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

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.

FIGURE 76-1 Portal venous system and systemic drainage of the small and large intestines. The stomach, pancreas, and small and large intestines have been partially removed to highlight portal venous vasculature.

FIGURE 76-2 Main portal vein and venous drainage of the stomach, spleen, and duodenum. The liver has been retracted to reveal portal venous vasculature.

FIGURE 76-3 Main portal vein and venous drainage of the stomach, pancreas, spleen, and duodenum. The liver, stomach, mesentery, and portions of the small intestine have been removed to highlight portal venous vasculature.

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 patients ³; 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

Portal Hypertension

The PV normally provides up to 80% of the total hepatic blood flow. Normal pressure in the PV ranges from 5 to 10 mm Hg, although clinically relevant alterations in portal pressures may be best considered in relative terms. The portosystemic gradient (PSG), or pressure difference between the PV and IVC (or the right atrium), is normally 3 to 6 mm Hg. In the setting of portal hypertension, the absolute portal pressure may rise above 11 mm Hg, and the portosystemic gradient may rise above 6 mm Hg.

A number of different factors can result in increased pressure in the portal system. These can be divided into prehepatic, intrahepatic and posthepatic causes (Table 76-1).

TABLE 76-1 Causes of Portal Hypertension

Prehepatic	Intrahepatic	Posthepatic
Portal vein thrombosis	Cirrhosis Schistosomiasis Noncirrhotic portal fibrosis

Right-sided heart failure

Hepatic outflow obstruction (Budd-Chiari syndrome)

Constrictive pericarditis

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.

1 The first group is represented by collaterals between the left gastric (coronary vein) and short gastric veins of the portal system with the intercostal veins, esophageal vein, and azygos tributaries of the IVC. This group may manifest clinically through sequelae of esophageal and gastric fundal varices (Fig. 76-4).

2 The second group, located in the anterior abdominal wall, is composed of communication between the vestiges of the umbilical circulation of fetal life and veins of the anterior abdominal wall. These collaterals produce varices radiating from the umbilicus, most often referred to as caput medusae.

3 The third group, located in the retroperitoneum, comprises collateral formation between the splenic vein and the left renal vein. These collaterals are often referred to as spontaneous splenorenal shunts.

4 The fourth group is located at the anal canal where the superior rectal vein, tributary of the portal venous system, anastomoses with the middle and inferior rectal veins. These veins may become dilated and pressurized, resulting in symptomatic rectal varices.

FIGURE 76-4 Esophageal varices from portal hypertension. This digitally subtracted fluoroscopic image was obtained during a transjugular intrahepatic portosystemic shunt (TIPS) procedure following injection of contrast through a catheter inserted into the splenic vein. Large esophageal varices are indicated by arrowheads. MPV, main portal vein; SV, splenic vein.

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

General Anatomic Description

The abdominal systemic venous circulation courses through the IVC. Proximal to the right atrium, the systemic and portal venous circulations unite to drain the abdominal and pelvic organs.

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.

FIGURE 76-5 Location of major vena caval inflow relative to the spine. The renal veins typically join the inferior vena cava between L1 and L2. The convergence of the common iliac veins most often occurs at the L5 vertebral level.

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).

FIGURE 76-6 Abdominal and pelvic venous return to the inferior vena cava. The abdominal and pelvic organs, except for the kidneys, have been removed to reveal the inferior vena cava and inflowing veins.

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.

Renal Veins

The renal veins are located anterior to the renal arteries and drain into the IVC. The left renal vein is the longer than the right and courses between the aorta and origin of the SMV. The left renal vein receives blood from the left testicular or ovarian, left inferior phrenic, and left suprarenal veins.

Right Inferior Phrenic Vein

The right inferior phrenic vein follows the course of the inferior phrenic artery and drains into the IVC. Note the different drainage pattern from the left inferior phrenic vein, which drains into the left renal vein.

Right Testicular or Ovarian Vein

The right testicular or ovarian vein drains into the IVC. The left testicular or ovarian vein drains into the left renal vein. Of note, valves are present in the testicular veins and are occasionally present in the ovarian veins. Incompetent valves may account for cases of pelvic congestion syndrome and male infertility (see subsequent discussion).

Right Suprarenal Vein

The right suprarenal vein drains directly into the IVC, superior to the orifice of the right renal vein. The left suprarenal vein drains into the left renal vein.

Hepatic Veins

The hepatic veins drain the liver parenchyma and do not contain valves. Most commonly, three large hepatic veins emerge from the posterior superior surface of the liver—the right, middle, and left hepatic veins. In addition, small accessory veins drain directly into IVC. These additional veins generally drain the caudate lobe or the right hepatic lobe.

