Study findings also suggest that prompt attention to incontinence events is needed to prevent moisture-associated skin damage (incontinence-associated dermatitis) even when absorbent pads are used.

Establishment of incontinence‑associated dermatitis rat models and assessment of the therapeutic effects of zinc oxide, painless skin protective film and silicone dressing

“…In addition, long-term skin contact with urine or feces causes excessive moisture on the cortex to overwhelm the stratum corneum cortex structure, and exhibit excessive hydration or maceration ( 25 ). When the digestive enzymes present in the feces encounter the urea present in the urine, they are used to produce repeated cycles of chemical stimulation, leading to inflammation and decomposition of the cortex ( 9 , 26 ). In the present study, two methods were used to construct the IAD rat model.…”

“…Currently, the prevention and treatment of IAD include: i) Correcting the causes of diarrhea and incontinence; ii) reducing urine and stool irritation; iii) correct cleaning, moisturizing and skin care; iv) maintaining the skin pH; and v) regular observation and evaluation (7)(8)(9). Since the presence of high moisture and corrosive enzymes in the intestinal juice can cause destructive damage to the skin, leading to peeling and erosion of the cortex, barrier products such as petrolatum, polydimethylsiloxane and zinc oxide ointment are necessary to protect patients with IAD (10).…”

Moisture-Associated Skin Damage

“…68 Some of these areas are anterior, others are posterior, and some are bilateral. Symptoms of IAD include the sensations of itching, stinging, burning, and discomfort of the affected areas 63–65…”

“…The pathophysiology of IAD is only partially understood. Research in healthy volunteers has shown that exposure of healthy skin to synthetic urine results in inflammation within a relatively brief period of time (4 hours) 65. A study that exposed the skin of healthy volunteers to synthetic urine and stool found that both prompted the release of inflammatory cytokines (IL-1α, IL-1RA, IL-1β, TNF-α, and IL-8) and that exposure to synthetic urine was associated with a higher rise in IL-1α whereas exposure to synthetic stool was associated with a greater rise in TNF-α 69.…”

“…Research in healthy volunteers has shown that exposure of healthy skin to synthetic urine results in inflammation within a relatively brief period of time (4 hours). 65 A study that exposed the skin of healthy volunteers to synthetic urine and stool found that both prompted the release of inflammatory cytokines (IL-1α, IL-1RA, IL-1β, TNF-α, and IL-8) and that exposure to synthetic urine was associated with a higher rise in IL-1α whereas exposure to synthetic stool was associated with a greater rise in TNF-α. 69 Exposure of the skin to synthetic urine and a controlled period of occlusion have also been found to increase inflammation of the skin and permeability to environmental water and other irritants.…”