eMedicine Specialties > Radiology > Gastrointestinal

Esophageal Varices

Cenon Buencamino, MD, Department of Medical Imaging, St. Mary's Hospital and Medical Center

Updated: Nov 5, 2008

Introduction

Background

Click on Images below to enlarge.

Normal venous flow through the portal and systemic circulation. IMC = inferior mesenteric vein; IVC = inferior vena cava; SVC = superior vena cava.

Redirection of flow through the left gastric vein secondary to portal hypertension or portal venous occlusion. Uphill varices develop in the distal one third of the esophagus. IMC = inferior mesenteric vein; IVC = inferior vena cava; SVC = superior vena cava.

Direction of venous flow with superior vena cava (SVC) obstruction proximal to the azygous vein. Flow is redirected through the azygous vein into the systemic circulation. Downhill varices develop in the upper one third of the esophagus. IMC = inferior mesenteric vein; IVC = inferior vena cava.

Direction of flow with superior vena cava (SVC) obstruction involving or distal to the azygous vein. Flow is redirected through the azygous vein, the esophageal veins, and into the portal circulation. Flow enters the systemic circulation through the inferior vena cava (IVC). Downhill varices develop the entire length of the esophagus. IMC = inferior mesenteric vein.

Using a thin-barium technique, radiographic appearances of esophageal varices were described first by Wolf in his 1928 paper, "Die Erkennug von osophagus varizen im rontgenbilde," or "Radiographic detection of esophageal varices."³ In 1931, Schatzki established the basis for the modern-day fluoroscopic detection of esophageal varices by refining positional and physiologic maneuvers to optimize visualization.

Today, more sophisticated imaging with computed tomography (CT) scanning, magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), and endoscopic ultrasonography (EUS) plays an important role in the evaluation of portal hypertension and esophageal varices.^4,5,6,7,8

This article discusses the relevant anatomy, pathophysiology, and radiographic characteristics of esophageal varices with a focus on uphill varices secondary to portal hypertension.

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Pathophysiology

Esophageal varices may be called uphill or downhill depending on the direction of the venous flow to the central circulation. Uphill varices are more common and result from portal hypertension (see Images 2, 5-7). Portal hypertension generates hepatofugal flow (reversal of flow), which diverts venous blood uphill in the cephalic direction through the left gastric vein to the venous plexus of the esophagus. The resulting esophageal varices are most prominent in the lower- to mid-thirds of the esophagus, especially at the gastroesophageal junction.

Solitary gastric varices identified with either endoscopy or barium techniques are also usually a result of portal hypertension. If isolated gastric varices are visualized during radiologic examination, one must critically look for associated esophageal varices. Only a minority of isolated gastric varices are a result of splenic vein obstruction.

The many etiologies of portal hypertension can be classified into 3 basic categories as follows:

• Presinusoidal, at the level of the portal vein
  • Periportal fibrosis (schistosomiasis)
  • Portal vein thrombosis
  • Umbilical vein infection (neonates)
  • Protein C deficiency
  • Trauma
  • Appendicitis
  • Hepatocellular carcinoma
  • Chronic active hepatitis
  • Congenital hepatic fibrosis
  • Early primary biliary cirrhosis
  • Sarcoid
  • Toxin
  • Arsenic
  • Polyvinyl chloride
• Sinusoidal, at the level of the liver parenchyma
  • Cirrhosis related to ethyl alcohol consumption
  • Hepatitis B, hepatitis C, and hepatitis D
  • Hemochromatosis
  • Wilson disease
  • Acute hepatitis related to ethyl alcohol consumption
  • Vitamin A toxicity
  • Drug-induced portal hypertension
  • Methotrexate use
  • Azathioprine use
  • Tropical splenomegaly syndrome (hepatic sinusoidal lymphocytosis or malaria in endemic areas)
• Postsinusoidal, at the level of the hepatic veins
  • Veno-occlusive disease (bone marrow transplant patients)
  • Budd-Chiari syndrome
  • Inferior vena cava obstruction
  • Thrombosis/thromboembolic disease
  • Tumor within the inferior vena cava (renal cell carcinoma)
  • Tumor-compressing inferior vena cava

Downhill varices are a result of obstruction of the SVC (see Images 4, 8-9).^1,2,9 Downhill varices have 2 presentations depending on the level of obstruction. When the SVC is obstructed superior to the azygous vein, venous blood is redirected downhill as it flows caudally from the head and upper extremities, through the esophageal veins, and into the azygous vein. Blood then enters the systemic circulation through the azygous vein. Resulting varices develop in the mid- to upper-thirds of the esophagus. When obstruction occurs at or inferior to the azygous vein, flow continues in the caudad direction through the venous plexus of the esophagus and cardiac veins and continues into the portal circulation.

Blood enters the central venous system through the inferior vena cava (IVC). In this setting, varices develop throughout the entire esophagus. The most common etiologies of downhill varices are lung carcinomas and large mediastinal tumors. Occasionally, obstruction may be a result of mediastinal fibrosis or substernal goiter. Previous central intravenous-line placement or intravenous-line infections are also in the differential diagnosis of SVC obstruction. Because malignancy is the most common etiology of SVC obstruction, few patients survive long enough to develop varices or variceal hemorrhage.

Case reports describe idiopathic esophageal varices or a single idiopathic esophageal varix presenting as an esophageal mass on barium studies. These cases were confirmed either surgically or endoscopically, but no underlying etiologies of the esophageal varices were identified. A proposed explanation for their appearance is intrinsic congenital weakness of the venous channels of the esophagus; however, no scientific proof supports this proposal.

The hepatic venous-pressure gradient (HVPG) is an accurate estimate of portal venous pressure. The HVPG is determined angiographically by subtracting the free hepatic venous pressure from the hepatic venous wedge pressure. Hepatic venous wedge pressure is an indirect measurement of portal venous pressure and is analogous to the relationship of the pulmonary wedge pressure to the left atrial pressure in right heart catheterization.

Usually, the HVPG is less than 5 mm Hg. Portal hypertension is diagnosed when the HVPG exceeds 5 mm Hg. Clinical findings, such as splenomegaly and thrombocytopenia, may develop with HVPG readings of greater than 5 mm Hg. Development of esophageal varices is a late complication that develops when the HVPG rises above 12 mm Hg. As a result, the deep intrinsic veins of the esophagus become tortuous and dilated over time, with sustained elevated venous pressure.

