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.

Address correspondence to:
Paul Takahashi, MD
Mayo Clinic
Department of Internal Medicine
200 First St. SW
Rochester, MN 55905
Phone: 507-284-2511
E-mail: takahashi.paul@mayo.edu

     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). Descriptive analysis documenting the demographic and medical comorbid characteristics of cases and controls was performed, and the difference in mean PAT score between cases and their matched controls was assessed utilizing a Wilcoxon matched pairs signed rank test, given the small numbers of persons per analysis group.⁵

Results

     Seven individuals (1.1% of sample) were identified with a history of pressure ulcer in the period of interest. There were no significant differences between cases and controls for basic demographic and medical comorbidities (Table 1). Average tonometry score in the cases was significantly worse (ie, lower) than in the controls (1.31 versus 1.76, respectively; P = 0.04), and all 7 cases met the PAT score criterion for ED (ie, tonometry score < 1.9), compared to 8 of 14 controls ([57%], McNemar chi-square = 4.17, degrees of freedom [df] = 1; P = 0.04).

Discussion

     The findings from this study show a potential relationship between poor EF and pressure ulcer history. A history of pressure ulcers appears to be associated with poorer EF in ambulatory elderly persons. Endothelial dysfunction has not been previously reported as a risk factor associated with pressure ulcer development. Pressure- induced vasodilation may protect against pressure-induced ischemia and potential skin breakdown. Persons with ED may possess an impaired response predisposed to ulcer development. Although the sample sizes were small, the association of EF with prevalent ulcer history was significant. However, sample size does limit the ability to evaluate interactions of ED with conventional incident ulcer risk factors or explore a multivariable approach. Additionally, as this was a community-based sample of ambulatory elderly, results within this population may not reflect other populations in whom ulcer risk is high—persons in skilled nursing facilities or those who have a spinal injury.

Conclusion

     Future work with a larger sample, including populations at high risk for ulcer development, can further elucidate the association of EF with ulcer development. Given the ability to noninvasively assess EF, and the ability to conduct the testing in NH or other non-office based practice settings, further study should look at the potential use of this patient characteristic to help predict potential pressure ulcers as well as wound healing.