12.2 Portal Venous System & Hepatic Vasculature

Portal Venous Anatomy and Normal Hemodynamics

The main portal vein (MPV) forms posterior to the neck of the pancreas, at about the L2 level, by the union of the superior mesenteric vein (SMV) and the splenic vein; the inferior mesenteric vein usually joins the splenic vein just before the confluence. The MPV then ascends within the hepatoduodenal ligament — anterior to the IVC, with the hepatic artery and common bile duct — and splits at the porta hepatis into right and left portal veins. In a fasting adult at quiet respiration the MPV measures up to about 13 mm; a diameter persistently greater than 13 mm is a supportive sign of portal hypertension, though diameter alone is neither sensitive nor specific.

Normal portal venous flow is hepatopetal — directed toward the liver — and appears on spectral Doppler as a continuous, mildly undulating monophasic tracing with gentle respiratory phasicity, at velocities around 15–40 cm/s (commonly quoted near 15–18 cm/s in a fasting subject). Flow increases after a meal as splanchnic perfusion rises. Complete loss of respiratory variation, or frankly pulsatile flow, suggests transmission of elevated right heart pressures; reversed (hepatofugal) flow is never normal and indicates severe portal hypertension.

Portal Veins Versus Hepatic Veins: Telling Them Apart

A core scanning skill — and a frequent exam target — is distinguishing the two venous systems on gray scale and Doppler:

The middle hepatic vein runs in the main lobar fissure and is a handy landmark separating the right and left lobes; the right hepatic vein divides the right lobe into anterior and posterior segments, and the left hepatic vein divides the left lobe into medial and lateral segments. Their triphasic waveform runs in the order A, S, D: a retrograde A wave from atrial contraction at end-diastole, then a large antegrade S wave during ventricular systole, then a second antegrade D wave in ventricular diastole. (A small V wave from atrial overfilling may interrupt between S and D — that reversal is not the atrial contraction.) Stiff, cirrhotic, or transplanted livers may blunt this pattern to monophasic flow.

Portal Hypertension

Portal hypertension exists when the portal venous pressure gradient exceeds roughly 5–10 mmHg (a hepatic venous pressure gradient above 10 mmHg is clinically significant). The commonest cause in the United States is cirrhosis; obstruction may be prehepatic (portal vein thrombosis), intrahepatic (cirrhosis), or posthepatic (Budd-Chiari, right heart failure). Sonographic signs form a classic list:

• Hepatofugal (reversed) portal flow — the single most specific Doppler sign
• Portosystemic collaterals: a recanalized paraumbilical vein (hepatofugal flow in the ligamentum teres/fissure, producing a Cruveilhier-Baumgarten pattern), coronary (left gastric) varices, and splenorenal shunts
• Splenomegaly (spleen length beyond about 12–13 cm)
• Ascites — anechoic free fluid in Morison pouch, the pelvis, and around the liver
• MPV diameter >13 mm with reduced or stagnant velocity

A TIPS (transjugular intrahepatic portosystemic shunt) may be placed to decompress the system; surveillance Doppler tracks its velocity because abnormally low or high shunt velocities (roughly outside 90–190 cm/s) suggest stenosis.

Portal Vein Thrombosis and Cavernous Transformation

Portal vein thrombosis appears as echogenic material within the lumen with absent or partial color filling; predisposing factors include cirrhosis with stagnant flow, hypercoagulable states, abdominal infection (pylephlebitis), pancreatitis, and hepatocellular carcinoma — which can produce tumor thrombus showing internal arterial flow, distinguishing it from bland clot. When thrombosis becomes chronic, the body recruits tiny periportal collateral channels that bypass the occluded segment; on imaging this cavernous transformation looks like a tangle of small anechoic vascular channels with hepatopetal flow replacing a discrete main portal vein at the porta hepatis.

Budd-Chiari Syndrome

Budd-Chiari syndrome is obstruction of hepatic venous outflow at the level of the hepatic veins or the IVC. Acute findings include hepatomegaly, ascites, absent or reversed hepatic vein flow, and inability to demonstrate normal hepatic vein drainage into the IVC. A hallmark chronic finding is caudate lobe hypertrophy — the caudate is spared because its emissary veins drain directly into the IVC, bypassing the obstructed main hepatic veins — with compensatory atrophy of the remainder of the liver. Membranous IVC webs and hypercoagulable disorders are typical causes.

Doppler Technique for the Portal System

Hepatic vascular Doppler is performed after fasting 6–8 hours with the patient supine or in a left lateral decubitus position, using a curved 2–5 MHz transducer through subcostal or right intercostal windows. Sample the MPV where it crosses the hepatic artery at the porta hepatis, keeping the angle of insonation at or below 60 degrees and placing the sample volume in mid-vessel; document flow direction relative to the liver, mean velocity, and respiratory phasicity. Because portal velocity is low, use a low wall filter and low pulse repetition frequency (PRF) to avoid losing the signal. Evaluate the splenic vein and SMV at the confluence, the three hepatic veins near the IVC, and search the ligamentum teres, splenic hilum, and gallbladder fossa for collaterals. Comparing pre- and post-prandial velocities can unmask latent portal hypertension: a healthy system shows a robust velocity increase after eating, whereas a cirrhotic liver blunts the response.