The Laplace law applies, as it does in all other hollow, tubular structures under pressure in the body. Wall tension is directly correlated with the tendency for a single varix to bleed. Wall tension can be calculated by using the following equation, in which T is the wall tension, Q is the flow, L is the length of the vessel, h is the viscosity of the blood, r is the radius of the vessel, and x is the mural wall thickness:

T = QLhpr⁴ (r/x)

Thus, a varix with a long, wide, and thin wall has high wall tension and an increased risk of bleeding.

In cirrhotic patients, an added factor of increased portal venous flow further adds to the problem. Patients with cirrhosis have an overall hyperdynamic circulation. As more collateral vessels develop, portal pressure decreases and triggers compensatory vasodilatation of the splanchnic circulation. The vasodilatory response is mediated at the cellular level primarily by the release of nitric oxide and prostacyclin, which result in increased volume and flow to portal circulation.

Most patients with cirrhosis also develop hypoalbuminemia, which leads to ascites. The third-space effect of fluid creates relative hypovolemic hypotension that triggers a renin-angiotensin–mediated response to retain fluid. Retaining more fluid volume results in more third-space hemodynamic shifts, and a cycle is created.

Frequency

United States

Most esophageal varices are a result of portal hypertension secondary to cirrhosis. Cirrhosis of the liver is the third leading cause of death after cancer and cardiovascular disease in people aged 25-65 years. The leading cause of cirrhosis in the Western world is alcoholic liver disease, closely followed by viral hepatitis. In recent years, cirrhosis has become strikingly more prevalent as more cases of hepatitis C are discovered. The lifetime incidence of esophageal varices is approximately 50% for all patients with cirrhosis. The annual risk of developing esophageal varices is 5-15%.

International

The prevalence, incidence, and etiology of cirrhosis may differ depending on geographic location, but the international incidence and annual risk rates of esophageal varices are similar to those in the United States. Outside the Western world, the leading causes of cirrhosis are hepatitis B and hepatitis C. Periportal fibrosis secondary to schistosomiasis (mansoni and japonicum, not haematobium) infection is also a major cause of portal hypertension worldwide. Periportal fibrosis is a chronic granulomatous inflammatory reaction resulting in fibrosis of the parenchyma adjacent to a portal tract and around the portal vein and is also called pipe-stem fibrosis.

Mortality/Morbidity

Many studies have been conducted to determine the risk of esophageal variceal hemorrhage. The North Italian Endoscopic Club for the Study and Treatment of Esophageal Varices evaluated the prediction of esophageal variceal hemorrhage on the basis of the patient's clinical status and the severity of the varices at endoscopy.¹⁰ The investigators used the endoscopic grade of the esophageal varices (see Preferred Examination), Child classification, and identification of red wheals (dilatated intraepithelial veins) to determine a patient's risk of hemorrhage.

The study found that the patient's Child classification was a major factor in predicting esophageal variceal hemorrhage; for example, the risk of hemorrhage in a patient with Child class A and grade 3/3 esophageal varices and no red wheals is only 15% compared with 42% in a patient with Child class C esophageal varices with identical endoscopic appearances.¹⁰

Nevens et al discussed the risk of hemorrhage in direct correlation with increasing portal venous pressure.¹¹ The authors determined that the risk of hemorrhage at portal venous pressures of 13 mm Hg is only 9% with an exponential increase to 72% if the portal venous pressure rises to 17 mm Hg.

Therapy to prevent first esophageal variceal hemorrhage is usually pharmacologic. Nonselective beta-blockers, such as propranolol and nadolol, are used, as well as nitrates. Sclerotherapy and banding procedures may also be performed under endoscopic guidance.

The true risk of hemorrhage for downhill esophageal varices is unknown, because most patients die as a result of the underlying etiology. See Intervention for a description of the acute treatment of patients with esophageal varices.

Race

No specific racial predilection exists for developing uphill or downhill esophageal varices. Racial differences may vary depending on the etiology of the esophageal varices.

Sex

No specific sex predilection exists for developing uphill or downhill esophageal varices. Sex differences may vary depending on the underlying etiology of the esophageal varices.

Age

Patients' ages may vary depending on the underlying etiology of the esophageal varices.

Anatomy

Venous drainage of the esophagus can be divided into 3 parts. The upper one third of the esophagus to approximately the level of the aortic knob is drained primarily by the supreme intercostal, bronchial, and inferior thyroid veins. The middle one third is drained by the azygous, hemiazygous, and accessory hemiazygous veins.

Venous drainage from the upper two thirds of the esophagus enters the central venous circulation via the SVC. The lower third is drained by the periesophageal plexus, which compose the intraepithelial channels, superficial venous plexus, and deep intrinsic veins coursing from the mucosa to the muscularis layers of the esophagus. This complex drains into the anterior branch of the left gastric vein (into the main left gastric [coronary] vein) and enters the portal circulation at the splenic vein or directly into the portal vein.

Paraesophageal varices are derived from the adventitial veins that drain into the posterior branch of the left gastric vein. Perforating veins run through the muscularis layer of the esophagus and connect the periesophageal plexus to the adventitial veins.

Presentation

Clinically, portal hypertension may be suggested in patients with cirrhosis. Clinical signs of cirrhosis include ascites, testicular atrophy, gynecomastia, and cutaneous spider angiomas. The last 3 signs are related to the inability of the liver to metabolize normal levels of estrogen in the body.

Abnormal laboratory test results, such as low albumin levels and a high international normalized ratio (INR), reflect hepatocellular failure. Hypoalbuminemia and coagulopathy develop because the liver is unable to synthesize important proteins, such as coagulation factors II, V, VII, IX, and X; albumin; and prealbumin. Elevated ammonia levels are due to impaired metabolism of amino acids. Clinically, such levels may result in hepatic encephalopathy.

Encephalopathy may be precipitated by changes in diet, dehydration, infection, and bleeding. Other liver function results, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyltransferase (GGT), and bilirubin levels, may be within the reference range or only mildly elevated. In patients with hepatitis C, the only abnormal finding may be a mildly increased ALT level, which may be 1.5-2 times higher than the reference range.

