Cath Lab Digest

History

Seventy-seven-year-old Ms. G was admitted to Manor Oak Life Center, Buffalo, NY, on July 24, 2000 with a diagnosis of sacral pressure ulcer, anemia, reflex sympathetic dystrophy, hypertension, and fractured left forearm. She had fallen at home and remained in a decubitus position for a prolonged period until she was hospitalized June 15, 2000 through July 24, 2000. The acute injuries were treated (including surgical debridement of the Stage IV pressure ulcer) in the hospital through July 24 by her attending physician and various consulting specialists.

When she was admitted to the Life Center, Ms. G was ambulating with a walker and assistance for short distances. She was able to understand and comply with instructions and wanted to return home as quickly as possible. A single mother of an adult mentally retarded son, she was concerned because her son had required social service intervention for temporary placement when she was hospitalized and he would continue to require placement until her return home. These circumstances and the location of the wound dictated that the wound be completely healed before she returned home.

Wound Description

A sacral pressure ulcer was located 9.0-cm superior and slightly lateral to the anus over the sacral base. On July 24, the wound measured 3.0 cm x 4.0 cm x 3.0 cm. Undermining of 1.0 cm to 3.0 cm was present on the inferior margins from 9 o'clock to 3 o'clock, which rendered a thick (4.0 mm) epibole (rolled edges) (see Figure 1). The wound bed was pale with a ceiling of yellow hydrated fibrous tissue. The peripheral margins were hyperpigmented and indurated. A scant amount of sanguineous drainage was noted and no signs of infection were observed. Ms. G did not complain of pain at the time of examination, yet was perceptive to tactile stimulation.

Diagnosis

The sacral pressure ulcer was classified as Stage IV, using the National Pressure Ulcer Advisory Panel (NPUAP) staging system, where a Stage IV pressure ulcer is defined as a full-thickness skin loss with extensive destruction, tissue necrosis or damage to the muscle, bone, or supporting structures (ie, tendon, joint capsule).

Epibole, also clinically referred to as rolled-over edges, is often seen in chronic wounds with poor healing dynamics, especially inadequate granulation.¹ The migrating front of epithelial cells is unable to cover the cavity so they descend down and curl under at the edges. Wound edges that roll over will ultimately cease in migration secondary to contact inhibition once epithelial cells of the leading edge come in contact with other epithelial cells. Continued tissue trauma will result in thickening, rolling inward of the epidermis, fibrosis, and scarring.

In a case where reepithelialization has ceased, "knocking down the edges" may be necessary so the normal process of epithelialization can continue once the proliferation phase (granulation) of repair has caught up. Various methods are used clinically to reduce the edges, including the application of chemical pharmaceuticals (ie, silver nitrate) and sharp and surgical debridement. Each method poses a risk of inflammation, setback, and infection.