Acute renal insufficiency following aortic surgery: A discussion of the pathogenesis and a consideration of gangrene of an extremity as a complication

Abstract

Eleven patients with acute renal insufficiency following aortic resectional surgery have been studied. All the patients were men; eight had aneurysms; three had occlusive vascular disease; and in each instance the lesion was distal to the renal artery. In five of the eight patients the aneurysms had ruptured, emphasizing the association of ruptured aneurysm and subsequent renal failure. Six of the patients survived, which is most encouraging in view of the coexistence of significant cardiovascular disease in ten of the eleven patients. A cerebrovascular accident, bronchopneumonia, rupture of the aorta and in two instances refractory hypotension were the principal causes of death in the five fatalities in which uremia was considered of secondary importance. Extensive renal infarction occurred in three of the patients. Nine of the eleven patients had sustained periods of significant hypotension and the renal failure may have had its origin in this circulatory stress. The current state of knowledge concerning the pathogenesis of acute renal insufficiency under these circumstances is reviewed and the opinion expressed that efforts directed at the relief of renal vasoconstriction are rational and should be pursued. The recommendation to infiltrate the renal pedicle during aortic surgery, especially in patients in whom rupture of an aneurysm has occurred, is supported. In three of the eleven patients gangrene of the lower extremity developed, a complication of particular significance in the oliguric subject. In these three patients potassium intoxication developed, and the rate of clinical deterioration seemed out of proportion to the rate of progression of the uremia. Amputation was performed in all three patients. In the difficult decision regarding the choice of treatment in these or other patients manifesting less obvious signs of vascular insufficiency, assistance has been sought in measurements of the PO 4: blood urea nitrogen ratio and the plasma-creatine concentration. Both of these values are elevated in the presence of devitalized muscle but with further studies high values were also found in other patients with uremia who were free of this complication. The plasma creatine concentration may exceed the creatinine concentration in uremia. The choice as to conservative management, debridement or amputation in patients with devitalized muscle cannot be made on a basis of biochemical data alone and for the present must remain a matter of judgment.