In addition to esophageal varices, clues to developing portal hypertension in cirrhotic patients include splenomegaly, caput medusae, and internal hemorrhoids. Abnormal hematologic findings may also be identified in all 3 cell lines produced by the bone marrow (ie, white blood cells [WBCs], red blood cells [RBCs], platelets).

Thrombocytopenia develops with increased platelet sequestration resulting from splenomegaly. Anemia resulting from extravascular hemolysis also develops as a result of splenomegaly. Leukopenia may develop in patients with advanced cirrhosis as a result of fibrosis of the space of Disse, in which reserves of WBCs ordinarily reside. Therefore, cirrhotic patients are considered to be immunocompromised.

Hepatopulmonary syndrome is a complication in chronic liver disease that leads to idiopathic abnormalities of pulmonary blood flow and subsequent arterial hypoxemia. Transplantation has been the only successful treatment in patients with hepatopulmonary syndrome. Hepatorenal syndrome occurs before renal failure secondary to renal cortical vasoconstriction as a result of hemodynamic disturbance from cirrhosis, portal hypertension, and ascites.

In patients with downhill esophageal varices, swelling of the upper extremities, face, and neck is the most common clinical manifestation. Arm claudication may also be a rare clinical symptom.

Preferred Examination

• Grade 1 – Small, straight esophageal varices
• Grade 2 – Enlarged, tortuous esophageal varices occupying less than one third of the lumen
• Grade 3 – Large, coil-shaped esophageal varices occupying more than one third of the lumen

The esophageal varices are also inspected for red wheals, which are dilatated intra-epithelial veins under tension and which carry a significant risk for bleeding. The grading of esophageal varices and identification of red wheals by endoscopy predict a patient's bleeding risk, on which treatment is based (see Morbidity/Mortality).

CT scanning and MRI are identical in their usefulness in diagnosing and evaluating the extent of esophageal varices. These modalities have an advantage over endoscopy because CT scanning and MRI can help in evaluating the surrounding anatomic structures, both above and below the diaphragm. CT scanning and MRI are also valuable in evaluating the liver and the entire portal circulation.

These modalities are used in preparation for a transjugular intrahepatic portosystemic shunt (TIPS) procedure or liver transplantation and in evaluating for a specific etiology of esophageal varices. These modalities also have an advantage over both endoscopy and angiography because they are noninvasive. CT scanning and MRI do not have strict criteria for evaluating the bleeding risk, and they are not as sensitive or specific as endoscopy. CT scanning and MRI may be used as alternative methods in making the diagnosis if endoscopy is contraindicated (eg, in patients with a recent myocardial infarction or any contraindication to sedation).

In the past, angiography was considered the criterion standard for evaluation of the portal venous system. However, current CT scanning and MRI procedures have become equally sensitive and specific in the detection of esophageal varices and other abnormalities of the portal venous system. Although the surrounding anatomy cannot be evaluated the way they can be with CT scanning or MRI, angiography is advantageous because its use may be therapeutic as well as diagnostic. In addition, angiography may be performed if CT scanning or MRI findings are inconclusive.

Ultrasonography, excluding EUS, and nuclear medicine studies are of minor significance in the evaluation of esophageal varices.

Limitations of Techniques

Although endoscopy is the criterion standard in diagnosing and grading esophageal varices, the anatomy outside of the esophageal mucosa cannot be evaluated with this technique. Therefore, imaging modalities such as CT scanning, MRI, and EUS are also performed for a more complete evaluation.

Barium swallow examination is not a sensitive test, and it must be performed carefully with close attention to the amount of barium used and the degree of esophageal distention. Barium swallow images may help in detecting only 50% of esophageal varices.

On CT scans and MRIs, esophageal varices are difficult to see at times. However, in severe disease, esophageal varices may be prominent. CT scanning and MRI are useful in evaluating other associated abnormalities and adjacent anatomic structures in the abdomen or thorax. On MRIs, surgical clips may create artifacts that obscure portions of the portal venous system. Disadvantages of CT scanning include the possibility of adverse reactions to the contrast agent and an inability to quantitate portal venous flow, which is an advantage of MRI and ultrasonography.

Differential Diagnoses

Esophagitis, Infectious
Portal Hypertension
Portal Vein Thrombosis

Other Problems to Be Considered

Klippel-Trenaunay syndrome – Very rare, congenital venous malformations and varicosities usually involving only 1 limb; occasionally involves the venous system of the abdomen

Parkes-Weber syndrome – Very rare, similar to Klippel-Trenaunay syndrome but with the angiographic appearances of an arteriovenous malformation

SVC obstruction – Downhill varices

Varicoid carcinoma of the esophagus

Radiography

Findings

Plain radiography

Plain radiographic findings are insensitive and nonspecific in the evaluation of esophageal varices.

• Plain radiographic findings may suggest paraesophageal varices. Anatomically, paraesophageal varices are outside the esophageal wall and may create abnormal opacities. Esophageal varices are within the wall; therefore, they are concealed in the normal shadow of the esophagus.
• Ishikawa et al described chest radiographic findings in paraesophageal varices, as confirmed with CT scans, portal venography, or both, in 352 patients with portal hypertension.¹⁴ The most common finding on chest radiographs was obliteration of a short or long segment of the descending aorta without a definitive mass shadow. Other plain radiographic findings included a posterior mediastinal mass and an apparent intraparenchymal mass. On other images, the intraparenchymal masses were confirmed to be varices in the region of the pulmonary ligament.
• On plain radiographs, a downhill varix may be depicted as a dilatated azygous vein that is out of proportion to the pulmonary vasculature. In addition, a widened, superior mediastinum may be shown. A widened, superior mediastinum may result from dilatated collateral veins or the obstructing mass.

Barium study

Uphill esophageal varices. Barium swallow demonstrates multiple serpiginous filling defects primarily involving the lower one third of the esophagus with striking prominence around the gastroesophageal junction. The patient had cirrhosis secondary to alcohol abuse.

Uphill esophageal varices on mucosal relief barium swallow.

Uphill esophageal varices on barium swallow.