The right hepatic vein courses along the right hepatic fissure, dividing the right lobe into anterior (segments V and VIII) and posterior segments (VI and VII).

The middle hepatic vein courses along the middle hepatic fissure and divides the right hepatic lobe from the left hepatic lobe. This vein drains the medial aspect of the left lobe (segment IV) and large portions of the right lobe (segment V). The middle and left hepatic veins typically unite into a common trunk before draining into the IVC.

The left hepatic vein drains the left lateral segments (segments II and III) and also receives tributaries from segment IV. As noted, this vein generally unites with the middle hepatic vein proximal to draining into the IVC.

The caudate lobe vein directly drains the caudate lobe into the IVC.

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.¹⁰^–¹² 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).

FIGURE 76-7 Hepatic venogram in Budd-Chiari syndrome. This digitally subtracted fluoroscopic image from a right hepatic venogram demonstrates tortuous intrahepatic venous collaterals from hepatic venous outflow obstruction.

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

FIGURE 76-8 Nutcracker syndrome. This axial CT image demonstrates severe narrowing of the left renal vein as it passes between the superior mesenteric artery and aorta (arrowhead). Ao, aorta; LRV, left renal vein; SMA, superior mesenteric artery.

PELVIS: SYSTEMIC VENOUS CIRCULATION

General Anatomic Descriptions

The systemic venous drainage of the pelvis primarily flows through the common iliac veins and their tributaries. The right and left common iliac veins merge at the level of the fifth lumbar vertebra to form the IVC.

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”).

External Iliac Veins

The external iliac vein is the continuation of the common femoral vein at the level of the inguinal ligament. On the right, it is first medial and then posterior to the corresponding artery. On the left, the vein runs medial to the corresponding artery (Fig. 76-9). The tributaries of each external iliac vein include the inferior epigastric, deep circumflex iliac, and pubic veins.

FIGURE 76-9 Venous drainage of the female pelvis, anterior view. The pelvic organs have been removed to highlight the complex venous drainage of the pelvis.

The inferior epigastric vein courses along the corresponding artery, draining into the external iliac vein about 1.25 cm above the inguinal ligament. Marching superiorly, the deep circumflex iliac vein joins the external iliac vein about 2 cm above the ligament, whereas the pubic vein serves as the conduit between the obturator veins and external iliac vein.

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 1: Venous Origin Outside the Bony Pelvis

The superior gluteal veins receive tributaries from the buttock and enter the pelvis through the greater sciatic foramen. The inferior gluteal veins drain the upper portion of the posterior thigh and enter the pelvis through the greater sciatic foramen. The internal pudendal veins begin in the deep veins of the penis and prostatic venous plexus in the male and the uterovaginal plexus in the female (Figs. 76-10 and 76-11). These veins course alongside the corresponding artery to form a single vein draining into the internal iliac vein. The internal pudendal veins also receive tributaries from the urethral bulb, perineal, and inferior rectal veins.

FIGURE 76-10 Lateral view of the venous drainage of the female pelvis. The right pelvic veins are depicted, emphasizing the venous plexuses of the bladder, female genitalia, and rectum.

FIGURE 76-11 Lateral view of the venous drainage of the male pelvis. The male venous plexuses for the genitalia, bladder, and rectum are depicted.

The obturator vein enters the pelvis through the superior aspect of the obturator foramen. It is typically positioned between the ureter and the internal iliac artery as it drains into the internal iliac vein.

Group 2: Lateral Sacral Veins

The lateral sacral veins accompany the corresponding arteries on the anterior surface of the sacrum and drain into the paravertebral and internal iliac veins. Note that the median sacral veins run alongside the median sacral artery anterior to the sacrum before merging into a single vein, which usually joins the left common iliac vein.

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.

FIGURE 76-12 Posterior view of rectal venous drainage.

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.

Normal Variants

Developmental anomalies of the IVC may result in variability in pelvic venous outflow, although relatively rarely. On occasion, the left common iliac vein has been seen to ascend into the abdomen, receive the left renal vein, and subsequently cross anterior to the aorta to join the inferior vena cava.³

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.

FIGURE 76-13 Left common iliac vein thrombosis from May-Thurner syndrome. This digitally subtracted fluoroscopic image from a selective contrast injection of the left common iliac vein demonstrates a thrombus near the confluence with the inferior vena cava (large arrowhead). There are numerous small venous collateral pathways to bypass the obstructed vein (small arrowheads).

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.

FIGURE 76-14 Dilated pelvic veins in pelvic congestion syndrome. This digitally subtracted fluoroscopic image from contrast injection of pelvic veins in a patient with pelvic pain demonstrates numerous tortuous and dilated varicose veins (arrowheads).

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.