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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



be the more lethal, since the associated loosely at- 

 tached thrombus was more predisposed to break 

 into emboli. Recent experimental and clinical evi- 

 dence suggests, however, that phlebothrombosis is 

 merely the silent forerunner of thrombophlebitis and 

 that the two diseases are stages of the same process 



(H. 29, 55)- 



Other terminology is dependent upon whether or 

 not superficial or deep veins are involved for which 

 the terms superficial and deep thrombophlebitis are 

 applied. The process of course is named according 

 to the particular vein or veins involved. When in- 

 fection is a predominant accompaniment, the term 

 "septic" or "suppurative" thrombophlebitis is ap- 

 plied. 



An interesting rare variant of thrombophlebitis, 

 the Trousseau syndrome, or "migratory thrombo- 

 phlebitis," should perhaps be mentioned. This dis- 

 ease may involve either superficial or deep veins, in 

 one or more sites, either concurrently or separated by 

 considerable lengths of time. The importance of this 

 svndrome is related to the frequency with which 

 underlying serious disease is present, especially, 

 thromboangiitis obliterans, polycythemia vera, occult 

 carcinoma (usually of the stomach, pancreas, or 

 lung), or collagen disease (14). 



The outstanding finding in typical acute superficial 

 thrombophlebitis is pain and tenderness over the 

 involved area, but embolic phenomena may occur. 

 Deep thrombophlebitis especially predisposes to 

 embolism. In deep thrombophlebitis the main 

 physiologic disturbance is obstruction to venous 

 blood flow. Pain of various types may be a feature 

 and is helpful in diagnosis, but edema is the most 

 objectively demonstrable physiologic alteration. The 

 degree of this disturbance is obviously dependent on 

 the size and location of the involved vein, the extent 

 of the thrombus, and the adequacy of collateral 

 circulation. When a large trunk such as the iliofemoral 

 or axillary vein is involved with a long thrombus also 

 compromising collateral flow, considerable obstruc- 

 tion to venous flow may occur and the increase in 

 venous pressure may be marked. This is in contrast 

 to simple ligation of a venous trunk in which col- 

 lateral circulation is not adversely affected. 



Edema formation, secondary to venous occlusion 

 in thrombophlebitis, is much more than a simple 

 process of increased venous pressure with resultant 

 increase in mechanical transudation of fluid into 

 the tissue space, but this factor seems to be important. 

 The importance of associated lymphatic obstruction 



in thrombophlebitis in the production of the edema 

 is debated and not yet clarified. Certainly, fibrotic 

 reactions in long-standing edema with a high protein 

 content of the extracellular fluid impairs lvmph flow. 



Appropriate to the present discussion are studies 

 concerning possible vasomotor or sympathetic factors 

 in the pathogenesis of the manifestations in thrombo- 

 phlebitis. That arterial spasm may occur in some 

 patients with deep vein thrombophlebitis is not 

 denied, but whether or not it is a significant factor 

 in most instances is debatable. In some patients 

 during the acute stages of the disease spasm may he 

 so severe that pulsations in the large arteries disappear 

 for several hours. Several patients with actual ischemic 

 gangrene have been reported. The terms "phlegmasis 

 alba dolens" and "phlegmasia cerulea dolens" have 

 been used in some of these patients to describe the 

 associated color changes thought to be due to ac- 

 companying arterial spasm. 



Some studies (68) suggest that vasoconstrictor 

 impulses are initiated by the thrombosed segment 

 of vein which produces spasm of both arterioles and 

 venules in the distant portions of the limb. Experi- 

 mental and clinical evidence has been presented in 

 favor of the idea that the thrombosed venous segment 

 initiates a detrimental spinal reflex arc with the 

 sympathetic nerves as its efferent arm. The induced 

 arterial, arteriolar, venous, and venular spasm was 

 said to propagate edema formation by increased 

 venous pressure with augmentation of filtration pres- 

 sure, by relative anoxia of capillary endothelium 

 with increased fluid transudation and by retarded 

 lymph flow secondary to reduced "pumping action" 

 from the arterial and arteriolar vessels in spasm. 

 Rather dramatic clinical improvement in patients 

 following paravertebral sympathetic blocks, both in 

 subsidence of pain as well as edema, has been re- 

 ported. 



Subsequent experimental studies on mesenteric 

 vessels of young dogs support some of these concepts 

 (56). It was found that after acute occlusion of the 

 main stem vein the artery reflexly underwent spasm, 

 whereas the vein became moderately dilated. On 

 release of the occlusion there was a period of residual 

 arterial constriction, whereas the vein returned to its 

 preocclusion caliber. After sympathectomy, however, 

 it was noted that all reflex arterial constriction, as 

 well as the residual arterial constriction that followed 

 release of the occlusion, were abolished. It was noted 

 that during occlusion the vein became dilated to a 

 diameter exceeding that of the control. Although 