A thick barium suspension or paste should be used to increase adherence to the mucosal surface. Ideally, single swallows of a small amount of barium should be ingested to minimize peristalsis and to prevent overdistention of the esophagus. If the ingested bolus is too large, the esophagus may be overdistended with dense barium, and the mucosal surface may be smoothed out, rendering esophageal varices invisible. In addition, a full column of dense barium may white out any findings of esophageal varices. Too many contiguous swallows create a powerful, repetitive, stripping wave of esophageal peristalsis that squeezes blood out of the varices as it progresses caudally.

Effervescent crystals may be used to provide air contrast, but crystals may also cause overdistention of the esophagus with gas and thereby hinder detection of esophageal varices. In addition, crystals may create confusing artifacts in the form of gas bubbles, which may mimic small varices.

The Valsalva maneuver may be useful to further enhance radiographic detection of esophageal varices. The patient is asked to "bear down as if you are having a bowel movement" or asked to "tighten your stomach muscles as if you were doing a sit-up." The Valsalva maneuver increases venous return and also prevents further peristaltic waves. The Valsalva maneuver also traps barium in the distal esophagus and allows retrograde flow for an even coating.

Barium study findings are as follows:

• Esophageal varices appear as tortuous, serpiginous, longitudinal filling defects that project into the lumen of the esophagus. These defects are seen best on relief projections of the esophagus.
• Esophageal varices may appear as thickened folds with rounded expansions etched in white because of barium trapped in the grooves of adjacent varices. This appearance may differentiate esophageal varices from the thickened esophageal folds of esophagitis.
• In a filled esophagus, varices may be identified as a scalloped border, which is a more specific sign of esophageal varices, especially if found in conjunction with the aforementioned findings.
• In the differential diagnosis, varicoid carcinoma of the esophagus is important. Varicoid carcinoma demonstrates a similar appearance to esophageal varices, but it has a more-rigid appearance that does not change or become distended with positioning, repetitive swallows, or use of the Valsalva maneuver.

Degree of Confidence

Plain radiographic findings suggestive of paraesophageal varices are very nonspecific. Any plain radiographic findings suggesting paraesophageal varices should be followed up with CT scanning or a barium study to differentiate the findings from a hiatal hernia, posterior mediastinal mass, or other abnormality (eg, rounded atelectasis). Similarly, barium studies or CT scan findings suggestive of esophageal varices should be followed up with endoscopy. Endoscopic follow-up imaging can be used to evaluate the grade and appearance of esophageal varices to assess the bleeding risk. The results of this assessment direct treatment.

False Positives/Negatives

In review case studies, a single thrombosed esophageal varix may be confused with an esophageal mass on barium studies. With endoscopy, the 2 entities can be differentiated easily.

The only normal variant is a hiatal hernia. The rugal fold pattern of a hiatal hernia may be confused with esophageal varices; however, a hiatal hernia can be identified easily by the presence of the B line marking the gastroesophageal junction.

Computed Tomography

Findings

Computed tomographic appearance of esophageal varices. Arrow points to enhancing vascular structures within the wall of the esophagus projecting into the lumen.

Computed tomography scan shows large, enhancing paraesophageal varices just to the left of the esophagus. Note the ascites and cirrhosis.

Computed tomography sections demonstrate esophageal varices protruding into the lumen, as well as paraesophageal varices.

Computed tomography scan showing esophageal varices. Note the extensive collateralization within the abdomen adjacent to the spleen as a result of severe portal hypertension.

Helical CT scanning and CT portal venography are becoming more important preprocedural tools before performing TIPS and transplantation. A variety of techniques have been described for the CT evaluation of the portal venous system. Most involve a helical technique with a pitch of 1.5-1.7– and 5-mm collimation. For imaging, 100-150 mL of 60% iodinated contrast is administered into an 18-gauge (preferred) peripheral intravenous line with a 60- to 80-second delay. The images are reconstructed in 5-mm increments. The amount of contrast material and the delay time are slightly greater than those in conventional helical CT scanning of the abdomen. The difference in technique ensures adequate opacification of both the portal venous and mesenteric arterial systems.

• On nonenhanced studies, esophageal varices may not be depicted well. Only a thickened esophageal wall may be found. Paraesophageal varices may appear as enlarged lymph nodes, posterior mediastinal masses, or a collapsed hiatal hernia.
• On contrast-enhanced images, esophageal varices appear as homogeneously enhancing tubular or serpentine structures projecting into the lumen of the esophagus. The appearance of paraesophageal is identical, but it is parallel to the esophagus instead of projecting into the lumen. Paraesophageal varices are easier to detect than esophageal varices because of the contrast of the surrounding lung and mediastinal fat.

On contrast-enhanced CT scans, downhill esophageal varices may have an appearance similar to that of uphill varices, varying only in location. Because the etiology of downhill esophageal varices is usually secondary to SVC obstruction, the physician must be aware of other potential collateral pathways that may suggest the diagnosis. Stanford et al published data based on venography.¹⁸ They described 4 patterns of flow in the setting of SVC obstruction as follows¹⁸ :

• Type 1 – Partial occlusion of the SVC with patency of the azygous vein
• Type 2 – Near-complete or complete obstruction of the SVC, with patency and antegrade flow through the azygos vein and into the right atrium
• Type 3 – Near-complete or complete obstruction of the SVC with reversal of azygous blood flow
• Type 4 – Complete obstruction of the SVC and 1 or more major caval tributaries, including the azygos system

In a retrospective investigation, Cihangiroglu et al analyzed CT scans from 21 studies of patients with SVC obstruction.¹⁹ They described as many as 15 different collateral pathways. Of their total cohorts, only 8 could be characterized by using the Stanford classification. In the setting of SVC obstruction, the most common collateral pathways were the (in decreasing order of frequency): (1) azygous vein, (2) thoracoepigastric vein, (3) mediastinal vein, and (4) internal mammary vein.¹⁹ The azygous vein collateral is most likely to develop downhill esophageal varices; however, any collateral vessel identified in the chest wall or mediastinum in the setting of SVC obstruction should prompt the radiologist to look for esophageal varices.

