Venous Anatomy of the Abdomen and Pelvis

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CHAPTER 76 Venous Anatomy of the Abdomen and Pelvis

The venous drainage of the abdomen is primarily mediated through the portal venous system and the inferior vena cava (IVC). These two systems are separate from each other in their organ drainage, but unite proximal to the IVC’s diaphragmatic hiatus to return blood from the abdomen and pelvis to the right atrium. The venous drainage of the pelvis is largely mediated through the common iliac veins, which unite to form the IVC. It is important to remember that abdominal and pelvic venous vasculature are highly variable; therefore, canonical representations are frequently oversimplifications.

ABDOMEN: PORTAL VENOUS CIRCULATION

General Anatomic Description

The portal venous system is composed of the veins that drain the abdominal viscera, spleen, pancreas, and gallbladder. Nearly 80% of hepatic inflow comes from the portal vein. Visceral blood enters the liver via the portal vein, which ramifies to smaller caliber veins, eventually reaching the hepatic sinusoidal level. From there, post-sinusoidal blood drains into the hepatic veins, which route all of the venous outflow from the liver to the IVC and systemic circulation.

Detailed Description of Specific Areas

Portal Vein

The portal vein (PV) is approximately 7 to 8 cm long in adults and is formed by the union of the splenic vein and superior mesenteric vein at the level of the second lumbar vertebra.1 It lies posterior to the pancreatic head and anterior to the IVC (Figs. 76-1 to 76-3). The PV enters the liver at the porta hepatis, where it runs posterior and medial to the bile duct and posterior and lateral to the hepatic artery. At the porta hepatis, the PV divides into the right and left PVs. Of note, the adult PV and its tributaries are devoid of valves. However, in the fetus and for a brief postpartum period, valves can be found in portal tributaries.

Conventionally, the right PV first receives blood returning from the cystic vein and then enters the right hepatic lobe, where it divides into anterior and posterior trunks, supplying hepatic segments 5 through 8. The left PV, which is longer but typically smaller in caliber, is discussed in terms of a more proximal transverse portion and more distal umbilical portion. The left PV supplies hepatic segments 1 through 4. Along its course, the left PV merges with the paraumbilical veins and ligamentum teres (obliterated left umbilical vein) and is united to the IVC by the ligamentum venosum (obliterated ductus venosus).

Inflow to the PV is supplied by the superior mesenteric, splenic, right gastric, left gastric (coronary), paraumbilical, and cystic veins.

Superior Mesenteric Vein

The superior mesenteric vein (SMV) drains the small intestine, cecum, appendix, and the ascending and transverse portions of the colon (see Fig. 76-1). It courses posterior to the head of the pancreas and horizontal segment of the duodenum, and lies anterior to the IVC. The SMV unites with the splenic vein to form the main PV.

Mesenteric tributaries of the SMV include the jejunal, ileal, ileocolic, right colic, and middle colic veins. The nonmesenteric supply to the SMV comes from the right gastroepiploic and inferior pancreaticoduodenal veins.

The jejunal and ileal veins are named after their respective arteries and conform to the same arcade distribution. They drain the jejunum and ileum into the SMV, typically on the left side.

The ileocolic vein is formed by the union of the anterior and posterior cecal veins, appendicular veins, the last ileal vein, and a colic vein. The ileocolic vein can anastomose with the ileal veins and right colic vein and it eventually drains into the SMV on the right.

The right colic vein drains the right colon and can anastomose with the ileocolic and middle colic veins into the SMV. The middle colic vein drains the transverse colon via its left and right branches.

The right gastroepiploic vein courses along the greater curvature of the stomach and drains the greater omentum, distal body, and antrum of the stomach into the SMV. It can form connections with the left gastroepiploic vein and can serve as collateral circulation in the setting of splenic vein thrombosis.

The pancreaticoduodenal veins drain the head of the pancreas and duodenal wall into the SMV. These veins conform to the same anatomy as the pancreaticoduodenal arteries, with anterior and posterior venous arcades between the superior and inferior pancreaticoduodenal veins.

