Identifying, managing and preventing skin maceration: a rapid review of the clinical evidence.

OBJECTIVE: To identify the clinical empirical evidence for identifying, managing and preventing skin maceration in human subjects. METHOD: A rapid review of the current literature was undertaken between 5 September and 19 September 2016 using the electronic databases CINAHL, MEDLINE, PUBMED and Cochrane, with the key words: skin macerat*, wound macerat*, moisture associated skin damage, wound exudate and hyper-hydration of skin, Results: Of 526 papers found using an electronic database search, four were identified as fitting the search parameters, and a further two were retrieved from a manual search of reference lists. There were three themes that emerged: how to identify and measure maceration, how to manage and reduce maceration once it has already occurred, and how to prevent skin maceration. Hyper-hydration can reach greater skin depths than previously thought, thus engendering more extensive damage potential, which in turn can impact on treatments and healing time. Realistically, the deeper the hyper-hydration issue, the more extensive the damage and it will take longer to recover-a problem compounded if the hyper-hydration is due to incontinence and skin is also exposed to urine and/or faeces. In relation to wound management, the authors advocate the removal of moisture away from the wound or skin, either through superabsorbent dressings, or by allowing the excess moisture to evaporate through semi-permeable dressings to reduce maceration, enhance patient comfort and encourage healing. However, we found no evidence regarding the limits of hydration of the dermis and epidermis and thereby the optimal conditions for managing exuding wounds and promoting skin health. Each of the six papers in this review calls for further research to help identify, treat and prevent maceration. CONCLUSION: Maceration causes patients' discomfort and pain as well as prolonging healing time and deserves more focused research. This rapid review highlights how limited the clinical empirical research is on identifying and managing skin maceration from an early stage so that health professionals may be better equipped to prevent it. Further clinical research is also needed to determine when levels of hydration in the skin become damaging. The small number of studies within this review show that skin maceration can be avoided, but clearer guidance is needed.

Bullous pemphigoid induced by cephalexin.

Two young men developed severe bullous eruptions with a distinctive clinical picture of severe flexural involvement and extensive mucosal ulceration. Biopsies showed subepidermal bullae and associated inflammation consisted of predominantly neutrophils. Both had IgG and C3 staining of the dermal-epidermal junction on direct immunofluorescence. Bullous pemphigoid was diagnosed on the basis of clinical, histopathological and immunofluorescence findings. Both cases occurred after recent ingestion of cephalexin. We believe they represent the first reported cases of bullous pemphigoid induced by cephalexin.

Salmeterol tachyphylaxis in steroid treated asthmatic subjects.

BACKGROUND: Tachyphylaxis to the protection afforded by salmeterol to broncho-constrictor stimuli after regular use has been described in patients with mild asthma not receiving inhaled corticosteroids. The present study was performed to investigate whether airway tachyphylaxis occurs in symptomatic asthmatic subjects receiving inhaled corticosteroids, the group for whom salmeterol is recommended in clinical practice. METHODS: Thirty one adult patients with symptomatic chronic asthma who were receiving inhaled corticosteroids were randomised in a double blind manner and on a 2:1 basis to receive salmeterol 50 micrograms (n = 22) or placebo (n = 9) twice daily. Baseline forced expiratory volume in one second (FEV1) was measured during the run-in period, on day 0, and after four and eight weeks of regular treatment (following a 36 hour test drug washout period). Airway responsiveness to methacholine was measured one hour after administration of the test drug on these occasions. Diary cards were kept throughout the study and for a two week follow up period. RESULTS: Baseline FEV1 was not significantly different between the treatment groups or between visits. There was significant bronchodilatation one hour after salmeterol administration at 0, four, and eight weeks. No significant tachyphylaxis of the bronchodilator action of salmeterol was seen. Protection against methacholine induced bronchoconstriction reduced from 3.3 doubling dilutions after the first dose of salmeterol to two doubling dilutions after four and eight weeks of regular treatment. Symptom scores and "rescue" salbutamol use were significantly reduced during salmeterol treatment and daytime improvements were maintained into the follow up period. CONCLUSIONS: Inhaled corticosteroids did not prevent tachyphylaxis to the protection afforded by salmeterol to methacholine induced bronchoconstriction. The clinical significance, if any, of these findings remains to be defined.

Dehydration deaths in infants and young children.

Dehydration in developed countries is an uncommon but important mechanism resulting in the death of infants and children. The clinicopathological features of a series of 37 fatal dehydration cases autopsied at the Adelaide Children's Hospital over a 33-year period (1961-1993) are presented. Causative factors for dehydration included gastroenteritis (21 cases), gastroenteritis with high environmental temperature (one case), high environmental temperatures (six cases), neglect/failure to thrive (four cases), mental retardation/chromosomal abnormality (three cases), congenital adrenal hyperplasia (one case), and unsuspected cystic fibrosis (one case). The mean age at death was 11.4 months (range 2 weeks to 6.25 years; median 6 months; 95% confidence interval 6 months to 1 year and 4 months; male-to-female ratio, 19:18). Sixteen of the 22 cases of fatal gastroenteritis (73%) occurred during the fall/winter months (March to August). There were a total of seven aboriginal or part aboriginal children in the group (19%). Children with mental retardation were at higher risk of dehydration, and previously unsuspected cases of child abuse/neglect also presented with lethal dehydration. Vitreous humor electrolyte levels and immunoassay for rotavirus were useful diagnostic adjuncts.

Ploidy studies in adenomatous polyps of the colon.

The nuclei of colonic adenomatous polyps and some colonic carcinomas have a normal diploid profile. The remaining carcinomas are aneuploid, and this change most probably occurs after the dysplasia that determines invasiveness, because even adenomatous polyps with carcinoma in situ are diploid.