In a study by Zhao et al, the investigators evaluated the use of 64-row multidetector CT portal venography for characterizing paraesophageal varices in 52 of 501 patients with portal hypertensive cirrhosis and esophageal varices.²⁰  Of the 52 cases of paraesophageal varices, 50 showed an origin from the posterior branch of left gastric vein, whereas the others were from the anterior branch. Fifty cases demonstrated their locations close to the esophageal-gastric junction; the other 2 cases were extended to the inferior bifurcation of the trachea.²⁰

Regarding collateral circulation, 4 cases of single periesophageal varices communication, 3 cases of single hemiazygous vein, 1 case of single IVC, 41 cases of mixed type (collateral communications of at least 2 of the above mentioned types), and 3 cases of undetermined communications were identified. Among all the cases, 43 patients showed the communications between paraesophageal varices and periesophageal varices, whereas the hemiazygous vein (43 cases) and IVC (5 cases) were also involved.²⁰
 
Zhao et al concluded that "64-row multidetector computed tomography portal venography could display the location, morphology, origin, and collateral types of paraesophageal varices, which provides important and referable information for clinical management and disease prognosis."²⁰

Degree of Confidence

CT scanning is a minimally invasive method used to detect moderate to large esophageal varices and to evaluate the entire portal venous system. CT scans also help in evaluating the liver, other venous collaterals, details of other surrounding anatomic structures, and the patency of the portal vein. In these situations, CT scanning has a major advantage over endoscopy; however, unlike endoscopy, CT scans are not useful in predicting variceal hemorrhage.

Compared with angiography, CT scanning is superior in detecting paraumbilical and retroperitoneal varices and at providing a more thorough examination of the portal venous system without the risk of intervention. In the detection of esophageal varices, CT scanning is slightly better than angiography. As many as 25% of esophageal varices detected at endoscopy may be missed on angiograms. CT scanning and angiography are approximately equal in the detection of varices smaller than 3 mm. If CT scans do not demonstrate small varices, they are unlikely to be seen on angiograms.

False Positives/Negatives

Contrast-enhanced CT scanning is essential for evaluating esophageal varices. Contrast enhancement greatly increases the sensitivity and specificity of the examination and reduces the rate of false-positive or false-negative results. On nonenhanced CT scans, esophageal varices may mimic soft-tissue masses, enlarged lymph nodes, or other gastrointestinal tract abnormalities (eg, hiatal hernia).

Magnetic Resonance Imaging

Findings

Maximum intensity projection magnetic resonance image of the normal portal venous system. PV = portal vein; SMV = superior mesenteric vein; SV = splenic vein. Courtesy of Ali Shirkhoda, MD, William Beaumont Hospital, Royal Oak, Mich.

Maximum intensity projection magnetic resonance image of the portal venous system. A = abdominal aorta; AS = spleen; IVC = inferior vena cava; L = liver. Courtesy of Ali Shirkhoda, MD, William Beaumont Hospital, Royal Oak, Mich.

Maximum intensity projection magnetic resonance image of the portal venous system demonstrates extensive esophageal varices (arrows) in conjunction with splenic and gastric varices. L = liver. Courtesy of Ali Shirkhoda, MD, William Beaumont Hospital, Royal Oak, Mich.

Most imaging protocols are based on time-of-flight or phase-contrast methods. Improved images can be obtained by using a contrast-enhanced, breath-hold, fat-saturated, segmented, 3-dimensional (3-D), gradient-echo technique. This approach involves imaging during 3 sequential breath holds, 6 seconds apart, after the injection of paramagnetic contrast material. Data from the 3 acquisitions are processed by using a maximum intensity projection (MIP) algorithm. The MIP technique provides imaging of the entire vascular anatomy at different phases, and it provides excellent resolution in a short time (see Images 17-19).

Esophageal varices and other portosystemic collateral vessels are demonstrated as serpiginous contrast-enhanced vessels in the portal venous phase. Downhill esophageal varices appear similar to uphill varices. The advantage of MRI over CT scanning in evaluating downhill esophageal varices is its superior ability in evaluating soft tissues. Therefore, if SVC obstruction caused by a tumor is identified, the adjacent soft-tissue structures of the mediastinum, thoracic inlet, and brachial plexus can be evaluated.

Degree of Confidence

Similar to CT, MRI is becoming a more common examination in pre-TIPS and pretransplantation evaluations. The only major disadvantages of MRI compared with CT are its limited availability and cost; otherwise, CT and MRI are equal in imaging the portal venous system and in detecting esophageal varices. An advantage of MRI over CT includes the ability to quantitate the peak velocity and to determine the direction of venous blood flow. As a result, MRI rivals ultrasonography when a bolus-tracking technique is used. Other advantages include better characterization of liver tumors and avoidance of iodinated contrast material.

False Positives/Negatives

In patients with severe portal hypertension, stagnant or to-and-fro flow may produce low or no signal intensity in a patent vessel, which may be mistaken for nonobstructive thrombus or occluded vessel. Surgical clips may create artifacts that obscure portions of the portal venous system. In imaging patients with portal hypertension, ascites may create significant motion artifact that degrades image quality and may result in a nondiagnostic study. Paracentesis is recommended prior to examination in patients with a large amount of ascites.

Ultrasonography

Findings

Duplex Doppler ultrasonography is excellent for evaluating the velocity and direction of flow in the portal venous system, and this imaging modality is also good for evaluating portal vein patency. Sonography also provides an adequate evaluation of the size and echotexture of the liver. In the evaluation and detection of esophageal varices, conventional ultrasonography is limited and not clinically useful.²¹

EUS is a procedure performed by gastroenterologists, sometimes in conjunction with radiologists, to evaluate the esophagus. The procedure is used primarily in the evaluation and staging of esophageal and pancreatic carcinomas, but it has also played a role in the evaluation and treatment of esophageal varices.

While the patient is under light sedation, a 13-mm side-view endoscope with a small ultrasound probe (7.5 or 12 MHz) at its tip is introduced into the esophagus. Once the desired placement is confirmed endoscopically, a water-filled balloon is inflated around the probe in close contact with the mucosal surface of the esophagus. Occasionally, sodium chloride solution is also introduced into the lumen to eliminate any air artifact. Axial images in a 180° or 360° field of view are generated. The images demonstrate all 5 layers of the esophagus, in alternating echogenic and hypoechoic layers, starting with the echogenic mucosa.

