Abstract: Vascular disease is a known risk factor for pressure ulcer development, but the underlying mechanisms of this association are less established. The authors evaluated the relationship between endothelial function (EF) and history of pressure ulcers in a nested case-control study of community-dwelling elderly, 60 years and older. Endothelial function was measured using peripheral arterial tonometry, and persons with a history of pressure ulcers in the past 5 years (n = 7) were matched 2:1 by age and gender to controls with no history of pressure ulcers (n = 14). Overall endothelial function was significantly worse in persons with pressure ulcers compared to controls (1.32 versus 1.76, respectively; P = 0.04), and the prevalence of endothelial dysfunction was higher among cases than controls as well (100% versus 43%, respectively; P = 0.04). Other vascular risk factors were similar in both groups. Endothelial dysfunction appears to be associated with pressure ulcer history and may reflect an underlying vascular etiology through which ulcer risk is mediated.

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Paul Takahashi, MD
Mayo Clinic
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     Some theories on the etiology of pressure ulcers suggest pressure induced anoxia and relative ischemia to the skin as a vascular cause for elevated risk of incident pressure ulcers or nonhealing wounds.¹ Endothelial dysfunction (ED) is defined as an inappropriate vasodilatory response of the vessels in the face of physiologic or pharmacologic stress, and ED has been associated with cardiovascular and cerebrovascular disease as well as cognitive impairment.² However, a role for ED in the development of pressure ulcers or pressure ulcer healing is not well examined. Small studies involving diabetic foot ulcers did not show differences in healing in those patients with presumed ED (diabetics) versus controls.³ There are no reports in the literature of an association of ED with pressure ulcers. The primary objective of this study was to evaluate the association between vascular endothelial function and development of pressure ulcers in healthy subjects more than 60 years old.

Methods

     This was a nested, case-control study undertaken within a longitudinal cohort study of endothelial function among an ambulatory community dwelling cohort of cognitively intact persons age 60 and older (n = 612). The study and the informed consent form were reviewed and approved by the local Institutional Review Board. Cases were defined as cohort members with a history of incident pressure ulcers within the 5 years preceding EF testing, as determined by a medical records review utilizing the Mayo Clinic medical records linkage system.⁴ Cases were matched by age (± 3 years) and gender in a 2:1 ratio to control cohort members without a history of pressure ulcers within the same period. Endothelial function was measured via peripheral arterial tonometry ([PAT], EndoPAT-2000, Itamar Medical, Framingham, MA) by a trained study coordinator blinded to the study hypotheses and using a standardized protocol. Medical records were abstracted by trained, blinded personnel for conventional vascular and ulcer risk factors including age (years), gender, weight (kg), systolic and diastolic blood pressure (mmHg), history of coronary artery disease (CAD), hypertension (HTN), stroke, and tobacco use (current or previous).