Esophageal varices

From Wikipedia, the free encyclopedia

Esophageal varices

Classification and external resources

Gastroscopy image of esophageal varices with prominent cherry-red spots

ICD-10

I85

ICD-9

456.0-456.2

DiseasesDB

9177

MedlinePlus

000268

eMedicine

med/745 radio/269

MeSH

D004932

In medicine (gastroenterology), esophageal varices (or oesophageal varices) are extremely dilated sub-mucosalveins in the lower third
[1]

of the esophagus. They are most often a

consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding. Esophageal varices are diagnosed with endoscopy.
Contents
[2]

[hide]

1 Pathogenesis 2 Treatment 3 Prevention 4 Histology 5 See also 6 References 7 External links

[edit]Pathogenesis

The majority of blood from the esophagus is drained via the esophageal veins, which carry deoxygenated blood from the esophagus to the azygos vein, which in turn drains directly into the superior vena cava. These veins have no part in the development of esophageal varices. The remaining blood from the esophagus is drained into the superficial veins lining the esophageal mucosa, which drain into the left gastric vein (coronary vein), which in turn drains directly into the portal vein. These superficial veins (normally only approximately 1mm in diameter) become distended up to 12 cm in diameter in association with portal hypertension. Normal portal pressure is approximately 9 mmHg compared to an inferior vena cava pressure of 2-6 mmHg. This creates a normal pressure gradient of 3-7 mmHg. If the portal pressure rises above 12 mmHg, this gradient rises to 7-10 mmHg.
[3]

A gradient greater than 5 mmHg is considered portal

hypertension. At gradients greater than 10 mmHg, blood flow though the hepatic portal system is redirected from the liver into areas with lower venous pressures. This means that collateral circulation develops in the lower esophagus, abdominal wall, stomach, andrectum. The small blood vessels in these areas become distended, becoming more thin-walled, and appear as varicosities. In addition, these vessels are poorly supported by other structures, as they are not designed for high pressures. In situations where portal pressures increase, such as with cirrhosis, there is dilation of veins in the anastomosis, leading to esophageal varices. Splenic vein thrombosis is a rare condition that causes esophageal varices without a raised portal pressure. Splenectomy can cure the variceal bleeding due to splenic vein thrombosis. The most common cause of esophageal varices is from aging changes in the vessels. Varices can also form in other areas of the body, including the stomach (gastric varices), duodenum (duodenal varices), and rectum (rectal varices). Treatment of these types of varices may differ.
[edit]Treatment

Esophageal varices seven days post banding, showing ulceration at the site of banding.

In emergency situations, the care is directed at stopping blood loss, maintaining plasma volume, correcting disorders in coagulation induced by cirrhosis, and appropriate use of antibiotics (usually a quinolone or ceftriaxone, as infection by gram-negative strains is either concomitant or a precipitant). Blood volume resuscitation should be done promptly and with caution. Goal should be hemodynamic stability and hemoglobin of over 8. Resuscitation of all lost blood leads to increase in portal pressure leading to more bleeding. Volume resuscitation can also worsen ascites and increase portal pressure. (AASLD guidelines) Therapeutic endoscopy is considered the mainstay of urgent treatment. Two main therapeutic approaches exist: 1. Variceal ligation, or banding. 2. Sclerotherapy. In cases of refractory bleeding, balloon tamponade with Sengstaken-Blakemore tube may be necessary, usually as a bridge to further endoscopy or treatment of the underlying cause of bleeding (usually portal hypertension). Methods of treating the portal hypertension include: transjugular intrahepatic portosystemic shunt (TIPS), or a distal splenorenal shunt procedure or a liver transplantation. Nutritional supplementation is not necessary if the patient is not eating for four days or less.
[4]

Terlipressin and octreotide (50mcg bolus IV followed by 25-50mcg/h IVF for 1 to 5 days) have also been used.
[5]

[edit]Prevention

In ideal circumstances, patients with known varices should receive treatment to reduce their risk of bleeding.
[6]

The non-selective -blockers (e.g., propranolol 10 mg PO TID, timolol or nadolol 20 mg

PO OD) and nitrates (e.g. isosorbide mononitrate (IMN) 20 mg BD to TID) have been evaluated for secondary prophylaxis. Non-selective -blockers (but not cardioselective -blockers like atenolol) are preferred because they decrease both cardiac output by 1 blockade and splanchnic blood flow by

blocking vasodilating 2 receptors at splanchnic vasculature. The effectiveness of this treatment has been shown by a number of different studies.
[7]

However, non-selective -blockers do not prevent the formation of esophageal varices.