Varices are identified as multiple, well-circumscribed, hypoechoic or anechoic structures that have a tubular or serpiginous appearance; they are located in the submucosal layer. Some EUS probes have color Doppler capability and permit the demonstration of flow. EUS has been used to guide sclerotherapy for precise injection of the sclerosing agent. EUS has also played a role in postsclerotherapy follow-up to predict the recurrence of esophageal varices. The prediction is made by identifying and measuring the size of the surrounding paraesophageal and perforating veins.

Degree of Confidence

Burtin et al evaluated 58 patients with cirrhosis and 16 control subjects by using endoscopy and EUS.²² Esophageal varices were detected more often with endoscopy (88%) than with EUS (55%). In addition, Burtin et al reported that higher-grade esophageal varices, as determined endoscopically, were more readily detected with EUS.

Esophageal varices are graded 0-3 on the basis of their protrusion into the esophageal lumen. A significant increase in the rate of EUS detection was found between grade 1 esophageal varices (25%) and grade 2 varices (73%).²² This increase is believed to be because grade 0 and 1 esophageal varices are easily compressed out by the inflated balloon and are not as readily detectable.

Even with a water-filled esophagus, the overall detection rate for esophageal varices with EUS is only 60%. Endoscopic detection of esophageal varices alone remains the criterion standard, with EUS adding little more information to the evaluation.

False Positives/Negatives

With color Doppler ultrasonography, esophageal varices can be identified easily. However, in patients with a thrombosed varix due to either idiopathic causes or sclerotherapy, the appearance may resemble those of other submucosal masses, such as cystic duplications, leiomyomas, or leiomyosarcomas. These masses are more likely to be solitary or rounded, and they are not tubular or serpiginous as are varices. Case reports describe a solitary thrombosed idiopathic varix, but these are extremely rare. A clinical history of cirrhosis or other causes of portal hypertension is helpful in evaluating such masses.

Nuclear Imaging

Findings

Nuclear medicine does not play a clinically useful role in the evaluation or diagnosis of esophageal varices. In occasional case reports in the literature, variceal hemorrhage was identified as a source of upper gastrointestinal tract bleeding seen on a tagged-RBC scan.

One group from Japan used abdominal blood pool, single photon emission CT (SPECT) scanning as a tool to evaluate success and predict recurrence of esophageal varices after sclerotherapy. More literature has been generated regarding the use of EUS imaging, with good results. To date, positron emission tomography (PET) scanning has no role in the evaluation of portal hypertension or esophageal varices.

Angiography

Findings

Before the advent of flexible endoscopy, angiography was the criterion standard in diagnosing esophageal varices.

• Angiographic findings of esophageal varices appear similar to those of serpiginous varicose veins in contiguity with the left gastric or azygous veins, depending on whether the course is uphill or downhill.²³
• Multiple small collateral vessels may be depicted in the upper chest, head, and extremities in the setting of downhill esophageal varices.
• Parasplenic, gastric, and umbilical varices may be seen in association with uphill esophageal varices.

Three major angiographic approaches to the imaging and evaluation of the portal venous system and esophageal varices are used. The approach, advantages, and disadvantages of each are as follows²³ :

• Indirect arterial portography
  • This procedure involves obtaining arterial access through the arm or groin and selectively cannulating the celiac or superior mesenteric arteries. A bolus of contrast agent is injected to obtain mesenteric angiograms and delayed images of the portal venous and splanchnic venous systems.
  • Intra-arterial injections of vasodilators, such as prostaglandin E or papaverine, may increase the amount of contrast agent that reaches the venous system to improve vessel opacification.
  • The technique is useful for defining the anatomy before the performance of shunt procedures and for evaluating the collateral circulation, including esophageal varices.
  • Major complications include bleeding at the arterial puncture site and dissection or pseudoaneurysm of any artery along the path of the procedure.
• Percutaneous transhepatic portography (TIP)
  • This technique involves direct puncture of a main portal venous branch under ultrasonographic guidance, fluoroscopic guidance, or both.
  • The patient receives a local anesthesia at the midaxillary line and the 10th intercostal space.
  • A 22-gauge Chiba needle is inserted parallel to the table and slightly inferiorly. The needle is withdrawn while contrast material is injected until a portal branch is opacified.
  • Once the vessel is identified, a 5-French (5F) catheter is inserted by using the Seldinger technique.
  • Venography may be performed through the catheter.
  • This procedure may also help in evaluating the venous anatomy and in identifying collaterals. TIP has the added benefit of better opacification of the main and intrahepatic portal venous system in the setting of hepatofugal flow.
  • Intervention, such as variceal embolization, may be performed by using this approach.
  • Although the risk is low with the procedure, morbidity rates are increased compared with those of indirect portography. Potential additional complications include subcapsular hematoma, hemobilia, biloma formation, and perforation of a hollow viscus.
• Hepatic phlebography
  • This technique involves venipuncture of the common femoral or common jugular vein and advancement of a catheter to the level of the hepatic veins through the IVC or SVC, respectively.
  • The primary purpose of the procedure is not to thoroughly evaluate the portal circulation but to evaluate hepatic venous anatomy and to search for postsinusoidal etiologies of portal hypertension.
  • Iodinated contrast material or carbon dioxide may be injected through a catheter wedged in a hepatic vein to obtain digital subtraction (DSA) images of the hepatic venous system and, possibly, the portal venous system (in hepatofugal flow).
  • The liver parenchyma may be roughly evaluated for indirect signs of cirrhosis (pruned-tree venographic appearance), malignancy, and intrahepatic venous-to-venous anastomoses.
  • Indirect measurement of the portal venous pressure may be obtained by measuring the difference between the free hepatic venous pressure and hepatic venous wedge pressures.
  • Interventions, such as transvenous liver biopsy and the TIP shunt (TIPS) procedure, may be performed by using this approach.
  • Complications of the procedure are minimal, with a small possibility of infection and bleeding at the venipuncture site.

Degree of Confidence

Angiographic images may cause as many as 25% of esophageal varices to be missed, and the technique is inferior to endoscopy. Detection is slightly better with a percutaneous technique, but it potentially creates more morbidity than the indirect method. Hepatic phlebography is not a technique designed for the detection of esophageal varices.

False Positives/Negatives

The major disadvantage of angiography is incomplete opacification of the portal venous system, either because of extreme hepatofugal flow, to-and-fro flow, or the dilution of the contrast medium. Incomplete opacification may create problems in evaluation for portal vein thrombosis or in detecting collateral pathways, including esophageal varices. Incomplete opacification is more of a problem with the indirect portography technique.

