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Oesophageal Varices

Prevalence

Alcholic & Viral infections are leading causes of liver disease, which in turn lead to varicies. The risk of bleeding from oesophageal varices in the first year after identification is 30%. Oesophageal varices develop in approximately 8% of patients with chronic liver diseases per year for the first two years and in 30% of patients by the sixth year.

Foundation

The causes of oesophageal varices are anything that can cause portal hypertension. Some examples are in the table that follows.

Causes Osophageal varicies

Pre-hepatic Portal vein thrombosis.

Portal vein obstruction – congenital atresia/stenosis.

Increased portal blood flow – fistula.

Increased splenic flow.

Intra-hepatic Cirrhosis due to various causes, including alcoholic, chronic hepatitis

(eg viral or autoimmune).

Idiopathic portal hypertension (hepatoportal sclerosis).

Acute hepatitis (especiallyalcoholic)

Schistosomiosis

Congenital hepatic fibrosis. Myelosclerosis.

Post-hepatic Compression (eg from tumour).

Budd Chiari syndrome

Constrictive pericarditis &rarely right-sided heart failure

Determinants of increased risk of variceal bleeding

These are also the same factors that increase the risk of portal hypertension:

Circadian rhythms.

Decompensation of liver disease.

Malnourishment.

Alcohol intake

Physical exercise.

Bacterial infection (cause of initial, and recurrence of, bleeding).

Increased intra-abdominal pressure. Aspirin.

Non-steroidal anti-inflammatory drugs (NSAIDs).

Appearance

Manifestations

Dysphagia/odynophagia(pain on swallowing; uncommon).

Haematemesis (most commonly), melaena.

Abdomnal pain

Confusion secondary to encephalopathy (even coma).

Features of liver disease and specific underlying condition.

Symptoms

Melaena.

Pale.

Peripherally shut down.

Pallor.

Signs of sepsis may also commonly be present.

Hypotension and tachycardia (ie shock).

Reduced urine output.

Signs of chronic liver disease.

Reduced Glasgow Coma Scale

invetigations

Endoscopy is required at an early stage.

INR.

Renal Function

Full blood count-haemoglobin may be low; MCV may be high, normal or low; platelets may also be low; WCC may be raised.

Clotting including

Liver Function Tests

Group and cross-match.

Investigations as indication for the underlying cause of portal hypertension.

CXR – patients may have aspirated or have chest infection. Aseptic tap may be needed if bacterial peritonitis is suspected.

Wellness Program

Management for acute variceal haemorrhage consists of vasoactive drugs, endoscopic band ligation and antibiotics prophylaxis. Transjugular intrahepatic portosystemic shunt (TIPS) is reserved for those who do not respond or are unlikely to respond to initial standard management.

Health Guidance and Recommendations

Terlipressin should be offered to patients with suspected variceal bleeding at presentation.

Treatment should be stopped after definitive haemostasis has been achieved, or after five days, unless there is another indication for its use.

Prophylactic antibiotic therapy should be offered at presentation to patients with suspected or confirmed variceal bleeding. Antibiotic use significantly reduces the mortality of patients who develop acute UGIB in association with chronic liver disease.

Oesophageal varices:

Band ligation should be used for patients with upper GI bleeding from oesophageal varices.

TIPS should be considered if bleeding from oesophageal varices is not controlled by band ligation. There is sufficient evidence to show that stent insertion is effective for selected patients with oesophageal varices in whom other methods of treatment have failed to control bleeding.

Gastric varices:

TIPS should be offered if bleeding from gastric varices is not controlled by endoscopic injection of N-butyl-2-cyanoacrylate.

Endoscopic injection of N-butyl-2-cyanoacrylate should be offered to patients with Upper GI bleeding from gastric varices.

REVITALIZATION

Patients should be monitored with a cardiac monitor, blood pressure, pulse rate and urine output (catheterise until the patient is stabilised).

Cross Matched Blood transfusion is necessary to build up circulatory volume to normal.

Assess airway – can easily be compromised, especially if reduced Glasgow Coma Scale.

Oxygen should be provided and intravenous access gained if possible.

Wide-bore access is needed, with a minimum of two cannulae (central access may also be required).

40% oxygen to be provided if tachypnoeic or confused.

Fluid resuscitation should be begun with rapid infusion of crystalloid and colloid solution.

There is some concern that saline infusions may worsen ascitis but the nature of the emergency warrants their use.

A nasogastric tube should be inserted to assess the severity of the bleeding and to lavage gastric contents before performing endoscopy.

Correct anaemia and coagulopathy: blood transfusion will be necessary. Many of the patients will have a coagulopathy, and so give intravenous vitamin K immediately. If INR is prolonged, also give fresh frozen plasma. platelet transfusion may be required.

Inserting a central venous line/pulmonary artery catheter in haemodynamically unstable or elderly patients can be considered, or for those with cardiac or pulmonary disease, to monitor fluid balance (overuse can produce oedema, ascites and hyponatremia.

Endoscopy

Urgent endoscopy is necessary for variceal haemorrhage. Emergency fibre optic endoscopy confirms the diagnosis and source of bleeding.

