Endarteritis

ENDARTERITIS (from Greek endon- within), inflammation of the inner lining of arteries, belongs to the number of frequently occurring lesions of the vascular system. In acute form it is observed: 1) in bacteriemias of the most diverse origin due to fixation of pathogenic agents circulating in the blood at some point in the arterial system (as for example this can often be seen in scarlet fever, streptococcal infections, typhus and the like); 2) as a metastasis from some infectious focus due to septic embolism of some small vessel (for example in endocarditis, osteomyelitis and the like); 3) by transition of a purulent or necrotic process to the intima from the middle and outer tunics, which can become infected either per contiguitatem from surrounding tissues (when the artery passes through a corresponding inflammatory focus) or through vasa vasorum (see Periarteritis); 4) in the so-called hyperergic inflammation of the vascular wall, for example in nodular periarteritis, tuberculosis, sepsis, rheumatism and the like, as well as in experimental animals with repeated parenteral administration of foreign protein. In the first two cases, the process begins with a limited necrosis of the intima and the adjacent part of the media, to which thrombosis rapidly joins, and in the presence of pus-forming agents also leukocytic infiltration in the surrounding parts of the wall (see Artery). In small arteries, total necrosis of the vessel often immediately occurs over a certain extent, and the cellular reaction develops already in the surrounding tissues. Hyperergic inflammation usually manifests as an initial focal, so-called fibrinoid necrosis of the inner tunic and some part of the middle tunic (in small vessels often the entire vessel wall) with a subsequent more or less marked proliferative reaction from the adventitia. (For specific changes in the inner tunic in tuberculosis, actinomycosis and syphilis of the arteries - see Artery.) A large place and important significance in the pathology of the arterial system belongs to the more slowly progressing nonspecific lesion of the inner lining of arteries in the form of so-called endarteritis productiva, s. obliterans. The essence of the process comes down to proliferation of cellular elements of the intima, which leads to thickening of the wall and narrowing, and ultimately to closure of the vessel lumen. It is observed: 1) physiologically in newborns and in the first days after birth at obliteration of vessels that function only in embryonic life (Botallo's duct, umbilical arteries), and here a significant stimulus for proliferation is apparently the drop in blood pressure in the corresponding vessel; 2) with prolonged pathological decreases or increases in blood pressure in the arteries, for example when they lose their contractile ability due to calcification of the middle tunic, or conversely with prolonged hypertensions; 3) with traumatic injuries to arteries: wound application, ligation, suturing (see Artery); 4) as reactive proliferation of the intima, which is observed under the influence of various irritants acting both from the side of the bloodstream (for example nicotine in smokers; toxic bacterial products in patients with pneumonia, typhoid fever, scarlet fever; abnormal metabolic products in those suffering from gout, diabetes and the like, and apparently constitutional predisposition also plays a significant role in the occurrence of such proliferations), and from the surrounding tissue (for example when the artery passes through a tuberculous, purulent, lymphogranulomatous and the like focus, even if the artery itself is not involved in this process); 5) during organization of thrombi or emboli, which also occurs due to proliferation of intimal cellular elements and ultimately leads to thickening of the inner tunic or even complete closure of the lumen; finally 6) in a process of not yet fully clarified etiology consisting of proliferation of the inner lining of arteries of the extremities (especially lower ones) and often leading to gangrene of the latter. In the development of this last type of process, in addition to the causes listed under items 2, 4, 5, other insufficiently studied moments undoubtedly also play a role, determined by some as primary juvenile atherosclerosis (with subsequent formation of thrombi at altered places of the wall and their organization), by others as a special peculiar disease of the vessels - so-called thrombangiitis obliterans, or Buerger's disease, and finally by others as vasomotor disorders in the form of frequent and prolonged vascular spasms occurring either under the influence of hyperadrenalinemia or as a constitutional angioneurosis (for more details see Gangrene, spontaneous gangrene, Raynaud's disease).