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.
Esophageal and paraesophageal varices are abnormally dilated veins of the esophagus. They are native veins that serve as collaterals to the central venous circulation when flow through the portal venous system or superior vena cava (SVC) is obstructed.
Esophageal varices are collateral veins within the wall of the esophagus that project directly into the lumen. The veins are of clinical concern because they are prone to hemorrhage. Paraesophageal varices are collateral veins beyond the adventitial surface of the esophagus that parallel intramural esophageal veins. Paraesophageal varices are less prone to hemorrhage. Esophageal and paraesophageal varices are slightly different in venous origin, but they are usually found together.1,2
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
Hemorrhage is a major complication in patients with esophageal varices, occurring in approximately one third of patients. The mortality rate for each bleeding episode is approximately 30%. If the underlying etiology of the esophageal varices remains untreated, as many as 70% of patients who develop hemorrhage die within 1 year of the initial bleeding episode.The risk of bleeding is highest during the first year of diagnosis, and esophageal variceal bleeding usually occurs near the gastroesophageal junction. Bleeding ceases spontaneously in one half of patients without intervention, but the risk of rebleeding is high, especially in the first 48 hours. Diagnosing esophageal varices is critical so that treatment and close follow-up care may be started to prevent the first episode of hemorrhage.
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
Endoscopy is the criterion standard for evaluating esophageal varices and assessing the bleeding risk.1,2,5,12,13 This procedure is performed by a surgeon or a gastroenterologist with the patient under light sedation. The procedure involves using a flexible endoscope inserted into the patient's mouth and through the esophagus to inspect the mucosal surface. When esophageal varices are discovered, they are graded according to their size, as follows:- 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
More on Esophageal Varices |
 Overview: Esophageal Varices |
| Imaging: Esophageal Varices |
| Follow-up: Esophageal Varices |
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| References |
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Further Reading
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
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