Intervention

On the detection of esophageal varices before the first occurrence of hemorrhage, medical therapy with propranolol or other nonselective beta-blockers is attempted as the initial treatment method. If the esophageal varices are of higher endoscopic grade, sclerotherapy or variceal ligation may be performed. In the setting of acute esophageal variceal hemorrhage, control of bleeding can be accomplished endoscopically in 80-90% of patients. Radiologic interventions in the treatment and management of esophageal varices include placement of a TIPS, embolization of the esophageal varices, or both.

TIPS is a minimally invasive procedure performed through the jugular vein (preferably the right), in which a shunt between the hepatic and portal veins is created to provide decompression of the portal venous system. The procedure is performed in the setting of acute or recurrent esophageal variceal bleeding that cannot be controlled medically or endoscopically.

Other indications for TIPS, other than control of esophageal variceal hemorrhage, include refractory ascites, cirrhotic hydrothorax, or portal gastropathy. TIPS can be performed as a bridge to eventual liver transplantation. To date, no significant data have demonstrated a benefit of TIPS in the prevention of refractory or recurrent hemorrhage in patients with Child class A esophageal varices or in the prevention of initial variceal hemorrhage.

Contraindications to TIPS include right- or left-sided heart failure, cardiac valve insufficiency, fulminate hepatic failure, unrelieved biliary obstruction, polycystic liver disease, hepatic malignancy, and portal vein thrombosis.

TIPS entails venous access through the right jugular vein with a micropuncture catheter set. The left internal jugular vein or right external jugular vein may be used if the right internal jugular vein is occluded.

• A long 10-12F catheter is advanced down the SVC and into the right hepatic vein. The right hepatic vein is preferred because of its size and proximity to the portal vein.
• A TIPS needle (16-gauge [16G] Colapinto, 21G Angiodynamics, or 14G Rosch-Uschida needle) is directed caudally and anteriorly toward the right portal vein. The right portal vein is approximately 0.5-1.5 vertebral-body widths to the right of the lateral margin of the spine between the 10th and 12th ribs.
• A small amount of contrast material may be injected into the periportal region to further aid localization.
• Once the portal vein is accessed, a floppy tip guidewire is advanced into the splenic or superior mesenteric vein, over which a 5F catheter is inserted into the main portal vein.
• The portosystemic gradient can be measured at this time by retrieving the sheath to the level of the right atrium. The central venous pressure can be measured in relation to portal venous pressure.
• A portal venogram may be obtained at this time.
• Then, the catheter can be exchanged for an 8-mm balloon for angioplasty of the parenchymal segment.
• A wall stent is deployed over the balloon. Commonly used stents include the self-expanding Nitinol, Smart, and Symphony stents, which have minimal or no shortening once they are deployed and which can create high amounts of radial force.

The goal of the TIPS procedure is to reduce the portosystemic gradient to less than 12 mm Hg. TIPS is successful in controlling esophageal variceal hemorrhage in approximately 97% of patients; however, a significant rebleeding rate of 5-32% is seen at 2 years. Most of the hemorrhage recurrence is within the first 6 months; this observation is comparable to recurrence after endoscopic therapy. Early complications include stent migration, thrombosis, or shunt dysfunction, as demonstrated by slow flow secondary to a competing shunt. Later complications include hepatic vein stenosis and pseudointimal hyperplasia within the stent lumen. The criterion standard method for detecting shunt stenosis is venography.

Stenosis is defined as a greater than 50% reduction of the shunt diameter. The preferred method for follow-up imaging after a TIPS procedure is Doppler ultrasonography. Doppler ultrasonography is an excellent noninvasive method for evaluating TIPS patency and flow. A baseline study should be performed the day after the procedure and then at 1 month, 3 months, 6 months, and then every 6 months.

TIPS patency is evaluated by measuring the shunt velocity in the proximal, distal, and middle portions. Direction of portal venous flow should be evaluated. The 1-year patency rate of TIPS is 20-66%. TIPS is associated with a morbidity rate of 10-20%, with a mortality rate of 1-2% immediately after the procedure. Major morbidities include portosystemic encephalopathy (17-36%), right- or left-sided heart failure, and intraperitoneal bleeding secondary to transcapsular puncture (up to 30%). Most morbidity is related to changing postprocedural flow dynamics and to bypassing the liver to clear metabolic toxins.

The role of embolization in acute esophageal variceal hemorrhage is controversial. Variceal embolization may be performed at the time of the TIPS procedure, or it may be performed by a percutaneous/transhepatic procedure to control bleeding. Embolization materials include ethanol, stainless steel coils, or bucrylate. Embolic agents are deployed or injected after selective catheterization of the left gastric vein.

In a study by L'Herminé et al involving 400 patients with variceal embolization, bleeding was controlled in 83%.²⁴ Recurrence occurred in almost 60% of patients in the first 6 months and 80% in 2 years. The study was performed before the TIPS procedure; therefore, data are from patients with uncorrected underlying portal hypertension. Theoretically, performing the TIPS procedure before embolization therapy may decrease the risk of rebleeding; however, no strong clinical data suggest that TIPS and embolization versus TIPS alone is better in preventing recurrent hemorrhage.

Medicolegal Pitfalls

• Misdiagnosis and failure to diagnose esophageal varices are the only major medical-legal issues.
• Russo et al compared the cost effectiveness of TIPS procedure versus endoscopic therapy for recurrent variceal hemorrhage. The group analyzed costs of the procedure and hospitalizations of patients undergoing TIPS, sclerotherapy, or ligation at 2 medical centers. The authors concluded that, in patients with recurrent hemorrhage, the TIPS procedure has lower recurrent variceal bleeding rates and is more cost-effective in the short-term than endoscopic therapy.

See also the Medscape topic Medical Malpractice and Legal Issues.

