Gastroenterology

• Liver cirrhosis is the result of chronic inflammation and damage to liver cells.
• The functional liver cells are replaced with scar tissue (fibrosis).
• Nodules of scar tissue form within the liver.
• Fibrosis affects the structure and blood flow through the liver, increasing the resistance in the vessels leading into the liver.
• The increased resistance and pressure in the portal system is called portal hypertension.
• Factors that can trigger or worsen hepatic encephalopathy include constipation, dehydration, electrolyte disturbance, infection, gastrointestinal bleeding, high protein diet, and medications, particularly sedative medications.
• Management of hepatic encephalopathy involves lactulose to promote the production of soft stools, antibiotics to reduce the number of intestinal bacteria producing ammonia, and nutritional support, which may require nasogastric feeding.
• Lactulose works in several ways to reduce ammonia: it speeds up transit time and reduces constipation, promoting bacterial uptake of ammonia, changing the pH of the contents of the intestine to become more acidic, and killing ammonia-producing bacteria.
• Rifaximin is the usual choice of antibiotic as it is poorly absorbed and stays in the gastrointestinal tract.
• Neomycin and metronidazole are alternatives to rifaximin.
• Management options for ascites include a low sodium diet, aldosterone antagonists, paracentesis, prophylactic antibiotics, transjugular intrahepatic portosystemic shunt (TIPS), liver transplantation, and spontaneous bacterial peritonitis (SBP).
• Spontaneous bacterial peritonitis (SBP) occurs in 10-20% of patients with ascites and has a mortality of 10-20%.
• Spontaneous bacterial peritonitis (SBP) involves an infection developing in the ascitic fluid and peritoneal lining without a clear source of infection.
• Spontaneous bacterial peritonitis can be asymptomatic.
• Presenting features of spontaneous bacterial peritonitis (SBP) include fever, abdominal pain, deranged bloods, ileus, hypotension, and the most common organisms are Escherichia coli and Klebsiella pneumoniae.
• Management of spontaneous bacterial peritonitis (SBP) involves taking a sample of ascitic fluid for culture before giving antibiotics, intravenous broad-spectrum antibiotics according to local policies, and hepatorenal syndrome involves impaired kidney function caused by changes in the blood flow to the kidneys relating to liver cirrhosis and portal hypertension.
• The exact pathophysiology of hepatorenal syndrome is still being debated, but it is thought that portal hypertension causes the portal vessels to release vasodilators, which cause significant vasodilation in the splanchnic circulation.
• Vasodilation in hepatorenal syndrome leads to reduced blood pressure, and the kidneys respond to the reduced pressure by activating the renin-angiotensin-aldosterone system, which leads to vasoconstriction of the renal vessels.
• Renal vasoconstriction combined with low systemic pressure results in the kidneys being starved of blood and significantly reduced kidney function in hepatorenal syndrome.
• Hepatorenal syndrome has a poor prognosis unless the patient has a liver transplant.
• Hepatic encephalopathy, also known as portosystemic encephalopathy, is thought to be caused by the build-up of neurotoxic substances that affect the brain.
• One toxin particularly worth remembering is ammonia, produced by intestinal bacteria when they break down proteins.
• Ammonia is absorbed in the intestines.
• Acutely, hepatic encephalopathy presents with reduced consciousness and confusion.
• Hepatic encephalopathy can present more chronically with changes to personality, memory and mood.
• Cirrhosis disrupts the ability of the liver to store glucose as glycogen and release it when required.
• Less protein is available for maintaining muscle tissue and muscle tissue is broken down for use as fuel.
• Management of cirrhosis involves nutritional support guided by a dietician, with regular meals, high protein and calorie intake, reduced sodium intake to minimise fluid retention, and avoiding alcohol.
• The portal vein comes from the superior mesenteric and splenic veins and delivers blood to the liver.
• Liver cirrhosis increases the resistance to blood flow in the liver.
• The increased back pressure on the portal system due to liver cirrhosis is called portal hypertension.
• The back pressure of blood results in splenomegaly.
• Back pressure in the portal system causes swollen and tortuous vessels at sites where collaterals form between the portal and systemic venous systems.
• Varices are asymptomatic until they start bleeding.
• Due to the high blood flow, bleeding from varices can cause patients to exsanguinate very quickly.
• Prophylaxis of bleeding in stable oesophageal varices involves non-selective beta blockers first-line, variceal band ligation if beta blockers are contraindicated, and vasopressin analogues which cause vasoconstriction and slow bleeding.
• Prophylactic broad-spectrum antibiotics are shown to reduce mortality in patients with cirrhosis.
• Urgent endoscopy with variceal band ligation is necessary in the management of bleeding oesophageal varices.
• Other options to control the bleeding include Sengstaken-Blakemore tube and Transjugular intrahepatic portosystemic shunt (TIPS).
• Ascites refers to fluid in the peritoneal cavity, caused by the increased pressure in the portal system.