deep circumflex iliac vein

The deep veins typically accompany arteries, and artery and vein have the same name, e.g., radial artery and radial vein. In contrast, the superficial or subcutaneous veins typically travel alone. The deep and superficial veins have frequent interconnections, i.e., anastomoses; in general, veins have more anastomoses than do arteries. Throughout the body, the pattern of veins is more variable than is the pattern of arteries.

The walls of most veins have three layers: an endothelial lining, which folds at intervals into leaflets that act as one-way valves, a thin middle layer often containing smooth muscle, and a thin outer layer composed of fibrous connective tissue. In contrast, the veins of the brain have no valves, and the largest venous channels in the brain are not veins but rather endothelial-lined spaces in the dura mater called 'dural sinuses' or 'venous sinuses'; dural sinuses receive blood from cerebral veins and deliver blood to other dural sinuses or to the internal jugular vein.

The venous circulation of the brain begins with venules that run from inside the brain to the surface where they bend 90° and run along the surface inside the pia mater. Anastomosing venous plexuses collect in the pia to form the cerebral veins, which eventually cross the subarachnoid space and empty into dural sinuses. The dural sinuses interconnect and eventually empty into the internal jugular veins.

The internal jugular vein is forms in the base of the skull by the merger of the inferior petrosal and sigmoid sinuses. As the vein descends through the neck, tributary veins include the facial, lingual, pharyngeal, superior thyroid, and middle thyroid veins.

The right internal jugular vein is often the blood vessel used for medical access to the central venous circulation and to the right side of the heart.

Etiology

The development of varicose veins of the legs is promoted and aggravated by pregnancy, obesity, genetics, chronic constipation, straining at stool, and occupations requiring prolonged standing. Esophageal varices are caused by portal hypertension that accompanies cirrhosis of the liver or mechanical obstruction and occlusion of hepatic veins.

Symptoms

Most varicose veins of the legs are asymptomatic, although they may be cosmetically undesirable. Esophageal varices and hemorrhoidal varices may bleed profusely. See: illustration

Treatment

In hemorrhage, elevation of the extremity and firm, gentle pressure over the wound will stop the bleeding. The patient should not be permitted to walk until the acute condition is controlled. Sclerotherapy, rubber band ligation, or octreotide may be used to control bleeding caused by hemorrhage from esophageal varices.

Patient care

The patient with lower extremity varicosities is taught to avoid anything that impedes venous return, such as wearing garters and tight girdles, crossing the legs at the knees, and prolonged sitting. After the legs have been elevated for 10 to 15 min, support hose are applied. The patient should not sit in a chair for longer than 1 hr at a time. Walking is encouraged for at least 5 min every hour. The patient should elevate the legs whenever possible, but no less than twice a day for 30 min each time, and should avoid prolonged standing. Exercise, esp. walking, is encouraged to promote the muscular contraction that moves blood through the veins and minimizes venous stasis. Signs of thrombophlebitis, a complication of varicose veins, include heat and local pain. If surgery is performed, elastic stockings or antithrombus devices are applied postoperatively, and the foot of the bed is elevated above the level of the heart. Analgesics are prescribed and administered as needed. Circulatory assessment (color and temperature of toes, pedal pulses) is carried out according to protocol or the surgeon’s orders. The patient is watched for complications such as bleeding, infection, and neurosensory problems. Overweight patients must lose weight.