An intestinal cell-mediated chromosome aberration test for the detection of genotoxic agents.

The use of rat-liver S9 in genotoxicity tests may not reflect true metabolism by whole cells, particularly cells of target organs. We have tested mucosal cells of the mouse small intestine for the capacity to mediate activation/inactivation of chemical carcinogens. Mucosal cells were isolated by pronase digestion. Three million cells were co-cultured with Chinese hamster ovary fibroblasts during a 3-h exposure to chemical clastogens. In the presence of the mucosal cells, aflatoxin B1 (100 microM) was activated to produce chromosome aberrations in 30% of Chinese hamster ovary cell metaphases. 4-Nitroquinoline 1-oxide was deactivated by intestinal cells, while benzo[a]pyrene and dimethylbenz[a]anthracene were not activated by the cells. The clastogenicity of the phenolic compounds caffeic acid (0.28 mg/ml) and clorogenic acid (0.25 mg/ml) was eliminated by the mouse intestinal preparation. The pyrrolizidine alkaloid monocrotaline was activated by intestinal cells. The results suggest the presence of specific activation and deactivation enzymes in the intestinal mucosa. The intestine cell-mediated chromosome aberration test could provide a means to measure tissue-specific activation and deactivation capabilities.

Lesion detection with single-photon emission computed tomography (SPECT) compared with conventional imaging.

We have evaluated analytically and experimentally the effectiveness of both conventional nuclear medicine imaging and single-photon emission computed tomography (SPECT) imaging to detect small photon-deficient areas (approximately the size of the system's resolution) with a relatively uniform background. The experimental model is based on the Tc-99m sulfur colloid study of the liver. The experimental data were obtained from a liver phantom containing two small photon deficient areas, nominally 1 and 1.5 cm in diameter. The liver phantom was placed in a water-filled Alderson body phantom and scanned with the cold defects located both centrally and peripherally. Lesion image contrast for both conventional and SPECT imaging is proportional to the lesion uptake ratio and is degraded by the system's finite spatial resolution and Compton-scattered photons. However, for conventional imaging the contrast is significantly degraded by the effect of radionuclide superposition (as modified by attenuation), while for SPECT imaging the contrast is essentially independent of these effects. This results in a significant increase in lesion-to-background contrast with SPECT as compared with conventional imaging. The measured SPECT image contrasts for the 1- and 1.5-cm areas of low uptake averaged more than five times the measured image contrasts for the conventional system.

Mouse alcohol dehydrogenase isozymes: products of closely localized duplicate genes exhibiting divergent kinetic properties.

Electrophoretic variants for the stomach isozyme (ADH-C2) and liver isozyme (ADH-A2) of alcohol dehydrogenase in strains of Mus musculus have been used in genetic analyses to demonstrate close linkage between the structural genes (Ahd-3 and Adh-1, respectively) encoding these enzymes. No recombinants were observed between these loci among 126 backcross animals, which places them less than 0.8 centimorgans apart. Previous studies have positioned Adh-3, and a temporal locus (ADh-3t), on chromosome 3 (Holmes, "79; Holmes et al., "80). Kinetic analyses on partially purified preparations of these isozymes have demonstrated widely divergent catalytic properties and inhibitor specificities. The liver isozyme exhibited Michaelis constants that were nearly 3 orders of magnitude lower than the stomach isozyme for various alcohol and aldehyde substrates. Moreover, aminopropyl pyrazole strongly inhibited ADH-A2 (Ki=1.2M), whereas ADH-C2 was insensitive to inhibition under the conditions used. It is proposed that Adh-1 and Adh-3 are products of a recent gene duplication event during mammalian evolution and that considerable divergence in the active sites of these enzymes and the "temporal" genes controlling loci expression in differentiated tissues has subsequently occurred.

Semliki Forest virus does not inhibit phosphatidylcholine biosynthesis in BHK-21 cells.

The mechanism by which Semliki Forest virus inhibits the incorporation of [methyl-3H]choline into phosphatidylcholine has been investigated. Decreased labeling of the lipid was not due to altered uptake of [methyl-3H]choline. The specific activities of choline kinase and CTP:phosphocholine cytidylyltransferase were unchanged. The previously observed inhibition (Vance, D. E. & Burke, D. C. (1974) Eur. J. Biochem. 43, 327-336) of CDP-choline:1,2-diacylglycerol phosphocholinetransferase was confirmed. Since the decreased activity of the phosphocholinetransferase may not have caused the reduced labeling of phosphatidylcholine, the amounts of this lipid and its precursors were measured. We observed changes in the concentration of phosphocholine (34 +/- 12 and 120 +/- 40 nmol x g cells-1 in mock- and virus-infected cells, respectively) and CTP (116 +/- 35 and 36 +/- 13 nmol x g cells-1 in mock- and virus-infected cells, respectively). Pulse-chase studies with [methyl-3H]choline demonstrated that, initially, most of the radioactivity was in phosphocholine. As it disappeared from this compound, it appeared in phosphatidylcholine. From these results, we calculated the rate of phosphatidylcholine biosynthesis to be 0.56 and 1.23 nmol x min-1 x g cells-1 in mock- and virus-infected BHK-21 cells, respectively. We conclude that phosphatidylcholine biosynthesis is not inhibited in Semliki Forest virus infected BHK cells, but rather is stimulated 6.75 h after infection. The decreased labeling observed during pulse studies with [methyl-3H]choline is due to dilution of the labeled choline into a pool of phosphocholine which is 3.5 times larger in the infected cells.