Venous Leg Ulcer Pain

Author(s): 
Siobhan Ryan, MD, FRCPC (Derm); Cathy Eager, RN, CWOCN, CWS; and R. Gary Sibbald, MD, FRCPC (Med)(Derm)

Treat the Cause
Venous disease may progress to ulcer formation. Ulcers are often serpiginous and seen around the ankle or lower calf region (gaiter area). Lipodermatosclerosis often precedes the development of venous ulcers but is not always present. Venous leg ulcers are the most common cause of all leg ulcers and increase in frequency with advancing age of the patient.1 The typical venous leg ulcer occurs around the medial aspect of the ankle or lower leg and is often shallow with irregular borders presenting on a background of skin changes related to chronic venous stasis.
Historically, venous ulcers have been considered to be relatively pain free. However, it is now known that a significant number of patients with venous ulcers will experience pain that has an impact on their quality of life (see Table 1).2-8 This pain may be constant or intermittent with procedures or dressing change. Evaluation of the location, frequency, and other factors associated with the pain are essential in the assessment and management of patients with venous disease. The clinician should keep in mind that patients may experience pain in the absence of an ulcer and may continue to have prolonged pain once an ulcer has healed.
Venous disease is a spectrum of changes that slowly evolve over time with a variety of associated pain symptoms ranging from discomfort and aching to deep, chronic pain. Acute, disabling pain may develop with each stage and will impact the plan of care for the patient (see Figure 1).
The management of pain is dependant on the diagnosis of the pain source (see Table 2). Clinically, dependent edema and a dilated saphenous vein are the early signs of venous disease. Patients with pitting edema and prominent varicose veins often will describe a dull aching or heaviness in their legs that progresses toward the end of the day or after prolonged periods of standing. Support stockings, ambulation, and leg elevation while sitting will often relieve these symptoms. Attention also should focus on other factors contributing to venous stasis disease such as obesity, sedentary life style, and other comorbid illnesses.
Assessment of the status of venous disease to determine the extent of venous incompetence or venous obstruction can be performed at the bedside or in a vascular laboratory. Measurement of the ankle brachial index (ABI) by Doppler is important to determine co-existing arterial disease. Use of inappropriate compression bandaging in a patient with arterial insufficiency may lead to worsening of the ulcer and more serious complications. Ulcers related to peripheral vascular insufficiency have always been considered quite painful, but this feature alone is not adequate to differentiate between an ulcer of venous stasis etiology and vascular insufficiency.
Lipodermatosclerosis. Long standing pitting edema leads to pigmentary changes on the distal one-third to one-half of each leg. This pigmentary change is related to deposition of hemosiderin from extravasated red blood cells and stimulated melanin. This change presents as reddish brown to dark brown nonpalpable discoloration that may initially be somewhat speckled and chronically becomes confluent and circumferential. Over time, this pigmented area becomes sclerotic, due to the leakage of fibrin, with a deep dermal fibrosis that may extend from the ankle to mid-way up the leg. It is often described as resembling an inverted "champagne bottle," as the upper one half of the leg remains edematous and has a much greater circumference than the lower sclerotic portion. Edema, sclerosis, and pigmentation together make the diagnosis of lipodermatosclerosis.
These clinical changes on the lower legs represent long-standing venous stasis and will vary in degree from patient to patient. The visible changes present do not always correlate with the degree of pain the patient feels.

References: 

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