Portal Hypertension and Varices

Ascites: Fluid in dependent recesses of peritoneal cavity

Splenomegaly: Spleen is enlarged > 500 cc

Varices: Well-defined, tubular or serpentine collateral vessels with same enhancement as adjacent veins

– Usually opacify on venous phase (not arterial phase)

Mesenteric edema: ↑ attenuation of mesenteric fat

Dilation of mesenteric veins : Portal vein > 13 mm

Slow or reversed flow in portal veins on ultrasound

– Slow flow in portal vein (< 15 cm/sec)

– Portal flow may be biphasic or completely reversed

– ↑ risk of portal vein thrombosis

Portal gastropathy, enteropathy, and colopathy

– May manifest as thickening of colon (especially right colon), small bowel, and stomach

Gallbladder wall thickening

PATHOLOGY

• Causes of portal hypertension divided into 3 categories

Pre sinusoidal: Portal vein/splenic vein thrombosis

Sinusoidal: Cirrhosis (most common), extensive hepatic tumor, or any severe hepatocellular disorder

Post sinusoidal: Right-sided heart failure, constrictive pericarditis, Budd-Chiari syndrome

• Varices (portosystemic collaterals) develop when portal pressures increase beyond critical value

Blood in portal venous system bypasses liver and empties into systemic veins via portosystemic collaterals

CLINICAL ISSUES

• Asymptomatic until varices rupture or ascites are infected

• 30% of patients with esophageal varices experience variceal hemorrhage within 2 years of diagnosis

• Many patients with cirrhotic ascites develop spontaneous bacterial (or rarely tuberculous) peritonitis

(Left) Graphic shows esophageal varices as serpiginous, longitudinally oriented submucosal venous collaterals extending into the gastric fundus.

(Right) Esophagram performed after endoscopic sclerosis of varices shows defects in the esophageal wall. Varices are usually pliable and easily compressed. Varicoid carcinoma could have a similar appearance.

(Left) Coronal CECT demonstrates multiple varices in the left upper quadrant in communication with the splenic vein and the left renal vein , which appears dilated, forming a splenorenal shunt.

(Right) Coronal CECT in a patient with cirrhosis and portal hypertension demonstrates thrombus in the portal and superior mesenteric veins, with calcification suggesting chronicity. Portal hypertension increases the risk of portal vein thrombus due to stasis and slow flow.

TERMINOLOGY

Definitions

• Portal hypertension: Elevated portal pressures due to resistance to portal flow, defined as absolute portal venous pressure of > 10 mm Hg or gradient between portal and systemic veins of > 5 mm Hg

• Varices: Abnormally dilated and tortuous veins due to rerouting of blood flow away from liver into lower pressure systemic veins through collateral pathways

• Ascites: Pathologic fluid accumulation in peritoneal cavity

IMAGING

General Features

• Best diagnostic clue

• Location

Ascites: Dependent recesses of peritoneal cavity

• Common features of portal hypertension

Ascites: Water density fluid in dependent recesses of peritoneal cavity

Splenomegaly: Spleen is enlarged > 500 cc

– CT or US can estimate or calculate splenic volume

– Usual upper limits: 13 cm in length and 6 × 8 cm in width and breadth, respectively

Varices: Well-defined, tubular or serpentine portosystemic collateral vessels with same enhancement as adjacent veins

– Usually opacify on venous phase images (not on arterial phase)

Mesenteric edema: Stranding and increased attenuation in mesenteric fat

Dilation of mesenteric veins (portal vein, superior mesenteric vein, and splenic vein)

– Portal vein is often dilated > 13 mm

Slow or reversed flow in portal veins on Doppler ultrasound

– Normal portal vein flow is hepatopetal (toward liver) with normal flow velocity of 15-40 cm/sec

– As portal hypertension progresses, portal blood flow velocities decrease

– Eventually, portal flow may be biphasic (alternating hepatopetal/hepatofugal flow) or completely reversed

– Stasis of blood flow in portal vein as well as hypercoagulability due to intrinsic liver disease increases risk of portal vein thrombosis

Portal gastropathy, enteropathy, and colopathy

– May manifest as thickening of colon (especially right colon), small bowel, and stomach

Gallbladder wall thickening: Due to combination of portal hypertension, hepatocellular dysfunction, and hypoproteinemia

• Varices: Types or locations

Left gastric venous collateral vessels

– Vascular channels in triangular fatty tissue between medial wall of upper gastric body and posterior margin of left hepatic lobe in lesser omentum

– Coronary (left gastric) vein ≥ 5-6 mm in diameter is considered abnormal

– Usually accompanied by esophageal or paraesophageal varices

Esophageal varices

– Dilated tortuous submucosal venous plexus of esophagus can be divided into “uphill” and “downhill” varices

Uphill varices (collateral blood flow into superior vena cava (SVC) from portal vein via azygous vein): Result from portal hypertension and found in distal 1/2 of esophagus

Downhill varices (collateral flow from SVC into inferior vena cava [IVC] or portal system): Usually due to SVC obstruction and found in proximal 1/3 of esophagus

– Tortuous or serpiginous longitudinal filling defects on esophagography

Varices may collapse during esophageal peristalsis or with distention of lumen

Best detected when esophagus is collapsed and esophageal mucosa coated with thick barium

– CECT has limited sensitivity for small esophageal varices, which may not be evident when collapsed

Can be simulated or hidden by esophagitis or hiatal hernia

– Endoscopy is most sensitive diagnostic tool

– Most clinically significant varices due to risk of bleeding

Paraesophageal varices

– Collateral vessels in posterior mediastinum behind esophageal wall connect coronary vein with azygos and hemiazygos veins and vertebral plexus

– Can mimic posterior mediastinal mass on chest x-ray

Recanalized paraumbilical vein

– Dilated collateral vein (≥ 3 mm) arising from left portal vein and coursing between medial and lateral segments of left hepatic lobe in anterior edge of falciform ligament

– Presence is virtually diagnostic of portal hypertension