PERIPHERAL VASCULAR DIS1 



[22 = 



During the next few minutes the part becomes bluer 

 and then definitely cyanotic. 



Lewis (48) made interesting observations on the 

 blood vessel reactions in the skin of the arm after 

 obstruction of the brachial artery by a pneumatic 

 cuff. After a few minutes of obstruction, reel and 

 white spots (Bier's spots) form in the cyanotic back- 

 ground of the surrounding skin. The red spots are 

 due to leakage of blood into the area from collateral 

 circulation through bone. The white spots are due to 

 intense contraction of the vessels responsible for 

 skin color, in particular, the subpapillary plexus of 

 veins. Lewis excluded cold temperature and central 

 and local nervous factors as primary causes of the 

 white spots. They are formed in previously dener- 

 vated areas. Through a careful series of experiments, 

 Lewis showed that in cutaneous areas in which the 

 circulation has been sufficiently reduced, vaso- 

 constrictor as well as vasodilator substances are 

 formed. The vasoconstrictor substances are released 

 locally in the tissue spaces and are not derived from 

 the blood. These substances act against potent 

 vasodilator factors known to be released when the 

 circulation is arrested. As noted by Lewis (48), these 

 white spots enlarge and coalesce progressively as the 

 skin is deprived of its circulation. He noted that at 

 death the skin is initially congested but shortly after- 

 ward the white spots appear, spread, and coalesce 

 until all but dependent parts of the skin are white or 

 universally blanched. Responses comparable to Bier's 

 spots have been described for organs other than the 

 skin (86). 



After its induction, if circulatory arrest to a limb 

 continues, nervous changes develop, distally at first 

 and then progress proximally up the extremity. 

 Numbness occurs within 15 min and is followed by 

 hypesthesia, first for pain and cold and last for 

 warmth. With respect to the arm, motor changes occur 

 in approximately 20 min, appearing first in the 

 thenar eminence. Within 25 min motor paralysis is 

 usually present in the thenar muscles and within 

 30 min in the interossi and extensor muscles of the 

 wrist. 



If the circulation is re-established within 30 to 60 

 min after its arrest, complete recovery usually occurs. 

 When arrest is prolonged, severe changes occur. 

 Within 6 to 1 2 hours there is muscle death and 

 whealing and blistering of the skin. After circulatory- 

 arrest for 12 to 20 hours there is nerve destruction 

 and after 24 to 48 hours, necrosis of the skin. 



Recent studies (33, 88) of pathologic changes from 

 acute ischemia in man have shown that after a few 



hours of circulatory arrest a muscle contracture similar 

 to rigor mortis develops. This does not progress 

 inevitably to fibrotic (Yolkmann's) contracture. 

 Although the latter is a frequent occurrence, the 

 initial contracture can be reversible. It was noted 

 that the early changes can be accompanied by little 

 or no obvious histologic alteration but somewhat 

 paradoxically, restoration of the circulation at this 

 stage often leads to sudden increase in the apparent 

 severity of muscle damage. It is thought that the 

 previous "normal" histology might be merely that 

 of dead or dying muscle preserved in a cool environ- 

 ment and that subsequent circulation of warm blood 

 results in the demonstrable vascular engorgement, 

 swelling, exudation, and focal hemorrhage with 

 release of myoglobin and consequent muscle pallor. 

 Depending on severity and duration, the involved 

 muscle can recover completely or suffer any degree 

 of damage (with subsequent fibrotic contracture) up 

 to complete necrosis. It was observed that skin is 

 more resistant to ischemic damage than is muscle, 

 and muscle can be irreversibly damaged even though 

 the skin remains viable. From these studies it was 

 difficult to place a definite length of time for circula- 

 tory arrest to produce irreversible change, but a gross 

 estimate was 1 2 hours or less. 



With respect to the clinical implications of the 

 above studies in the management of acute arterial 

 occlusion by thrombo-embolectomy, it is worthwhile 

 noting that blood in an artery distal to an occlusion 

 usually remains fluid for 8 to 12 hours (4). After- 

 ward the tendency to thrombosis and progressive 

 distal arterial occlusion increases rapidly. 



CLASSIFICATION OF PERIPHERAL VASCULAR DISEASE 



The classification of peripheral vascular disease 

 included in the Appendix to this chapter although 

 not all-inclusive is fairly complete. It represents a 

 modification of the classification suggested by the 

 Criteria Committee of the New York Heart Associa- 

 tion (15). It serves to emphasize the enormous prob- 

 lem and types of peripheral vascular disease. Each 

 entity in the classification represents a separate 

 complex experiment in nature. An adequate dis- 

 cussion of each would be impossible. For more elabo- 

 rate descriptions of these diseases and for references, 

 the reader may consult monographs on the subject 

 (1,3, 87, 104) and two recent symposia on peripheral 

 vascular diseases (95, 96). The diseases selected for 

 discussion here are the more common ones as well 



