文摘
Acute ischemia of an extremity constitutes an emergency. To initiate reasonable treatment steps knowledge of the underlying pathophysiology can help. During ischemia there is a drop in blood oxygen, which is required to allow the physiological energy generation. Inhibition of mitochondrial oxidative phosphorylation during ischemia leads to a rapid loss of cellular energy sources and thus affects the function of microsomal membrane pumps. This leads to altered intracellular electrolyte levels. The results are acidosis and cellular edema. By impairment of the endoplasmic reticulum, there is a persistent production of useless proteins, which interferes with the cell function sustainably. The fresh oxygen, rushing in during reperfusion, induces the formation of free radicals that additionally damage the tissue. In addition, leukocytes are submerged, promote an inflammatory response and provide further reactive oxygen species. Nitric oxide (NO) acts as a physiological radical scavenger and regulates the vascular tone. In the ischemic damaged vessels endothelium-mediated relaxation of NO does not work anymore. Furthermore, an increased filtration of fluid into the interstitial space and a rarefaction of the capillary vascular bed can be seen. Vasospasm and increased resistance further deteriorate blood flow. During reperfusion, it also comes to a distribution of metabolites and inflammatory cytokines in the whole organism, which can lead to inflammation in other organs like e.g. the lungs. Acute limb ischemia is a multifactorial process, which can lead to varying degrees of damage depending on the size of the affected area and the ischemic duration.