Normal Variants

In a study by Koc and colleagues, a total of 318 branching variants and anomalies of the portal venous system were observed in 307 (27.4%) of 1120 patients3; 72.6% of patients demonstrated conventional anatomy. The most frequent variation was trifurcation of the PV, detected in 12.4% of patients. In these individuals, the PV divided into a left portal branch, right anterior portal branch, and right posterior portal branch. The next most common variant was a right posterior portal branch as the first branch of the main portal vein, detected in 9.2% of cases. In 3.6% of patients, there were variants of PV origin in segments IV and VIII of the liver.

Another variant of the PV seen in very rare cases is infracardiac total anomalous pulmonary venous return (TAPVR), in which the pulmonary veins drain into the PV. The incidence of TAPVR is approximately 2% of all congenital heart defects and, in 15% of cases, the pulmonary veins drain into the portal venous system (type III).3,4

In most cases, the SMV is formed by its chief tributaries. However, in almost 13% of cases, the main trunk of the SMV is absent and large right and large left mesenteric branches join the splenic vein to form the portal vein.3,4

The inferior mesenteric vein demonstrates considerable anatomic variability. In a study by Graf, the inferior mesenteric vein drained into the splenic vein in 56% of patients, but in 18% it drained into the splenoportal angle, and in the remaining 26% drainage was observed into the superior mesenteric vein.5

Differential Considerations

The most common causes of portal hypertension include cirrhosis, noncirrhotic portal fibrosis, Budd-Chiari syndrome, and schistosomiasis. The increase in portal venous pressure results in the formation of multiple portosystemic collateral vessels. These vessels function to divert blood away from the region of increased pressure and into the systemic circulation. Four main groups of portosystemic collaterals will be discussed.

Patients with portal hypertension may be asymptomatic, but most manifest with variceal bleeding, ascites, splenomegaly, or encephalopathy. In variceal bleeding, 85% of cases result from variceal hemorrhage at the gastroesophageal junction. Bleeding from gastric and esophageal varices account for 17% of cases of acute massive upper gastrointestinal hemorrhage.6

Direct pressure recording of the PV through arterial portography or indirect measurement by wedged hepatic venography can be used to diagnose portal hypertension. However, portal hypertension can also be noted on computed tomography (CT) or ultrasound. CT signs of portal hypertension include dilated portal vein (>13 mm), splenomegaly, ascites, and portosystemic collaterals. Sonographic signs of portal hypertension include ascites, splenomegaly, PV enlargement (>13 mm measured in the anteroposterior direction), portosystemic collaterals, enlarged hepatic arteries, and hepatofugal (reversed) portal flow.

Treatment options for portal hypertension include medical management, surgical devascularization with portosystemic shunt formation, transjugular intrahepatic portosystemic shunt (TIPS), and liver transplantation.7

ABDOMEN: SYSTEMIC VENOUS CIRCULATION

Detailed Description of Specific Areas

The IVC is formed by the union of the common iliac veins at the level of the fifth lumbar vertebra (Fig. 76-5).1 It ascends to the right of the abdominal midline, anterior to the vertebral column, in the retroperitoneal space and traverses the tendinous portion of the diaphragm at the level of the eighth thoracic vertebra, draining into the right atrium. A semilunar valve is present at its atrial orifice (valve of the inferior vena cava), which in fetal life serves to direct blood through the foramen ovale into the left atrium, which becomes rudimentary in the adult.

Inflow to the Inferior Vena Cava

Inferior vena caval inflow comes from the lumbar, renal, right inferior phrenic, right testicular or ovarian, right suprarenal, and hepatic veins (Fig. 76-6).

Lumbar Veins

Four paired lumbar veins drain the lumbar musculature and vertebral plexus into the IVC.2 The lumbar veins are interconnected via longitudinal veins called the ascending lumbar veins, which allow for communication between the common iliac and iliolumbar veins. The ascending lumbar veins join the subcostal veins and form the azygos vein on the right and the hemiazygos vein on the left.

Normal Variants

In a large study by Koc and associates, 58.2% of patients demonstrated conventional hepatic vein anatomy.3 The most common hepatic vein variant (prevalence, 69.5% to 86%) is the presence of an inferior right hepatic vein (IRHV), which usually drains segment VI. Knowledge of the number of IRHVs and the distance from each IRHV to the IVC is important for surgical planning prior to liver transplantation. In cases of rare multiple IRHVs, some of these veins drain into the adrenal vein before joining the IVC (prevalence, 0.2%). Another common variant found in 65% to 85% of individuals is a common trunk for the middle and left hepatic veins proximal to their insertion into the IVC.

