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CHAPTER 30
atherosclerotic vascular changes in old age, and lesions of the nervous system such as
syringomyelia, multiple sclerosis and leprosy. In traumatic transverse lesions of the spinal
cord, this has been considered throughout thousands of years as one of the inevitable
complications, causing sepsis and early death. Although during the last quarter of this
century this concept was proved as false, it still occurs in spite of all the advances made
in this subject of medicine, not merely in the developing countries of Asia and Africa
but, alas, in the so-called highly developed countries.
Various names have been used to describe this condition, such as trophic ulcers,
decubitus, bed sores and pressure sores. In particular, the names bedsore and decubitus
are misleading, as this condition may not only occur in bedridden patients but in any later
stage of spinal cord lesions when the patient is wheelchair bound or able to walk. The
correct name is undoubtedly pressure sore, for, from the results of all research, the state
ment can be made:
Where there is no pressure there is no sore.
Mechanism
The mechanism underlying the causation of pressure sores in spinal cord sufferers has
been a subject of many discussions in the old and modern literature (Brown-Sequard,
1853; Charcot, 1881; Riddoch, 1917; Trumble, 1930; Munro, 1940; Nissen, 1941;
Guttmann, 1945, 1946, 1949, 1953, J 9^7; Dick, 1949; Exton-Smith & Sherwin, 1961;
Kermani
et al.,
1970; and others). The factors determining the formation of pressure
sores can be classified as intrinsic and extrinsic.
A. INTRINSIC FACTORS
The most important intrinsic factor is the lowering of tissue resistance to pressure,
which is most pronounced during the stage of spinal shock and flaccid paraplegia caused
by the interruption of the spinal vasomotor pathways resulting in loss of the vasomotor
control not only of the skeletal muscles, as is generally recognized, but also of the skin
and mucosa. The loss of vasomotor control leads to a lowering of the tone in the vascular
bed of the paralysed part of the body, especially the lower limbs. Therefore, a pressure
which under normal conditions will not produce blockage of the blood supply resulting
in ischaemia, will do so under these circumstances.
The second important intrinsic factor is the loss of sensation in the paralysed parts.
Normally, afferent impulses arising from an area exposed to pressure, causing blockage
of the blood circulation, elicit discomfort appreciated as numbness, pins and needles
sensation and pain. These sensations, which are the earliest signs of impending ischaemia,
normally readily initiate change of posture. Exton-Smith & Sherwin (1961) found the
incidence of pressure sore in a group of 50 elderly patients to be directly related to the
number of spontaneous movements they made during sleep. However, in transverse cord
lesions, these sensations are abolished, and, if the patient's attendant ignores this most
important fact and does not take appropriate measures to change the patient's position,
ischaemia with all its deleterious consequences on the tissues inevitably occurs.
The third intrinsic factor is the anatomical arrangement of certain parts of the body
