Are your pressure injury numbers high? This may be an indication that you should check to ensure the wounds being coded as pressure injuries are truly pressure injuries. Here is what you need to know.
Wounds from moisture-associated skin damage (MASD), friction, arterial insufficiency, venous insufficiency, peripheral neuropathy, and diabetes are commonly mistaken for pressure injuries. While identifying the proper etiology of the wound is important for coding and tracking purposes, it is even more important as the driver of management and prognosis. Unless the underlying etiology is addressed or reversed, the wound will not heal. If the wound is from pressure, the pressure must be minimized or removed; or if the wound is from edema in the lower extremity, the edema must be relieved.
The Proper Identification Process
The proper way to identify a pressure injury is to review the National Pressure Ulcer Advisory Panel’s (NPUAP) and the RAI User’s Manual definition of a pressure injury. The NPUAP explains that the primary cause of a pressure injury is intense and/or prolonged pressure. Essentially, due to pressure, the circulation to the tissue becomes limited or cut off, leading to tissue breakdown and tissue death. Pressure injuries are typically over bony prominences because there are two sources of pressure on the tissue: internal pressure from the bone and external pressure from the support surface. Thus the tissue becomes compressed between the bony prominence and the support surface. However, any medical or other device can cause pressure injuries in locations other than bony prominences. A pressure injury will generally mimic the shape of the device. In simple terms, the RAI User’s Manual states, “A pressure ulcer is localized injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure, or pressure in combination with shear and/or friction.
Common Causes of Pressure Injuries
As the RAI User’s Manual and NPUAP definition indicates, pressure injury can also be caused by shearing forces in combination with pressure. Shearing forces are caused when the skin stays in one position due to pressure and the bones and underlying tissue roll in the opposite direction. Shearing can happen when a resident slides down in the bed or wheelchair or when a staff member drags a resident into a position without lifting the resident off the surface first. By causing trauma and cutting off the blood supply, shearing forces can lead to rapid tissue breakdown. Two characteristics identify shearing forces as having contributed to the pressure injury: undermining and/or irregular wound edges. Undermining is the shelf-like effect at the wound edge when the skin is not anchored down to the underlying tissue, causing a shelf-like gap between the skin and underlying tissue. If the wound edges are irregular or elongated in shape, shearing forces have contributed to the development of the wound, as pressure injuries mimic the shape of the underlying bone or source of pressure.
If the skin breakdown is secondary to friction or moisture, it is not considered a pressure injury. Skin breakdown from friction involves only the top layer of skin and is thus very superficial. A friction injury is not considered a pressure injury, as there is very little to no pressure involved. Skin breakdown secondary to moisture will have irregular edges, cover a large area of skin, be superficial, and look raw and irritated. However, both friction and moisture can lead to pressure injuries. If the area receiving the friction starts to have more pressure it can turn into a shearing force and lead to a pressure injury. Skin that is compromised secondary to moisture can be more sensitive to pressure, leading to a pressure injury within the MASD area.
If the resident has wounds on the lower extremity and/or feet, evaluate for vascular and/or neuropathic causes rather than pressure. While pressure can exacerbate and contribute to the breakdown of vascular or neuropathic ulcers, it should not be considered the etiology. As with pressure injuries, the vascular or neuropathic wound’s underlying etiology must be addressed for prognosis and proper management. Unfortunately, many times the vascular compromise or neuropathy cannot be reversed, thus leading to non-healing, chronic, or declining ulcers.
If the wound on the lower extremity is anywhere on the calf of the leg, including the posterior calf and/or superior to the medial malleolus in the gaiter/sock area, the skin breakdown is typically secondary to venous insufficiency. The calf may have pitting or non-pitting edema, hemosiderosis (brown) staining, venous dermatitis (erythema, itching, vesicles, weeping, scaling, crusting), tinea pedis (fungal infection), varicose veins, lipodermatosclerosis (increased pigmentation and hardening of the skin), atrophie blanche (small white scarred areas), or maceration. A venous wound typically starts out superficially, with irregular wound margins, a wound base that is usually ruddy red and yellow adherent or with loose slough present, and moderate to heavy exudate. Residents with venous insufficiency are also prone to cellulitis.
If the wound is on the mid-tibial area (shin), lateral malleolus, phalangeal heads of the toes, toe tips, or web spaces, the wound is typically secondary to arterial insufficiency. Severe arterial insufficiency can cause necrosis of the entire foot. The lower extremity may have pallor on elevation; dependent rubor; purpura (small hemorrhagic spots); shiny, taut, thin, dry, hairless skin; atrophy of the skin, subcutaneous tissue, and muscle; skin that is cold to the touch; and/or dystrophic toenails. Pedal and/or posterior tibial pulses might be diminished or absent. Capillary refill is abnormal (more than three seconds). The resident might also report cramping of the calves when lying in bed or when ambulating or exercising. Arterial wounds are typically covered with eschar. When arterial wounds are open, granulation tissue is rarely present and the wound bed will present as pale, smooth, and dry.
If the wound is on the plantar aspect of the foot, metatarsal head, dorsal and distal aspects of the toes, inter-digital areas, inter-phalangeal joints, heels, or altered pressure points on the foot that have had painless trauma or repetitive stress, the wound is typically secondary to peripheral neuropathy. Neuropathy is the loss of innervation to the foot. Thus the muscles in the foot atrophy, leading to shifting of the foot bones. This causes structural changes in the foot such as clubbing of the toes. The resident might report burning or shooting pain in the foot. The foot might have thick callusing, cracks, and fissures. Reflexes and sensation in the foot will be diminished or absent. The wound edges tend to be callused and/or the wound will callus over the wound bed. Neuropathy can lead to Charcot foot, a condition causing weakening of the bones in the foot, which can lead to breaks in the bones and dislocation or collapse of the joints. Charcot foot can lead to a collapsed arch, giving the bottom of the foot a “rocker bottom” appearance.
Lastly, diabetic ulcers are caused by neuropathy and/or arterial insufficiency. If the resident has a diagnosis of a diabetic foot ulcer, you will need to assess whether the diabetic wound is from neuropathy, arterial insufficiency, or a combination of both, as this will determine the course of treatment and prognosis.
Get the Code and Care Correct
Proper coding of the MDS starts with proper identification of the wound etiology. Improper identification of the etiology can lead to falsely high numbers of pressure injuries and, more important, to inappropriate treatment and management of the wound.
For permission to use or reproduce this article in full or in part, please complete a permissions form.
Meet the volunteers who review LTC Leader articles and FAQ content. They represent the best and brightest minds in LTC, and we thank them.