a significantly reduced plasma albumin concentration cannot be regarded as a causative factor, since the oedema is unilateral. The aetiology of oedema formation is probably multifactorial, and further investigations are under progress to elucidate relevant pathogenetic factors.
CLI causes ultrastructural changes in the capillary endothelium and surrounding stroma. The presence of large gaps between endothelial cells as well as an increased capillary pressure may enhance transcapillary transudation, and are most likely the causative factors in the formation of the ischaemic oedema. The stromal haemorrhage as well as degeneration probably signifies a terminal stage of CLI.
HF waves are associated with CLI. Ischaemia also appears to influence the FFT-power of each frequency domain. Ischaemic oedema does not seem to affect the pattern of FM in the foot of patients with CLI.
a low plasma albumin concentration in patients with CLI agrees with the reduction in COP pl but cannot explain the oedema formation, since it is unilateral. The high P r may cause a high transcapillary filtration pressure, resulting in a relatively great net filtration and subsequent oedema formation.
A higher transcapillary concentration gradient for proteins in CLI limbs signifies an increase in the net osmotic pressure gradient across the capillary wall, which may be a potential oedema limiting factor.
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