[edit]Histology

[8]

Axial CT showing esophageal varices in liver cirrhosis with portal hypertension

Dilated submucosal veins are the most prominent histologic feature of esophageal varices. The expansion of the submucosa leads to elevation of the mucosa above the surrounding tissue, which is apparent during endoscopy and is a key diagnostic feature. Evidence of recent variceal hemorrhage includes necrosis and ulceration of the mucosa. Evidence of past variceal hemorrhage includes inflammation and venous thrombosis.
[edit]

Gastric varices
From Wikipedia, the free encyclopedia

This article does not cite any references or sources. Please help improve this article by adding citations toreliable sources. Unsourced material may be challenged and removed. (January 2008)

Gastric varices

Classification and external resources

Isolated gastric varices of Sarin classification IGV-1 seen on gastroscopy in a patient withportal hypertension

ICD-10

I86.4

Gastric varices are dilated submucosal veins in the stomach, which can be a life-threatening cause of upper gastrointestinal hemorrhage. They are most commonly found in patients with portal hypertension, or elevated pressure in the portal vein system, which may be a complication of cirrhosis. Gastric varices may also be found in patients with thrombosis of the splenic vein, into which the short gastric veins which drain the fundus of the stomach flow. The latter may be a complication of acute pancreatitis, pancreatic cancer, or other abdominal tumours. Patients with bleeding gastric varices can present with bloody vomiting (hematemesis), dark, tarry stools (melena), or frank rectal bleeding. The bleeding may be brisk, and patients may soon develop shock. Treatment of gastric varices can include injection of the varices with cyanoacrylate glue, or a radiological procedure to decrease the pressure in the portal vein, termedtransjugular intrahepatic portosystemic shunt or TIPS. Treatment with intravenous octreotide is also useful to shunt blood flow away from the stomach's circulation. More aggressive treatment including splenectomy (or surgical removal of the spleen) or liver transplantation may be required in some cases.
Contents
[hide]

1 Clinical presentation

2 Diagnosis and classification 3 Treatment 4 See also

[edit]Clinical

presentation

Axial CT showing varices of the fundus in liver cirrhosis with portal hypertension

Gastric varices can present in two major ways. First, patients with cirrhosis may be enrolled in screening gastroscopyprograms to detect esophageal varices. These evaluations may detect gastric varices that are asymptomatic. When gastric varices are symptomatic, however, they usually present acutely and dramatically with upper GI hemorrhage. The symptoms can include hematemesis, or vomiting blood; melena, passing black, tarry stools; or passing maroon stools or frank blood in the stools. Many patients with bleeding gastric varices present in shock due to the profound loss of blood. Secondly, patients with acute pancreatitis may present with gastric varices as a complication of thrombosis of the splenic vein. The splenic vein sits over the pancreas anatomically and inflammation or cancers of the pancreas may result in thrombosis, or clotting of the splenic vein. As the short gastric veins of the fundus of the stomach drain into the splenic vein, thrombosis of the splenic vein will result in increased pressure and engorgement of the short veins, leading to varices in the fundus of the stomach. Laboratory testing usually shows anemia and often thrombocytopenia (a low platelet count). If cirrhosis is present, there may be coagulopathy manifested by a prolonged INR; both of these may worsen the hemorrhage from gastric varices. In very rare cases, gastric varices are caused by splenic vein occlusion as a result of the mass effect of slow-growing pancreatic neuroendocrine tumors. [edit]Diagnosis

and classification

The Sarin classification of gastric varices identifies two types of gastroesophageal varices, where esophageal varices are found concurrently, and two types ofisolated gastric varices, found in the absence of esophageal varices.

Antral varices, of Sarin classification IGV-2, an unusual class of gastric varices.

Diagnosis of gastric varices is often made at the time of upper endoscopy. The Sarin classification of gastric varices identifies four different anatomical types of gastric varices, which differ in terms of treatment modalities. [edit]Treatment Initial treatment of bleeding from gastric varices focuses on resuscitation, much as with esophageal varices. This includes administration of fluids, blood products, and antibiotics. The results from the only two randomized trials comparing band ligation vs cyanocarylate suggests that endoscopic injection of cyanoacrylate, known as gastric variceal obliteration or GVO is superior to band ligation in preventing rebleeding rates. Cyanoacrylate, a common component in 'super glue' is often mixed 1:1 with lipiodol to prevent polymerization in the endoscopy delivery optics, and to show on radiographic imaging. GVO is usually performed is specialized therapeutic endoscopy centers. Complications include sepsis, embolization of glue, and obstruction from polymerization in the lumen of the stomach. Other techniques for refractory bleeding include:

Transjugular intrahepatic portosystemic shunts (TIPS) Balloon occluded retrograde transvenous obliteration techniques (BORTO)

Gastric variceal ligation, although this modality is falling out of favour Intra-gastric balloon tamponade as a bridge to further therapy

a caveat is that a larger balloon is required to occupy the fundus of the stomach where gastric varices commonly occur

Liver transplantation