The presence of multiple renal veins is the most common renal vein variation, with a prevalence of 9% to 30%. A circumaortic renal vein is the most common variation of the left renal vein, with a prevalence of 8.7%. Less commonly, a retroaortic left renal vein is noted, with a prevalence of 2.1%.3

In studies of IVC development in the domestic cat, variations of vena caval anatomy were classified based on abnormal regression or persistence of the various embryonic veins.8 In total, 14 theoretical variations were suggested. We will discuss the most common variations of the IVC.

A left-sided IVC forms when the left supracardinal vein persists, seen in 0.2% to 0.5% of the population. In most cases, a true left IVC unites with the left renal vein, crosses to the right side (anterior to the aorta), and joins the right renal vein, forming a normal right-sided IVC. This variation is important to recognize to prevent misdiagnosis (e.g., adenopathy) and for planning endovascular procedures in the abdomen.

In 0.2% to 0.3% of the population, a double IVC forms when both supracardinal veins persist. The two vessels often demonstrate marked size discrepancy. This anomaly should be suspected in the setting of recurrent pulmonary embolism following single IVC filter placement. In most cases, the left-sided IVC joins the left renal vein, which drains in a conventional fashion into the right-sided IVC. In 0.6% of individuals, there is azygos continuation of the IVC, with absence of the hepatic segments of the IVC.8

Differential Considerations

Budd-Chiari Syndrome

First discussed in 1845 by George Budd and then further detailed by Hans Chiari in 1899, the Budd-Chiari syndrome (BCS) is marked by obstruction of the hepatic venous outflow system. Hepatic venous obstruction can occur at any level from the small hepatic veins to the caval-atrial junction. Although BCS is rare, it can be a life-threatening condition that can present relatively acutely or develop gradually. Causes of BCS can be primary (e.g., congenital membranous webs), or secondary (e.g., polycythemia vera, paroxysmal nocturnal hemoglobinuria, hypercoagulable states, oral contraceptive–induced, or pregnancy).9 In approximately two thirds of cases, no cause can be established.

Classically, BCS manifests with the triad of abdominal pain, ascites, and hepatomegaly. However, patients often present with portal hypertension, variceal bleeding, and jaundice. The clinical presentation varies based on the chronicity of the disease process. In acute BCS, patients may experience sudden onset of right upper quadrant pain. In chronic BCS, hepatomegaly, ascites, and portal hypertension become evident.

Diagnosis may be achieved more invasively through hepatic venography or hepatic biopsy. Other noninvasive modalities such as magnetic resonance imaging (MRI), ultrasound, and CT serve as excellent diagnostic tools.1012 With CT and MRI, signs of BCS include ascites, hepatomegaly, nonvisualization of the hepatic veins, and prominent enhancement of the central liver, with enhancement of the periphery only on delayed images. The caudate lobe is usually spared because it drains separately into the inferior vena cava.

Multiple intrahepatic and extrahepatic venous collateral pathways exist in the setting of BCS.13,14 The intrahepatic collateral veins serve to divert blood away from the occluded hepatic veins, draining into a patent hepatic or systemic vein. These veins usually are curvilinear and tortuous, often resembling a comma—hence, the “comma sign” of BCS (Fig. 76-7).

Treatment options for BCS include medical managements of symptoms, surgery, transjugular intrahepatic portosystemic shunt formation, or liver transplantation.

Nutcracker Syndrome

First described in 1950, the nutcracker syndrome results from compression of the left renal vein between the aorta and the superior mesenteric artery (SMA).15

Typically, the space in which the left renal vein courses anterior to the aorta and deep to the SMA is 4 to 5 mm and is maintained by retroperitoneal fat and the third segment of the duodenum. The pathophysiology of this syndrome is not completely understood; however, if the aortomesenteric angle is narrow (perhaps because of abnormal SMA branching), left renal vein compression occurs (Fig. 76-8). Increased left renal vein pressures and surrounding venous collateral formation may be appreciated.16 The syndrome typically occurs in young, previously healthy patients. The most common clinical presentation is hematuria in the absence of renal pathology and presence of gonadal varices. Hematuria may be caused by rupture of congested renal vein tributaries into the renal collecting system. Diagnostic modalities include CT, ultrasound, and venography, with pressure gradient measurements obtained between the left renal vein and IVC. Treatment options include surgical intervention or minimally invasive intravascular stent placement.17