Endoscopy allows the bleeding point to be visualised and treated:

Band ligation is the first choice of treatment.

Urgent endoscopy in unwell patients is not without its risks, and adequate staffing and the presence of resuscitation facilities are required.

Emergency sclerotherapy is still widely used as a first-line therapy for variceal bleeding in patients with cirrhosis, especially when band ligation is not available. However, drug treatment may stop bleeding in the majority of these patients. There is no convincing evidence to support the use of emergency sclerotherapy for variceal bleeding in cirrhosis as the initial single treatment when compared with vasoactive drugs.

Vasoactive drugs

The use of vasoactive agents (terlipressin, octreotide or somatostatin) is associated with a significantly lower risk of acute all-cause mortality and transfusion requirements, and improved control of bleeding and shorter hospital stay.

Terlipressin is considered the vasoactive agent of choice in acute variceal bleeding. It should be given to all patients presenting with suspected variceal bleeding prior to endoscopy and following confirmation.

Terlipressin is an analogue of vasopressin and studies have shown it to be superior to placebo in variceal haemorrhage.

Vasopressin and terlipressin should not be used in severe hypovolaemic shock and patients with severe cardiac disease.

Variceal obturation with glue

This involves embolisation of varices with a glue-like substance (N-butyl-2 cyanoacrylate).

It is particularly good for gastric or gastro-oesophageal variceal bleeding.

However, there is a risk of embolisation to the lung, spleen or brain.

Balloon tube tamponade (Sengstaken-Blakemore tube)

Balloon tamponade should be considered as a temporary salvage treatment for uncontrolled variceal haemorrhage.

The Sengstaken tube (preferably kept in the fridge to stiffen rubber and make passage easier) is inserted through the mouth and into the stomach.

The gastric balloon is inflated with air and the gastric balloon in then pulled up against the oesophagogastric junction, compressing submucosal varices.

The Sengstaken tube also contains an oesophageal balloon which is only rarely required when the gastric balloon does not work.

If bleeding continues, it may be that the tube is wrongly positioned or bleeding is from another source.

Transjugular intrahepatic portosystemic shunt

Transjugular intrahepatic portosystemic stent shunting is recommended as the treatment of choice for uncontrolled variceal haemorrhage.

The hepatic vein is cannulated percutaneously via the internal jugular vein, using a needle under ultrasound or fluoroscopic guidance.

A tract is created through the liver from the hepatic to the portal vein – thus reducing portal pressure. This is dilated and an expandable metal stent inserted to create a shunt.

This has a high success rate but encephalopathy is found in 25% of cases (as portal blood diverted from the liver) and shunt occludes within one year in up to 50% of cases.

Operation

Oesophageal transection and gastric devascularisation are rare procedures but may have a role for patients with portal and splenic vein thrombosis who are not suitable candidates for shunt procedures and who continue to have variceal bleeding despite endoscopic and pharmacological treatment.

Liver Transplant is the treatment of choice for patients with advanced liver disease.

Other aspects of management of variceal haemorrhage

Sedatives to be avoided if possible.

Patients are best managed on ITU/HDU.

Antibiotic prophylaxis – infection occurs in up to 50% of patients and is associated with a worse outcome. It is thought that bacteria release endotoxins that enhance portal pressure and impair coagulation. Antibiotics are therefore given early, eg Ciprofloxacin

Obviation

No specific treatment has been shown to prevent the formation of varices.

Prevention of first variceal haemorrhage depends on the size/characteristics of varices. In patients with small varices and high risk of bleeding, non-selective beta- blockers are recommended, while patients with medium/large varices can be treated with either beta-blockers or oesophageal band ligation.

Prevention of recurrent variceal haemorrhage consists of the combination of beta-blockers and endoscopic band ligation.

Endoscopic screening

All patients with newly-diagnosed cirrhosis should have screening endoscopy, looking for oesophageal varices.

If there are contra-indications to beta-blockers, the varices should be banded or sclerosed.

In the long term, repeated endoscopic screening is usually required, eg 2- to 3-yearly in cases of small varices.

Patients who have survived an oesophageal variceal bleed should receive beta-blockers, ± nitrates and endoscopic screening and treatment.

The use of measures of hepatic vein pressure gradient with an aim to reduce it under 12 mm Hg is associated with a significant reduction in mortality.

Outlook

Patients who have bled once from oesophageal varices have a 70% chance of rebleeding.

Approximately one third of further bleeding episodes are fatal.

Associated renal, respiratory, cardiovascular and immune disorders account for 20-65% of mortality in patients with oesophageal varices.

The risk of death is maximal during the first few days after the bleeding episode and decreases slowly over the first six weeks.

CONCLUSION

Variceal haemorrhage occurs from dilated veins (varices) at the junction between the portal and systemic venous systems. Varices tend to be in the distal oesophagus and/or the proximal stomach, but isolated varices may be found in stomach, small or large intestine but more common in oesophagus. Majority of patients with varicies have chronic liver disease. Bleeding from varicies tends to be large volume though size of varicies depends on portal pressure which inturn related to severity of liver disease.