PERIPHERAL VASCULAR DISEASES 



1223 



patients with vasospasm than in normal subjects. In 

 patients with obliterative arterial disease (organic), 

 interruption of sympathetic innervation results in 

 little change or only a moderate increase in digital 

 cutaneous temperature, depending upon the degree 

 of obstructive disease (usually only to about 28 C). 

 A decline in cutaneous temperature from control 

 levels following sympathetic inhibition indicates 

 severe impairment of arterial circulation. This 

 response may be due to a pre-existing lack or dys- 

 function of sympathetic innervation in the diseased 

 area caused by ischemic degeneration of sympathetic 

 nerves. Rigidity of the diseased blood vessel walls 

 may be another factor. After induced sympathetic 

 inhibition, blood is apparently shunted away to 

 more healthy areas where the resulting decrease in 

 vascular resistance would be proportionately greater. 

 It should be remembered that tests dependent on 

 inhibition of sympathetic innervation are of value 

 clinically only in evaluation of the cutaneous circula- 

 tion and are of little or no value in the investigation 

 of the circulation to muscle. 



The above tests, however, are of a special or some- 

 what complex nature. More simply, sympathetic 

 inhibition may be induced by means of reflex vasodila- 

 tation. Reflex vasodilatation is produced by heating 

 a part of the body other than that which is being 

 tested. Application of a radiant heat tent over the 

 trunk may be used with the temperatures main- 

 tained at approximately 50 to 60 C. Responses can 

 be determined graphically by temperature or plethys- 

 mographic recordings (figs. 1, 2 A, B, and C) or other 

 suitable means. Normally, the unheated tested limb 

 may reach approximately 32 C when other parts of 

 the body are warmed. Reflex vasodilatation is 

 caused in large part by indirect sympathetic vaso- 

 constrictor inhibition resulting from the action of 

 warmed blood on central sympathetic temperature- 

 regulating centers (30), but in part also by increased 

 activity of the vasodilator fibers (100). 



Another simple clinical procedure is the histamine 

 wheal test (48, 93). The wheal formation of the 

 triple response produced by intradermal injection of 

 histamine is dependent upon the rate of local blood 

 flow and capillary pressure. The rate at which the 

 wheal forms is a rough indication of the status of 

 cutaneous circulation. Briefly, the test is performed 

 by slightly puncturing the skin several times with a 

 sharp needle through a drop of 1:1000 solution of 

 histamine acid phosphate. The subsequent reaction 

 is then observed. It has been stated that if a wheal 

 fails to appear within 3 to 5 min, ischemia of tissue 



is severe; if a wheal does not develop at all, gangrene 

 is imminent. Normally, the wheal develops in 3 min. 

 The mechanisms of the triple response have been 

 discussed in detail by Lewis (48, 49). 



EVALUATION OF THE STATUS OF THE MAIN ARTERIES. 



In the evaluation of the arterial circulation, one of 

 the most important and informative procedures is 

 a careful and methodical palpation of the main 

 arteries, including all the major branches from the 

 aorta to the digital ones. The abdominal portion of 

 the aorta is readily palpated. The thoracic aorta may 

 be palpated in advanced aneurysm formation. The 

 digital arteries of normal people are usually palpable. 

 When arterial spasm is present and the pulses are 

 weak, sublingual administration of 0.4 mg of nitro- 

 glycerin (24) or the inhalation of amyl nitrite may 

 release the vascular tone sufficiently to cause marked 

 accentuation of arterial pulses. Obviously, arteries 

 which have been totally and organically occluded 

 will remain impalpable after this procedure. 



For further information concerning functional 

 states of the main arterial circulation, one often 

 must employ more specialized procedures. With 

 the foregoing diagnostic procedures, however, this 

 is usually not necessary. 



EVALUATION OF THE STATUS OF THE VENOUS SYSTEM. 



The common signs of venous disease should be 

 observed and evaluated. One of the most frequent is 

 edema, which tends to be compressible or ""pitting" 

 in acute or subacute stages of formation but firm and 

 less compressible when of long duration. Abnormally 

 dilated and distended veins and venous varicosities 

 are frequently present. Ulcers are common in long- 

 standing venous insufficiency and tend to be located 

 over the medial lower one-third of the leg. Also 

 located in this area and frequently found in chronic 

 disease is the so-called ""stasis dermatitis," an atrophic, 

 pigmented, chronic, low-grade inflammatory area 

 of skin. 



Several simple clinical tests are available for 

 determining the competency of the venous valves 

 and the patency of the deep veins. They are usually 

 employed in the evaluation of varicose veins. Infor- 

 mation pertaining to the clinical tests may be found 

 in several publications (9, 54, 65, 67, 72, 7g, 80, 99). 

 The tests are well known and will not be repeated 

 in detail here, but briefly some are as follows: 



Brodie- Trendelenburg test (gg)- This test is designed 

 to test the valvular competence of the saphenous 

 and communicating venous system. It involves two 



