164 THE VASCULAR SYSTEM 



of the capillary cells and tissues. The appearance of a part in a 

 state of passive hypersemia is livid and bluish, swollen, pitted by 

 pressure ; its temperature is lowered. The degree of swelling 

 depends on the relative in and out flow of blood. It is little 

 in hypostatic congestion because of the feeble arterial supply. 

 Whether the tissues live or die depends on the maintenance of 

 some flow by collateral paths. 



When a vein is slowly closed by a thrombus, collateral path- 

 ways have time to enlarge. " Thrombosis of the common iliac 

 vein or vena cava inferior produces O3dema of the lower limbs 

 and compensatory enlargement of the cutaneous vessels of the 

 legs and abdominal wall. Thrombosis of the subclavian vein can 

 be compensated by collateral paths through the internal mammary 

 and intercostal veins, and even thrombosis of the innominate vein 

 fails to produce oedema if the laryngeal descending veins remain 

 open." The effects depend on the rapidity with which the throm- 

 bosis takes place, i.e. on the relative damage of the tissues by 

 deficient flow. If the inferior cava is thrombosed rapidly, general 

 oedema occurs below the level, and blood and albumen appear in 

 the urine if the renal veins are involved. Closure of the portal 

 vein by a tumour or of its branches by cirrhosis of the liver, leads 

 to congestion of the intestines, enlargement of the spleen, and 

 ascites. Here again the results are due entirely to deficient flow 

 and altered constitution of blood and tissue cells. The cranial 

 sinuses are liable to thrombosis. They are wide, of irregular 

 lumen, with Pacchionian granulations dipping into them, and in 

 some cases bands crossing them. The current is forwarded by 

 respiration but cannot be influenced directly by muscular con- 

 tractions. Hence thrombosis occurs in marasmic states, with 

 feeble respiration and deficient cardiac power. Sudden blockage 

 of an artery by ligature or embolus is of little effect so long as there 

 are adequate collateral anastomotic paths. These rapidly dilate, 

 and while the blocked artery shrinks up the anastomotic capillary 

 paths, where the flow is increased, develop the structure of arteries. 

 Retinal, coronary, renal, splenic, and cerebral arteries beyond the 

 circle of Willis behave as terminal arteries. Closure of these and 

 of the superior mesenteric artery in spite of its collateral paths, 

 leads to stasis and necrosis. It seems to be possible for an embolus 

 to be driven by the respiratory and muscular movements in a 

 retrograde fashion down the large veins by coughing or expiratory 