PELVIS: SYSTEMIC VENOUS CIRCULATION

Detailed Description of Specific Areas

Common Iliac Veins

The common iliac veins are formed by the union of the internal (hypogastric) and external iliac veins anterior to the sacroiliac joint.1,2 Typically, the right common iliac vein is shorter than the left and is positioned posteriorly and laterally to the corresponding artery. The left common iliac vein is positioned at first on the medial aspect of the corresponding artery but then courses posterior to the artery, and can be compressed between the spine and the artery (see later, “May-Thurner Syndrome”).

Internal Iliac Veins

The internal iliac vein is situated medial to the corresponding artery and, at the pelvic brim, joins the external iliac vein to form the common iliac vein. Tributaries of each internal iliac vein have often been separated into three groups.

The first group includes tributaries that originate outside the pelvis and includes the superior and inferior gluteal, internal pudendal, and obturator veins. The second group includes the lateral sacral veins, which lie anterior to the sacrum. The final group includes tributaries originating in visceral venous plexuses and includes the middle rectal, vesical, uterine, and vaginal veins.

Group 3: Venous Origin in Visceral Plexuses

The rectal venous plexus is positioned around the rectum and communicates with the vesical plexus (in males) and the uterovaginal plexus (in females; Fig. 76-10). The plexus consists of an internal submucosal portion and external muscular portion. At the anal canal, the plexus is composed of veins with longitudinal orientation, which are prone to become varicose, resulting in internal hemorrhoids. The internal portion of the plexus drains into the superior rectal vein and also communicates with the external portion.

The external portion of the plexus has various drainage sites. The most inferior aspect of the external rectal plexus is drained by the inferior rectal veins into the internal pudendal vein. The middle portion is drained by the middle rectal vein, which itself drains into the internal iliac vein. The most superior portion of the external rectal plexus drains into the superior rectal vein, which ultimately drains into the inferior mesenteric vein, a tributary of the portal venous system. This communication between the systemic and portal venous systems allows for portosystemic collaterals in the setting of portal hypertension.

The pudendal plexus receives the deep dorsal vein of the penis and branches from the bladder and prostate. This plexus communicates with the vesical plexus and subsequently the internal pudendal vein. There are venous communications between the prostatic plexus and pudendal plexus.

The dorsal veins of the penis are composed of superficial and deep veins. The superficial vein drains the prepuce and skin of the penis into the external pudendal vein. The deep vein drains the glans penis and corpora cavernosa into the prostatic venous plexus and communicates with the internal pudendal veins.

The vesical venous plexus is situated on the inferior aspect of the bladder and at the base of the prostate. It communicates with the prostatic venous plexus in males and the vaginal venous plexus in females.

The uterine plexus communicates with the ovarian and vaginal plexuses and is drained by a pair of uterine veins into the internal iliac vein. The vaginal plexus communicates with the uterine, vesical, and rectal plexus and is drained by the vaginal veins into the internal iliac veins.

Differential Considerations

May-Thurner Syndrome

May-Thurner syndrome (also known as iliac vein compression syndrome, Cockett syndrome, iliocaval compression syndrome, or pelvic venous spur) is characterized by obstruction of the left common iliac vein related to compression by the overlying right common iliac artery.1 The mechanism of obstruction is caused by the physical entrapment of the vein between the artery and the spine or by extensive intimal hypertrophy of the vein resulting from the chronic pulsatile force of the anteriorly situated common iliac artery.

Following examination of 430 cadavers in 1957, May and Thurner described iliac compression syndrome and documented decreased venous flow resulting from intimal changes.18 They theorized that the intimal changes resulted from continual compression of the left common iliac vein by the right common iliac artery. The transmitted arterial pulsation may cause opposing venous walls to contact, resulting in endothelial irritation and subsequent proliferation. This may explain the formation of intraluminal webs or spurs within the iliac vein, sometimes visualized using intravascular ultrasound. Sequelae of venous compression include reduction of venous outflow and deep vein thrombosis of the left iliofemoral system (Fig. 76-13). Other symptoms include leg swelling, varicosities, chronic venous stasis ulcers, and symptomatic pulmonary emboli.

