Chronic Wounds: Palliative Management for the Frail Population—PART II

Oscar M. Alvarez, PhD;1 Marge Meehan, RN, MIM;2 William Ennis, DO;3 David R. Thomas, MD, FACP;4 Frank D. Ferris, MD;5 Karen Lou Kennedy, RN, CS, FNP;6 Roisin Rogers, RN, MSN, CWCN;7 Marianne Bradley, RN, MS, CWOCN;8 Judith J. Baker, PhD;9 Adolfo Fernandez-Obregon, MD;10 George Rodeheaver, PhD;11

Venous ulcers. Definition. The venous system returns blood to the cardiopulmonary system. Injury as well as disease can prevent veins from effectively performing this job. There are four major disruptive mechanisms that prevent the vascular system from performing optimally: thrombus, embolism, dilation or varicosity, and hemorrhage.

Microcirculatory changes associated with chronic ulcers, diabetes, and repeated bouts of previous vessel damage lead to fibrin cuffs, causing a stained ring around the gator or ankle region of the lower extremity. The fibrin cuff is seen histologically around dermal vessels, which result in impaired cutaneous nutrition and, ultimately, ulceration.22 The action of neutrophils adhering to tissue damaged by ambulatory venous hypertension releases highly reactive substances generating free radicals and subsequent tissue injury.23

The degree to which any of these mechanisms lead to significant dysfunction or resultant ulceration depends mostly on the location of the involved vein. Obstruction of superficial veins rarely cause serious problems. However, if deep veins become occluded or obstructed, major peripheral problems can result.24

Once the venous system is impaired in its ability to return blood to the cardiopulmonary system, skin and subcutaneous tissues near the involved vein(s) are no longer receiving adequate oxygenation and nutrition. While it is widely accepted that venous insufficiency ulcers can result, the exact mechanism by which oxygenation and nutrition becomes compromised remains a constant debate.

Venous ulcers account for 90 percent of all chronic wounds found on the lower leg.25 The exact incidence among immobile patients, the population that is most likely to be frail, is unknown. Epidemiological studies from Western Australia suggest a prevalence of 0.62 per 1000 individuals with 90 percent of patients being 60 years or older. This group comprises 16.7 percent of the population with a relative prevalence of 3.3 per 1000 persons.26

Immobile patients offer a therapeutic challenge most notably because of their debilitated states and predictable recurrences of their ulcers. Although the pathophysiology of venous ulcers has been widely studied, the exact mechanisms that cause venous ulceration is the subject of widespread speculation. Gay27 and Homans28 made a connection between deep vein damage and ulceration. Under normal ambulatory conditions, the calf muscles serve to pump the blood back up to the heart. Without adequate use of calf muscles, blood that collects in the saphenous venous system and its tributaries cannot make its way swiftly to the deep veins to be compressed by the action of musculofascial compartment to make its way back up to the heart. The absence of competent one-way valves shifts the high venous pressure generated from the calf muscle contraction to the cutaneous vasculature. This all leads to chronic venous hypertension.29–31

Assessment. Physical evaluation of a patient with a chronic lower-extremity ulcer in which a vascular etiology is suspected begins with the same documentation of a comprehensive clinical history as is done to work up any chronic wound. For the frail patient, who probably has some degree of significant activity limitation, the examination becomes somewhat more complex. The frail patient requires a complete evaluation of clinical history, which must sometimes be obtained from family members, past physicians, and nursing staff responsible for the care of the patient. Aside from inquiring about possible causal trauma, which is not always readily recalled, many other areas deserve investigation.

It is also important to note the use of medications that may impair wound healing. Sensitizers like ethylene diamine, neomycin, and lanolin, among others, can produce a contact dermatitis.


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