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can also lead to direct tissue damage, death, and ulceration."

Venous stasis ulcers, described in Table 7-11, are frequently

present on the medial malleolus, where the long saphenous vein is

most superficial and has its greatest curvature. Venous ulcers may be

present on the foot or above the midcalf but are more likely to have

another primary etiology, such as trauma or infection. The leakage of

red blood cells over time results in the deposit of hemosiderin and

stimulated melanin, causing the characteristic hyperpigmenration

around the medial ankle. Other characteristics include a thin skin surface with a loss of hair follicles and sweat glands]4

Pressure Wounds

A pressure ulcer, sometimes referred to as a decubitus ulcer, is caused by

ischemia that develops as a result of sustained pressure in excess of capillary pressure on the tissue. The pressure usually originates from prolonged weight bearing on a bony prominence, causing internal ischemia at the point of contact. This initial point of pressure is where tissue

death first occurs. The tissue continues ro necrotize externally until a

wound is created at the skin surface. By this time, there is significant

internal tissue damage. Superficial tissue ulceration can be caused by

the effect of mechanical forces acting on localized areas of skin and

subcutaneous tissue, whether the forces are of low intensity over long

periods or are higher forces applied intennittently.J6.J7 The relationships between the amount of force applied, the duration of force, and the direction of the force contribute to the occurrence and severity of a

pressure ulcer. Not only can direct pressure create tissue ischemia, but

friction and shearing forces contribute as weI1.36-J8.40.41 Refer to Wound

Staging and Classification for the pressure ulcer grading system.

BURNS AND WOUNDS

471

All bed- or chair-bound individuals or any individuals who have an

impaired abiliry ro reposition themselves or weighr shifr are ar risk of

developing pressure ulcers. Common pressure ulcer sires include rhe

back of rhe head, rhe scapular spines, spinous processes, elbows,

sacrum, and heels when a parient is laying in supine. While side-lying,

a patient may experience increased pressure at the ear, acromion process, rib, iliac crest, greater trochanter, medial and lateral condyles, and rhe malleoli.38•39 A person's body weighr also plays a role in pressure ulcer development. A person who is tOO thin has more prominent bony prominences, whereas a person who is overweight has increased

pressure on weight-bearing surfaces.J9-41

Neuropathic or Neurotropic Ulcers

A /lel/ropathic or /lel/rotropic ulcer (see Table 7-11) is a secondary

complication that occurs from a triad of disorders, including peripheral vascular disease, peripheral neuropathy, and infection.42 Neuropathic ulcers are most commonly associated with diabetes. The development of ulcers and foot injuries are the leading causes of

lower-extremity amputation in people with diabetes·3 Additionally,

there is an increased incidence of atherosclerosis, which appears earlier and progresses more rapidly than in patients without diabetes.

However, many people with diaberes who develop foot ulcers have

palpable pulses and adequate peripheral blood flow."

Individuals with diabetes may also have changes in the mechanical

properties of the skin. Insulin is essential for fibroblastic and collagen

synthesis. A lack of insulin in type 1 diabetes can lead ro diminished

collagen synthesis that can cause stiffness and poor tensile strength of

tissue, both of which increase the suscepribility of wound development and decrease healing potential.'s

The peripheral and central nervous systems can be adversely

affected in diabetes. Peripheral neuropathy is common, and sensation

and strength can be impaired. Diminished light rouch, propriocep·

tion, and temperarure and pain perception decrease the ability of the

person with diabetes ro identify areas that are being subjecred ro

trauma, shearing forces, excessive pressure, and warm temperatures,

all of which can cause ulcers.' ..... •

Structural deformities can occur as the result of the neuropathies

that may be present secondary to diabetes. Any structural deformities, sllch as "hammer toes" or excessive pronation or supination, can create pressure points that lead to ischemia and a subsequent

ulcer.46-48

472

AClfTE CARE. HANDBOOK FOR PHYSICAL THERAPISTS

Excessive plantar callus formation may form at the sites of increased

pressure and in itself can increase the pressure to the affected area.44

The minor repetitive ischemia that occurs every time the person bears

weight on the pressure points in the tissue underlying the callus can

eventually cause the tissue to fail, and ulceration occurs.48

Peripheral mOtor neuropathy contributes to the development of an

equinus contracture at the ankle as stronger plantarflexors overcome

the weaker dorsiAexors. Weakness of the small intrinsic muscles of

the foot causes clawing of the toes. These foot deformities lead to

increased weight distribution through the forefoot and increased pressure under the metatarsal heads. The abnormal mechanical forces and intermittent forces can stimulate callus formation.44

A neuropathy of the autonomic nervous system is present in the

majority of individuals with diabetes and neuropathic ulcers. The

autonomic nervous system regulates skin perspiration and blood

flow to the microvascular system. Lack of sweat production contributes to the development of a callus. Altered cross-linkage between collagen and keratin results in predisposal to hyperkeratosis and callus formation. Beneath the callus, a cavity often forms as a response to the increased pressure and shear forces and fills with serous Auid,

causing a seroma. If the deep skin fissure comes in contact with an

underlying seroma, it can become colonized with bacteria and result

in ulcer formation.44

The immune system is also affected by elevated glucose levels and

their resultant problems. Edematous tissues and decreased vascularity,

which contribute to lack of blood Aow, decrease the body's abiliry to

fight infection because of its inability to deliver oxygen, nutrients, and

antibiotics to the area.49-SS

Although neuropathic ulcers are most often associated with diabetes, they may also occur in individuals with spina bifida, neurologic diseases, muscular degenerative disease, alcoholism, and tertiary

syphilis because of similar risk factors in these populations.JJ

Process of Wound Healing

Epidermal wounds heal by re-epithelialization. Within 24-48 hours

after an injury, new epithelial cells proliferate and mature. Deeper

wounds, which involve the dermal tissues and even muscle, go through

a rather complex and lengthy sequence of (1) an inAammatory

response, (2) a fibroplastic phase, and (3) a remodeling phasc.J7-41

BURNS AND WOUNDS

473

In the inflammatory phase, platelets aggregate and clOts form. leukocytes, followed by macrophages, migrate to the area, and phagocytosis begins. Macrophages also provide amino acids and sugars that are needed for wound repair. In preparing the wound for healing, they

stimulate the fibroplastic phase. During the fibroplastic phase, granulation begins. Granulation is indicative of capillary buds, growing into the wound bed. Concurrently, fibrocytes and other undifferentiated cells multiply and migrate to the area. These cells network to transform into fibroblasts, which begin to secrete strands of collagen,

forming immature pink scar tissue. In the remodeling phase, scar tissue marures. New scar rissue is characterized by its pink color, as ir is composed of white collagen fibers and a large number of capillaries.

The amount of time the entire healing process takes depends on the

size and type of wound. It may take from 3 days to several months or

more for complete closure to occur,49-5S

Factors That Can Delay Wound Healing

In addition to the problems indigenous to the wound, many other factors can delay wound healing. Age, lifestyle, nutrition, cognitive and self-care ability, vascular Status, medical complications, and medications all can affect wound healing. These factors may also be risk factors for the development of new wounds. These factors should therefore be included in the physical therapy assessment and considered when determining goals, intervenrions, and time frames.