986 Hyperemia of the Kidneys. 



be differentiated almost only on the strength of its acute 

 course. 



Venous hyperemia differs from renal inflammations by the 

 fact that the urine contains only little albumen and no real 

 form elements, and also by the existence of some basic disease 

 which has produced stasis of the blood in the kidneys. 



Treatment. ^ Arterial hyperemia disappears in a short 

 time after the removal of its cause, especially after an ap- 

 propriate regailation of the feeding. The administration of 

 irritating remedies should be avoided as much as possible, 

 especially in acute febrile diseases. 



The relief of blood stasis in the kidneys is possible only 

 by suitable treatment of the underlying disease, and it is 

 especially those remedies which raise the blood pressure that 

 enter into consideration (see chapter on valvular diseases). 



Literature. Augner, Mag., 1847. 95. — Dammann, D. t. W., 1898. 125. — 

 Friedberger, Z. f. pr. Vet.-Wiss., 1874. 292. — Pflug, Krankh. d. uropoet. Systems, 

 1876. — Williams, Vet. Journ., 1901. 263. (See also Lit. on Diabet. insipidus.) 



Hemorrhagic Infarct of the Kidneys. The formation of infarcts 

 in the kidneys is always a consequence of obstruction of the arteries, 

 by emboli carried from elsewhere or by thrombi which form at the 

 location of the infarct. Infarct formation is frequent after obstruc- 

 tion of smaller branches of the renal arteries by emboli, especially in 

 valvular disease, but this is not to be discussed here because it cannot 

 be diagnosed clinically, or at most presents the clinical picture of 

 chronic indurative nephritis if numerous infarcts have formed in 

 succession. Those infarcts need also not be considered here which 

 develop after the arrestment of pyogenic bacteria (see the chapter on 

 purulent nephritis). It is intended to discuss here only the hemorrhagic 

 infarction which occurs after complete occlusion or in marked stenosis 

 of the renal artery. It occurs probably only in the horse because 

 throml)osis of the larger blood vessels (usually produced by larvae 

 of sclerostoma) occurs with few exceptions only in this animal. It 

 appears to be not infreciuent, although it is usually mistaken for other 

 diseased conditions of the kidneys. The authors have observed four 

 cases within a short space of time and several cases are reported in 

 literature (Cadeac, Lustig, Ostermann), which permit the diagnosis 

 of a similar kidney disease. 



The cause of hemorrhagic infarct lies in the occlusion or marked 

 stenosis of one of the renal arteries, which causes the blood pressure 

 to fall in that kidney. Arterial blood then flows into the kidney 

 through the few anastomoses between the blood vessels of the kidney 

 and those of the capsule and the ureters ; on account of the considerable 

 size of the region which is excluded from the circulation the blood 

 remains under low pressure for a time or permanently. The great 

 diminution in the arterial blood pressure causes a stasis and extravasa- 

 tion of the blood. (Compare Vol. II.) 



The effect of an occlusion of the renal arteries was elucidated by Littea in 

 animal experiments. If the vascular obstruction was not complete or if it was 

 relieved after a short time, the circulatory disturbances retrogressed; but if in 



