Biomedical Engineering Reference
In-Depth Information
underlying illness however, to be the dominant evil. In 1749, the French physician
and economist François Quesnay assumed the 'nerves which attend the arteries'
responsible for the development of pressure sores. The most wide spread
hypothesis to date was introduced by the French surgeon Alexis Boyer in 1818
who ascribed pressure sore development to compression of blood vessels. Kers-
chensteiner reported in 1859, and later, in 1918 Wieting and Dietrichs about
pressure sores that initiate inside the tissue and progress towards the skin.
Furthermore in 1879, the French neurologist J. M. Charcot proposed that nerve
injury released some factor leading to sore formation. This theory prevailed in
spite of attempts by people like P. Marie and G. Roussy who, in 1914, argued that
pressure ulcers developed in all debilitated patients, not just in paraplegics.
From the numerous investigations in the last century, the works of Trumble
(Trumble 1930) and Landis (Landis 1930) are especially meaningful. In 1930, they
published their researches on the effects of prolonged pressure and critical
thresholds of reduced blood flow within blood vessels. The most frequently quoted
value of 32 mmHg (4.3 kPa) measured by Landis in the finger nail bed at the
arteriolar end of a capillary loop and 12 mmHg at the venule end are still in use,
especially among manufactures of body support devices. The claim in conjunction
with these values was that any exceeding pressures result in occlusion of the blood
vessels and lead to ischaemia and finally to cell death. In 1941, however, Landis
itself revised these thresholds to the range of 46-50 mmHg. Later in 1953, Husain
observed that local pressure on the skin affected more blood vessels in the skin and
in subcutaneous tissue than in muscle tissue while however, muscle tissue expe-
rienced higher damage (Husain 1953).
Besides the above mentioned investigations of Trumble and Landis which
support the hypothesis that prolonged pressure results in tissue necrosis as a result
of impaired capillary perfusion and thus leads to hypoxia of the skin and under-
lying tissues (cf. also Kosiak 1959, 1961; Daniel et al.1981; Larsen et al. 1979)
there exist two other main hypotheses regarding pressure sore etiology. One is that
shear strain and shear deformation as major mechanisms (Reichel 1958; Dinsdale
1974) or most recently (Celeen et al. 2008), and another one assumes that external
loads impairs interstitial fluid flow and changes interstitial pressure resulting in
nutritive injury to the affected cells and impaired lymphatic drainage of metabolic
waste products and thus breakdown of the metabolic cell processes, cf. e.g.
Krouskop (1983) or Miller (1981). The first hypothesis of the pathogenesis of
pressure sores has led to more recent studies focusing on the study of the effects of
loading magnitude and loading duration.
The existing knowledge has predominantly been established via in vivo and in
vitro animal experiments as briefly outlined in the following. An additional
overview about the subsequent sections is given in Bader et al. (2005).
