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 The liver has been retracted to reveal portal venous vasculature.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.