Special Concerns

• In children, esophageal varices are a consequence of extrahepatic obstruction of the portal vein rather than parenchymal liver disease.
  • Portal venous thrombosis may result from dehydration, sepsis, umbilical vein catheterization, and abdominal infection.
  • The diagnosis of esophageal varices is difficult, because all clinical laboratory, physical examination, and biopsy results may be normal.
  • Esophageal varices may be seen on images such as barium studies, CT scans, or MRIs.
• Detection is important because esophageal varices are a major cause of upper gastrointestinal bleeding in children.
  • After detection, sclerotherapy and variceal ligation have been shown to be superior treatment modalities.
  • TIPS and surgical shunts may also be considered, although success rates are not as promising.

Multimedia

Media file 1: Normal venous flow through the portal and systemic circulation. IMC = inferior mesenteric vein; IVC = inferior vena cava; SVC = superior vena cava.

Media file 2: Redirection of flow through the left gastric vein secondary to portal hypertension or portal venous occlusion. Uphill varices develop in the distal one third of the esophagus. IMC = inferior mesenteric vein; IVC = inferior vena cava; SVC = superior vena cava.

Media file 3: Direction of venous flow with superior vena cava (SVC) obstruction proximal to the azygous vein. Flow is redirected through the azygous vein into the systemic circulation. Downhill varices develop in the upper one third of the esophagus. IMC = inferior mesenteric vein; IVC = inferior vena cava.

Media file 4: Direction of flow with superior vena cava (SVC) obstruction involving or distal to the azygous vein. Flow is redirected through the azygous vein, the esophageal veins, and into the portal circulation. Flow enters the systemic circulation through the inferior vena cava (IVC). Downhill varices develop the entire length of the esophagus. IMC = inferior mesenteric vein.

Media file 5: Uphill esophageal varices. Barium swallow demonstrates multiple serpiginous filling defects primarily involving the lower one third of the esophagus with striking prominence around the gastroesophageal junction. The patient had cirrhosis secondary to alcohol abuse.

Media file 6: Uphill esophageal varices on mucosal relief barium swallow.

Media file 7: Uphill esophageal varices on barium swallow.

Media file 8: Downhill esophageal varices. Mucosal relief view shows the serpiginous varicoid filling defects in the proximal esophagus, with normal distal mucosa in this patient with superior vena cava obstruction.

Media file 9: Downhill esophageal varices on barium swallow examination. Notice the serpiginous filling defects proximally with normal-appearing esophagus distally.

Media file 10: Barium swallow demonstrating esophageal varices involving the entire length of the esophagus. This appearance may be seen in advanced uphill varices or downhill varices secondary to superior vena cava obstruction at or below the level of the azygous vein.

Media file 11: Varices involving the entire esophagus on barium swallow examination. Note the thickened folds with rounded expansions at the level of the gastroesophageal junction that are characteristic of esophageal varices findings on barium studies.

Media file 12: Full-column image of the esophagus with varices throughout its entire length. Note scalloping of the borders of the filled esophagus. This sign, in conjunction with thickened folds with rounded expansions and some degree of distensibility, is pathognomonic for esophageal varices. (See also Image 16.)

Media file 13: Computed tomographic appearance of esophageal varices. Arrow points to enhancing vascular structures within the wall of the esophagus projecting into the lumen.

Media file 14: Computed tomography scan shows large, enhancing paraesophageal varices just to the left of the esophagus. Note the ascites and cirrhosis.

Media file 15: Computed tomography sections demonstrate esophageal varices protruding into the lumen, as well as paraesophageal varices.

Media file 16: Computed tomography scan showing esophageal varices. Note the extensive collateralization within the abdomen adjacent to the spleen as a result of severe portal hypertension.

Media file 17: Maximum intensity projection magnetic resonance image of the normal portal venous system. PV = portal vein; SMV = superior mesenteric vein; SV = splenic vein. Courtesy of Ali Shirkhoda, MD, William Beaumont Hospital, Royal Oak, Mich.

Media file 18: Maximum intensity projection magnetic resonance image of the portal venous system. A = abdominal aorta; AS = spleen; IVC = inferior vena cava; L = liver. Courtesy of Ali Shirkhoda, MD, William Beaumont Hospital, Royal Oak, Mich.

Media file 19: Maximum intensity projection magnetic resonance image of the portal venous system demonstrates extensive esophageal varices (arrows) in conjunction with splenic and gastric varices. L = liver. Courtesy of Ali Shirkhoda, MD, William Beaumont Hospital, Royal Oak, Mich.

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Keywords

esophageal varices, esophageal varix, paraesophageal varices, portal hypertension, gastric varices, esophageal disease, dilated veins of the esophagus, SVC flow obstruction, portal venous flow obstruction, uphill varices, downhill varices, esophageal varix, esophageal hemorrhage, variceal hemorrhage, upper gastrointestinal hemorrhage, upper GI bleeding, cirrhosis

Contributor Information and Disclosures

Author

Cenon Buencamino, MD, Department of Medical Imaging, St. Mary's Hospital and Medical Center
Cenon Buencamino, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Radiology, American Institute of Ultrasound in Medicine, American Roentgen Ray Society, Radiological Society of North America, Society of Thoracic Radiology, and State Medical Society of Wisconsin
Disclosure: Nothing to disclose.

Medical Editor

Zahir Amin, MD, MBBS, MRCP, FRCR, Consulting Staff, Department of Imaging, University College Hospital, UK
Zahir Amin, MD, MBBS, MRCP, FRCR is a member of the following medical societies: British Institute of Radiology, British Medical Association, and Royal College of Radiologists
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Abraham H Dachman, MD, FACR, Professor, Department of Radiology, The University of Chicago School of Medicine; Director of CT, Department of Radiology, The University of Chicago Hospitals
Abraham H Dachman, MD, FACR is a member of the following medical societies: Radiological Society of North America
Disclosure: iCAD, Inc. Consulting fee Consulting; iCAD, Inc. Grant/research funds Other; GE Healtcare, Inc. Honoraria Speaking and teaching

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Eugene C Lin, MD, Clinical Assistant Professor of Radiology, University of Washington Medical School
Eugene C Lin, MD is a member of the following medical societies: American College of Nuclear Medicine, American College of Radiology, Radiological Society of North America, and Society of Nuclear Medicine
Disclosure: Nothing to disclose.

Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. American Association for the Study of Liver Diseases - Private Nonprofit Research Organization
American College of Gastroenterology - Medical Specialty Society.  1997 (revised 2007 Sep).  17 pages.  NGC:005907

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