Fig. 1.1
Venogram of persistent left SVC (arrow). Used with permission from [9]. (c)2011 Povoski and Khabiri; licensee BioMed Central Ltd. This image is from an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited [9]
Fig. 1.2
CT scan of left-sided SVC (arrow). From: Lawler LP, Fishman EK. Thoracic venous anatomy: multidetector row CT evaluation. Radiol Clin N Am. (2003); 41(3): 545–60 [10]. Used with permission
Inferior Vena Cava (IVC )
As with the SVC , duplication and/or a left-sided IVC is possible depending on persistence of the left supracardinal vein. If the left supracardinal vein fails to regress, a duplicated IVC is demonstrated (Fig. 1.3). If both supracardinal veins persist and join at the level of the renal veins, a double IVC is noted (Fig. 1.4).
Fig. 1.3
CT scan with axial views of duplicated IVC (arrows)
Fig. 1.4
CT scan with coronal views of duplicated IVC (arrows)
If the left supracardinal vein persists while the right supracardinal vein regresses, then a left-sided IVC is observed and is a mirror image of the normal anatomy—the right adrenal vein and right gonadal vein will drain into the right renal vein, whereas the left adrenal vein and left gonadal vein will drain directly into the left-sided IVC (Fig. 1.5). This anatomy would make IVC filter retrieval more challenging because of the angulation of the cava (Fig. 1.6) [11, 12].
Fig. 1.5
Venogram of a left-sided IVC
Fig. 1.6
IVC filter in left-sided cava (arrow)
Absence of the IVC arises when the right subcardinal vein fails to connect with the liver and blood is shunted directly into the right supracardinal vein. In this manner, blood from the caudal part of the body reaches the heart through the azygos vein and the SVC (Figs. 1.7 and 1.8). Occasionally systemic to portal shunting may occur causing portal hypertension. Flow is reversed from the systemic system into the portal system unlike traditional portal systemic shunts (Fig. 1.9).
Fig. 1.7
(A) Diagram of an absent IVC.The lower half of the body is drained by the azygos vein which enters the SVC . The hepatic vein enters the heart at the site of the IVC. (B) A venogram showing absence of the IVC. The venous return is through both ascending lumbar veins and the azygos and hemiazygos veins. This was thought to be congenital in origin because it was noted early in life and there was no history to suggest venous thrombosis
Fig. 1.8
(A) Venogram of congenital IVC atresia, (B) congenitally absent IVC filling azygos and hemiazygos systems. Note lumbar venous collaterals
Fig. 1.9
SMV filling portal vein venogram congenital absence of IVC . Large systemic to portal shunt
Renal Veins
Knowledge of the variants of the renal veins is important during open dissection of the pararenal aorta. Most efforts are focused on the left renal vein due to its course. A retroaortic left renal vein is observed when the posterior left renal vein persists and the anterior left renal vein regresses (ie, opposite to normal development). In some instances, when both the anterior and the posterior left renal veins persist, a circumaortic left renal vein is observed [13, 14] (Figs. 1.10 and 1.11). The incidence of major IVC and renal vein anomalies is summarized in Table 1.1 [15].
Fig. 1.10
(A) Anterior left renal vein , (B) circumaortic left renal vein
Fig. 1.11
Duplicate retroaortic left renal veins (arrow)
Table 1.1
Incidence of major inferior vena cava and renal vein anomalies
Venous anomaly | Incidence |
|---|---|
Circumaortic renal vein | 1.5–8.7% |
Duplicated inferior vena cava | 2.2–3.0% |
Posterior left renal vein | 1.8–2.4% |
Left-sided inferior vena cava | 0.2–0.5% |
Fetal Circulation
Before birth, oxygenated blood from the placenta courses through to the fetus via the umbilical vein. Most of this blood flows through the ductus venosus into the IVC, essentially bypassing the liver proper. Within the IVC , it is admixed with returning deoxygenated blood from the lower extremities prior to entering the right atrium. It is then guided through the foramen ovale to the left atrium by the terminal valve of the IVC . At this point, it mixes with desaturated blood from the head and upper extremities through the SVC .
Blood flows from the left atrium into the left ventricle. With the high pulmonary resistance in the fetus, most of the blood is now shunted through the ductus arteriosum in the proximal descending thoracic aorta, where ultimately the viscera are supplied and the blood then flows to the placenta through the two-paired umbilical arteries .
