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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.