The true prevalence of this disorder is unknown. May-Thurner syndrome is estimated to occur in 2% to 5% of patients undergoing evaluation for lower extremity venous disorders. Approximately 70% to 87% of cases are in females typically around 40 years of age. Early diagnosis of common iliac vein obstruction is important for prognosis. Iliac venography is the optimal diagnostic test because venous compression may be visualized in conjunction with pressure gradient measurements to determine the hemodynamic significance of the compression. Surrounding venous collaterals may be seen on iliac venography, either via conventional angiography or contrast-enhanced CT.

Treatment options for May-Thurner syndrome include endovascular thrombolysis followed by venous dilation and endovascular stent placement at the site of compression. Surgical options, including left common iliac vein bypass, may also be considered.

Pelvic Congestion Syndrome

It is estimated that 30% of all women experience chronic pelvic pain (CPP) during their lifetime. CPP is an enigmatic condition defined as noncyclic pain lasting longer than 6 months. Many different entities can result in CPP, including endometriosis, fibroids, and pelvic congestion syndrome (PCS). The medical literature suggests that 30% of chronic pelvic pain symptoms are caused by PCS.

PCS relates to ovarian and pelvic vein dilation, resulting in blood pooling and pain in the region of the uterus, ovaries, and vulva (Fig. 76-14). This condition is analogous to varicoceles in men.19 PCS is prevalent in women younger than 45 years of age (child-bearing age). The syndrome is uncommon in nulliparous women. It has been estimated that 15% of women between the ages of 20 and 50 years have pelvic varicose veins, although not all experience noncyclic pain. PCS has also been associated with polycystic ovaries and hormonal dysfunction. Symptoms of PCS include dull pain in the lower abdomen and lower back that increases on standing or with pregnancy, dyspareunia, dysmenorrhea, vaginal discharge, irritable bladder, and varicose veins involving the legs.

The diagnosis of PCS is challenging because other causes of CPP must be excluded. Useful modalities for the diagnosis of PCS include pelvic venography, MRI, ultrasound, and CT.20 On ultrasound, the ovarian and pelvic varicoceles are dilated and often tortuous, with surrounding dilated pelvic venous plexuses demonstrating reversed (caudal) flow within the ovarian vein. CT may demonstrate varicose veins surrounding the uterus and ovaries, with retrograde filling of dilated ovarian veins from the left renal vein in the arterial phase. Of note, dilated pelvic veins larger than 5 mm in diameter is consistent with varices and larger than 8 mm in diameter is suggestive of PCS, given the appropriate clinical symptomatology.

Numerous treatment options are available for PCS.21 Medical management with analgesics and hormones can be effective, but does not cure the underlying cause of pain. Surgical options including hysterectomy and bilateral salpingo-oophorectomy have been performed. However, minimally invasive options include endovascular embolization of the varicose ovarian veins using metallic coils (Fig. 76-15). This procedure is reportedly successful in terms of symptom relief in approximately 85% to 95% of patients.

Pertinent Imaging Considerations

Portal venous imaging requires attention to the timing of contrast injections for optimal opacification of portal structures, whether via conventional angiography, CT, or MRI.

During catheter angiography, indirect portograms are often well visualized in the late venous phases following injection of the celiac or superior mesenteric arteries. Alternatively, direct portography is possible from several approaches. Catheterization of the portal vein itself can be achieved from a transhepatic or transjugular route. The spleen may be injected with contrast, a technique known as splenoportography, or an umbilical vein may be large enough for direct puncture and subsequent portal imaging.

Cross-sectional portal venous imaging is commonly performed during multiphase CT or MR abdominal studies. The optimal portal venous scan delay from the time of peripheral venous contrast injection is routinely calculated using a timing bolus, in which peak aortic enhancement is determined. When additional scanning parameters such as contrast injection rates are taken into consideration, the results are often spectacular, with minimal contamination from nonportal vascular opacification (Fig. 76-16). CT portography combining catheter angiography with direct superior mesenteric arterial injections has emerged as a superior means to evaluate the portal venous system. In particular, when there is clinical concern for PV thrombosis or portal hypertension, CT portography may be invaluable for surgical planning.

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