Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - 5

CLINICAL PRACTICE GUIDELINE

Introduction
Normal Skin

S

kin is the largest single organ of the body.
Its main function is to isolate and protect the
body from the environment. When the skin
barrier is broken, it is no longer impregnable to
environmental trauma. Skin also helps insulate
the body, maintaining the core temperature within
a healthy range as regulated by the autonomic
nervous system. Blood flow from the interior
of the body to a venous plexus immediately
beneath the skin is the most efficient method f
or dissipating heat from the interior of the body
to the skin surface. Cold receptors in the skin
activate reflexes to raise the body temperature,
if needed, in part by promoting vasoconstriction.
Skin consists of two layers: the epidermis
and the dermis. The epidermis is the outermost
layer, which is in a constant state of renovation,
shedding old cells and acquiring new cells that
move upward from the dermis. The dermis is a
much thicker layer where hair cells, sebaceous
and sweat glands, and nerve receptors are based;
it is dense with capillaries. The dermis consists
mainly of collagen whereas the epidermis has
no collagen.

Epidermis

Dermis

excess excretion seems to cease during the
second year after the injury, but often increases
again with the development of a pressure ulcer
(Rodriguez et al., 1989). A prospective, controlled
study of 60 men with SCI who had a history of
pressure ulcers showed an increase in the urinary
excretion of two collagen metabolites. The
metabolite characteristic of skin collagen was
preferentially increased. The time elapsed from
the start of increased excretion to the appearance
of an ulcer in the epidermis ranged from 2 to 5
months (Rodriguez and Garber, 1994).
Type I collagen has the thicker, stronger
fibrils, which are responsible for the great
tensile strength of normal skin. Type III collagen
has much thinner, weaker fibrils, with a certain
degree of elasticity. After SCI, skin biopsies
show a decrease in the proportion of type I to
type III collagen in the skin below the level of
SCI (Rodriguez and Markowski, 1995). This
proportional increase in type III collagen
contributes to the fragility of skin affected by
denervation after SCI. Skin with greater tensile
strength has a higher ratio of type I collagen
to other types (Flint et al., 1984).
When skin biopsies taken below the level of
injury are compared to skin biopsies taken from
above the level of injury or from biopsies taken
from individuals who have not experienced SCI,
reductions have been found both in the total
amino acid content of skin as well as the activity
of enzymes involved in the biosynthesis of
collagen within the skin. (Rodriguez and ClausWalker, 1988).
ADRENERGI C RECEPTOR DENSI TY

Adipose
Tissue
Muscle
Bone

Changes in Skin after SCI
C O L L A G E N S Y NT HE S IS A ND DE GRA DAT ION

Collagen is the principal component of the
organic matrix of the dermis and is responsible
for its tensile strength. Soon after spinal cord
injury, increased levels of collagen metabolites
are excreted through urine, a marker of collagen
catabolism (Claus-Walker et al., 1977). This

The density of adrenergic receptors in
skin below the level of injury is decreased as
compared to adrenergic receptors in skin above
the level of injury (Rodriguez et al., 1986). This
decrease in density of adrenergic receptors is
likely related to changes seen in the vasomotor
control of the skin, as the decrease in the density
of adrenergic receptors seems to correlate with
other symptoms of vascular dysfunction in SCI,
such as the reduced blood supply and deficient
circulation, as well as the impaired response of
individuals with SCI to repeated surface pressure
loads (Patterson et al., 1993).
CHANGES I N UNDERLYI NG SOF T TI SSUE
COMPOSI TI ON AFTER SCI

Makhsous et al. (2008) used ultrasound
to quantitatively measure changes in soft tissue

5
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury

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