Venous Histology and Function
The vein wall is relatively thin compared to its arterial counterpart, but nevertheless it is composed of three layers—the intima, media, and adventitia.
The intima is actively antithrombogenic with in situ production of multiple glycosaminoglycan cofactors such as thrombomodulin, antithrombin, and tissue-type plasminogen activator [16, 17]. The single layer of endothelial cells allows a low-friction smooth surface for flow. Damage to the tunica intima from traumatic cannulation, hyperosmolar solutions or even inflammation will expose the subendothelial layer and activate the platelet cascade.
The tunica media consists of a band of smooth muscle cells combined with collagen and elastin, and is adrenergically innervated. This layer can withstand both longitudinal and circumferential stress; this allows elastic recoil to accommodate changes in flow and pressure. Histologically, the internal and external elastic laminae are very thin, if not absent. Traditionally, the presence or absence of the internal elastic lamina was a major criterion in distinguishing an artery from a vein on specimen analysis. Recent studies, however, suggest that smooth muscle pattern is more reliable (and carries a higher interobserver concordance) than an evaluation of the internal elastic lamina for vessel discrimination [18].
The tunica adventitia is well developed and in some instances contains longitudinally oriented bundles of smooth muscle. The veins of the lower extremities tend to be thicker than those more cephalad.
Veins function as storage organs and tend to hold upward of 70% of the blood volume being returned to the heart. Veins have thinner walls but larger diameters and a larger capacitance as compared to arteries, while maintaining a lower resistance. In addition, they tend to have a larger percentage of vasa vasorum, most likely due to the lower oxygen tension present within venous blood.
Venous flow is influenced by a variety of factors dependent on anatomic and physiological mechanisms. These included gravity, hydrostatic pressure, competence of unidirectional valves, respiration, and compressive forces generated by lower extremity (LE) muscle groups. In fact, approximately 90% of the deep venous return from the lower extremities is managed by the compartmental muscle groups of the thigh, calf, and foot [19].
Bicuspid (ie, having an anterior and a posterior cusp) unidirectional valves are identified within veins and are noted in increasing frequency caudally—they decrease in number centrally and are not present in the head and neck as the function of gravity promotes central flow [17, 20]. Valves function to decrease the hydrostatic pressure generated by the column of blood into lower pressure segments in addition to facilitating central flow of blood.
One in four external iliac veins (24%) contains a valve. More than 2/3 of these are competent. Valves in the common iliac vein are not as rare as formerly believed, but few, if any, are competent. Valves are not seen in the adult IVC . The femoral vein contains an average of three valves. Rarely, there may be none and uncommonly as many as six. Almost all of these are competent on macroscopic evaluation. The most common site for a valve in the femoral vein is just distal to the mouth of the profunda tributary (about 90% incidence). The second most common site is at or just distal to the inguinal ligament where over 2/3 of all femoral veins have a valve [21]. A variety of venous pathologies are present due to valvular incompetence and reflux, particularly in the lower extremities (Table 1.2). Several clinical syndromes are associated with congenital vascular malformations (Table 1.3).
