Issues and challenges in staging of pressure ulcers.

Wound assessment is a key element of effective wound care, and assessment of pressure ulcers includes accurate determination of wound stage. Although the original staging system established by Shea was based on his understanding of the pathology involved in pressure ulcer development, subsequent staging systems (and the one currently in use) were intended simply to establish the level of tissue damage. Recently, clinicians have drawn attention to numerous limitations associated with the current staging system, including the inability to differentiate between an inflammatory response involving intact skin and a deep tissue injury (deep bruising) underneath intact skin. This is a clinically significant difference because clinicians have noted that most inflammatory responses resolve with intervention, whereas most areas of deep tissue injury progress to full-thickness ulcers even when appropriate intervention is provided. A second area of controversy involves partial-thickness (Stage 2) lesions; because many of these lesions are caused by maceration and/or friction (as opposed to pressure) clinicians are frequently unclear regarding which of these lesions should be staged. In response to these concerns, the National Pressure Ulcer Advisory Panel convened a consensus forum and published white papers to clearly outline the issues; they solicited clinician feedback on the white papers and the Wound, Ostomy, Continence Nurses Society provided a written response. This article summarizes the key points of the white papers, WOCN Society response, and consensus forum discussion.     

The effects of household wealth on HIV prevalence in Manicaland,Zimbabwe – a prospective household census and population-based open cohort study

Introduction

Intensified poverty arising from economic decline and crisis may have contributed to reductions in HIV prevalence in Zimbabwe.

Objectives

To assess the impact of the economic decline on household wealth and prevalent HIV infection using data from a population-based open cohort.

Methods

Household wealth was estimated using data from a prospective household census in Manicaland Province (1998 to 2011). Temporal trends in summed asset ownership indices for sellable, non-sellable and all assets combined were compared for households in four socio-economic strata (small towns, agricultural estates, roadside settlements and subsistence farming areas). Multivariate logistic random-effects models were used to measure differences in individual-level associations between prevalent HIV infection and place of residence, absolute wealth group and occupation.

Results

Household mean asset scores remained similar at around 0.37 (on a scale of 0 to 1) up to 2007 but decreased to below 0.35 thereafter. Sellable assets fell substantially from 2004 while non-sellable assets continued increasing until 2008. Small-town households had the highest wealth scores but the gap to other locations decreased over time, especially for sellable assets. Concurrently, adult HIV prevalence fell from 22.3 to 14.3%. HIV prevalence was highest in better-off locations (small towns) but differed little by household wealth or occupation. Initially, HIV prevalence was elevated in women from poorer households and lower in men in professional occupations. However, most recently (2009 to 2011), men and women in the poorest households had lower HIV prevalence and men in professional occupations had similar prevalence to unemployed men.

Conclusions

The economic crisis drove more households into extreme poverty. However, HIV prevalence fell in all socio-economic locations and sub-groups, and there was limited evidence that increased poverty contributed to HIV prevalence decline.     

COPD stories of complex causal ‘truths’‘Sure I’ve smoked all my life/but I also put in 37 years at the mine’

Aims and objectives. Secondary analysis was conducted to interpret the causes of illness stories told by patients living with chronic obstructive pulmonary disease. Background. Despite the abundance of quantitative evidence regarding the causal relationship between smoking and chronic obstructive pulmonary disease, there is limited research that provides a contextual emic understanding of chronic obstructive pulmonary disease aetiology. Design. Interview data from two earlier focused ethnography studies were examined by retrospective interpretation, a type of secondary qualitative research. Chronic obstructive pulmonary disease causation stories were identified in both primary study data bases, but were not previously systematically examined. Methods. The analysis was completed using an eclectic, explicit narrative approach that involved the examination of causation story elements. Results. Participants told 104 causal stories about the development of their lung disease. They situated the aetiology of their chronic illness within a psychosocial reality. Conclusions. The causal stories told by participants demonstrate that those living with chronic obstructive pulmonary disease present a broader causal explanation for their illness, an orientation not commonly presented in the literature. They demonstrate the need for further examination of the important lay accounts of causes of illness in relation to chronic obstructive pulmonary disease. Relevance to clinical practice. Clinicians’ ability to hear an alternative understanding may be impeded when they only listen for what they already know, ‘facts’ concerning the relationship between smoking and chronic obstructive pulmonary disease. Addressing vulnerable persons in such a manner may impede patients’ efforts to be responsible for the development of their chronic illness and individualised care.     

Exfoliated buccal mucosa cells as a source of DNA to study oxidative stress.

The extent of oxidative DNA damage is considered a biomarker of carcinogenic process and could be investigated in population studies using easily obtained cells. The oxidized DNA base adduct 8-hydroxy-2-deoxyguanosine (8-OHdG) released by enzymatic hydrolysis of DNA is commonly assayed by high performance liquid chromatography with electrochemical detection. It is expressed as a ratio of 8-OHdG to unoxidized deoxyguanosine. We modified and improved this method, determined the optimal time for harvesting buccal mucosa cells (BMC), assessed whether they mirror peripheral circulating blood cell DNA damage, and compared the anticoagulants, heparin, and EDTA for consistency in measurement of leukocyte 8-OHdG. Thirty-one healthy participants, randomized into two groups, donated BMC and blood samples. Samples were collected at baseline and either 3 or 7 days after baseline. Results showed no correlation between 8-OHdG/deoxyguanosine ratios in BMC and peripheral blood leukocytes at any time point regardless of harvest time. BMC had much higher oxidative DNA damage, but displayed a 25.6% reduction in the oxidized DNA adduct level (P < 0.04) at 3 days after baseline. Leukocytes collected in heparin and EDTA had similar 8OHdG/deoxyguanosine ratios; however, EDTA was preferred, as it produced a clean nuclear pellet without hemoglobin contamination, and the results were less variable. This improved assay shows within subject stability over time in both leukocyte and BMC DNA damage, increasing the probability that small intervention differences can be detected in healthy subjects. Buccal cells provide an accessible pool of epithelial cells that represents higher levels of DNA damage than circulating leukocytes.     

CA-125: A potential prognostic indicator in patients with cervical cancer?

We evaluated 104 patients with newly diagnosed carcinoma of the cervix. Pre- and post-therapy and followup CA-125 levels were measured in 64 patients. Fifty-five patients (86%) had squamous cell carcinoma and 9 (14%) had adenocarcinoma of the cervix. At initial presentation 19 (30%) had CA-125 levels >35 U/ml, 12 (19%) had levels of 16–35 U/ml, and 33 (51%) had levels <16 U/ml. Of the 11 patients who had pre- and post-treatment levels >35 U/ml, 10 are dead of the disease and 1 is alive with persistent or recurrent disease. Of the 20 patients with elevated CA-125 levels at presentation who reverted to normal after therapy, 19 are clinically without evidence of disease at 14–46 months (median 27 months). Of the 33 patients with normal pre- and post-therapy CA-125 levels, 31 are clinically without evidence of disease. Two of these thirty-three patients had increasing CA-125 levels during routine follow-up and both have disease recurrence confirmed. There was no apparent correlation between CA-125 level and tumor type, tumor grade, or stage of disease. Our data suggest that patients with initially elevated CA-125 levels that revert to normal after therapy have a favorable prognosis. Persistent elevation of CA-125 levels during and after therapy in patients with carcinoma of the cervix was associated with a poor prognosis.