Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - 6

6

PRESSURE ULCER PREVENTION AND TREATMENT FOLLOWING SPINAL CORD INJURY

stiffness, thickness, and deformation at four
different anatomical locations-the ischial
tuberosity, greater trochanter, posterior mid-thigh,
and biceps brachii-in both persons without
SCI and in those with chronic SCI. Significant
differences were observed within the various
anatomical locations in both groups as well as
between the two groups. Those with SCI were
found to have significantly softer tissue over the
ischial tuberosity and mid-thigh areas. This
result may be attributable to denervation and
atrophy of muscles leading to a greater
proportion of fat to muscle.
C H A N G E S I N S KIN, S OFT T IS S UE VA S CULA RI TY,
A N D O X Y G E N ATION A FT E R S CI

Individuals with spinal cord injuryhave an
altered autonomic nervous system, with the
degree of alteration varying with the level and
completeness of injury. Injury to the spinal cord
interferes with this autonomic control and often
is responsible for a person with SCI to be unable
to compensate for extremes of cold and heat.
For example, in persons with complete injuries,
sweating is markedly decreased below the level
of injury, resulting in a decrease in the body's
natural cooling ability.
Deitrick and colleagues (2007) studied
small vessel blood flow in the lower limbs of
persons with SCI using duplex Doppler
sonography of the common femoral artery and
laser Doppler flowmetry of the foot. Cutaneous
blood flow measured during both the supine
and sitting positions was found to be decreased
in persons with SCI as much as 50% or more
while sitting as compared to blood flow in
persons without SCI. This confirms what others
have noted previously: that individuals with SCI
have a reduced blood supply (Bennett et al.,
1984) and reduced blood flow below the level
of injury (Lindan, 1961).
Hagisawa et al. (1994) measured changes
in blood content and oxygenation in superficial
vessels of the skin following an applied pressure
over the trochanter in individuals with and
without spinal cord injury. No substantial
differences were found in the reactive hyperemia
duration and intensity between groups. However,
there was a slower reflow rate after pressure
was removed in the SCI group. This slower reflow
rate was also noted by Schubert and Fagrell
(1991), who used laser Doppler flow
measurements to determine the response of
skin blood cell flow after local pressure was
applied over the sacrum and the gluteus maximus
muscle in individuals with and without SCI. A
smaller increase in temperature during occlusion

was found in the SCI group with no sensation
over the sacrum, compared to individuals who
had sensation over the sacrum or to the ablebodied group.
Studying transcutaneous oxygen tension,
Liu reported the subjects with paraplegia,
without pressure ulcers, had reduced tissue
oxygenation below the level of the spinal cord
lesion compared to ambulatory controls (Liu et
al., 1999). Others have shown that under the
same pressure load, individuals with SCI have a
reduction of the transcutaneous oxygen tension
five times the magnitude of the reduction
measured in those who did not have a spinal
cord injury (Hunt and Connally, 1978).

Pathophysiology
of Pressure Ulcers

A pressure ulcer is defined as localized injury
to the skin and/or underlying tissue usually over
a bony prominence, as a result of direct pressure
or shear (Black et al., 2007) and the resulting
deformation of the underlying soft tissues (Scales,
1990). In addition to the necessary direct
pressure or shear, there are multiple systemic,
internal, and external factors that contribute to
the development of pressure ulcers, including but
not limited to such divergent factors as skin
moisture level, nutritional factors, psychosocial,
and cognitive issues. To complicate this further,
even for the necessary factors of pressure and
shear, there is no known threshold value above
which a pressure ulcer will definitely occur,
especially since other quantifying factors, such
as the duration of pressure, all come into play.
Pressure ulcers result from the effect of
gravity on the body mass in contact with a
support surface. The forces at the contact point
are defined as direct pressure if the force vector
is perpendicular or shear pressure if the force
vector is tangential to the tissue contact surface.
The viscoelastic and microvascular properties of
the tissue determine its response to these forces
(Bader, 1990; Bogie et al., 1995; Reddy et al.,
1981). Prolonged stress due to pressure in the
tissue collagen network above the capillary and
lymphatic vessel tolerance to remain patent
(open) can result in occluded blood and
interstitial fluid flow, ischemia, pain, necrosis,
and sloughing of the dead tissues (Bennett et al.,
1984; Schubert et al., 1994).
Histologic features of chronic pressure
ulcers that have extended beyond the dermis into
underlying tissues include an accumulation of
fibrin on the inside edge, within which are
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