Table 1.2
Definition of clinical terms for venous dysfunction
International term | Definition |
|---|---|
Chronic venous disorder | The entire spectrum of morphological and functional abnormalities involving the vascular system |
Chronic venous disease | Any longer-lasting morphological or functional abnormality of the venous system, which is characterized by symptoms and/or abnormalities in diagnosis and/or requires therapy |
Chronic venous insufficiency (C3–C6) | Advanced chronic vascular disorder with functional disturbances of the venous system resulting in edema, skin changes, or venous ulcerations |
Venous symptoms | Symptoms caused by vascular disease such as a tingling sensation, pain, burning, muscle cramps, swelling, throbbing, heavy feeling, itching, restlessness, fatigue. Additional clinical signs and/or diagnoses suggest a relationship between symptoms and vascular disease |
Venous signs | Visible manifestations of vascular disturbance including vessel dilation (eg, telangiectasias, reticulated veins, varicose veins), edema of the legs, skin changes, and ulcerations as listed in the CEAP classification [22] |
Recurrent varices | Recurrent varices in a successfully treated region |
Residual varices | Varicose veins that persist after treatment and cannot be eliminated |
PREVAIT = presence of varices (residual or recurrent) after intervention | Varices present after intervention—residual or recurrent vessels |
Post-thrombotic syndrome | Chronic venous symptoms and/or signs that are seen as a result of deep leg thrombosis or its complications |
Pelvic congestion syndrome | Chronic symptoms such as pelvic pain, perineal discomfort, or postcoital pain or incontinence due to reflux or obstruction of pelvic or ovarian veins. Usually associated with vulvar, perineal, and/or leg varices |
Varicocele | Scrotal varices |
Table 1.3
Clinical syndromes associated with congenital vascular malformations
Syndrome | Inheritance | Type of vascular malformation | Location | Characteristic features | Treatment | Prognosis |
|---|---|---|---|---|---|---|
Parkes Weber | No | Arteriovenous malformation (AVM; intraosseal or close to epiphyseal plate), port-wine stain | Extremity, pelvis | Soft tissue and bony hypertrophy, varicosity (atypical), hemangioma | Observation, elastic support, embolization ± excision | Deep diffuse lesions have poor prognosis |
Klippel-Trenaunay | No | No or low-shunt AVM, venous or lymphatic VM, port-wine stain | Extremities, pelvis, trunk | Soft tissue and bony hypertrophy, varicosities (lateral lumbar to foot pattern), hemangioma, lymphangioma | Elastic support; seldom: epiphyseal stapling | Usually good |
Rendu-Osler-Weber (hereditary hemorrhagic telangiectasia) | Autosomal dominant | Punctate angioma, telangiectasia | Skin, mucous membrane, gastrointestinal (GI) tract, liver, lungs, kidney, brain, spinal cord | Epistaxis, hematemesis, melena, hematuria, hepatomegaly, neurologic symptoms | Transfusions, embolization vs. laser treatment ± excision | Good if bleeding can be controlled and no central nervous system (CNS) manifestations |
Sturge-Weber (encephalotrigeminal angiomatosis) | No | Port-wine stains | Trigeminal area, leptomeninges, choroid, oral mucosa | Convulsions, hemiplegia, ocular deformities, mental retardation, glaucoma, intracerebral calcification | Anticonvulsants, neurosurgical procedure | Guarded; depends on intracranial lesion |
Von Hippel-Lindau (oculocerebellar hemangioblastomatosis) | Autosomal dominant | Hemangioma | Retina, cerebellum | Cysts in cerebellum, pancreas, liver, adrenals, kidneys | Excision of cysts | Depends on intracranial lesion |
Blue rubber bleb nevus | Autosomal dominant | Cavernous venous hemangioma | Skin, GI tract, spleen, liver, CNS | Bluish, compressible, rubbery lesions, GI bleeding, anemia | Transfusions, electrocoagulation, excision | Depends on CNS and GI involvement |
Kasabach-Merritt | Autosomal dominant | Large cavernous hemangioma | Trunk, extremity | Thrombocytopenia, hemorrhage, anemia, ecchymosis, purpura | Compression, transfusion of blood, platelets | Death from hemorrhage or infection |
Maffucci (dyschondroplasia with vascular hamartoma) | Probably autosomal dominant | AVM, cavernous hemangioma, lymphangioma | Fingers, toes, extremity, viscera | Enchondromas, spontaneous fractures, deformed, shorter extremity, vitiligo | Orthopedic management | 20% chance of malignancy |
Adult Venous Anatomy
Head and Neck
The dural venous sinuses are endothelium-lined spaces between the periosteal and meningeal layers of the dura within the cranium. Large veins from the surface of the brain drain into these sinuses including the superior sagittal sinus, inferior sagittal sinus as well as the straight sinus, transverse sinus, petrosal sinus, and others—ultimately, they drain into the internal jugular veins. The internal jugular veins run anterior and lateral to the carotid arteries within the carotid sheath and are joined by multiple tributaries from the anterior face, cervical viscera, and upper neck. They commence at the jugular foramen in the posterior cranial fossa as the direct continuation of the sigmoid sinus. The internal jugular veins unite with the subclavian veins draining the upper extremities posterior to the sternal head of the clavicle where they form the brachiocephalic vein. Of note, the smaller more superficial external jugular veins, which accept some tributaries from the shoulder, drain into the internal jugular veins.
The internal jugular veins are the most common sites for the placement of a central venous catheter, especially for dialysis. They are easily accessible and easily compressible. The right internal jugular vein is preferred as it has a more direct route to the right atrium resulting in less central venous stenosis.
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