Transcript Slide 1
Dr Allister J Grant Consultant Hepatologist University Hospitals Leicester NHS Trust Anatomy &Physiology Anatomy &Physiology Anatomy &Physiology IVC Portal Vein Hepatic Artery Splenic Vein Gallbladder CBD SMV Anatomy &Physiology Liver Functions Nutrition/Metabolic – stores glycogen (glucose chains) – releases glucose when if no insulin – absorbs fats, fat soluble vitamins – manufactures cholesterol Bile Salts – lipids derived from cholesterol – dissolves dietary fats (detergent) Bilirubin – breakdown product of haemoglobin Liver Functions Clotting Factors – manufactures most clotting factors Immune function – Kupfer cells engulf antigens (bacteria) Detoxification – drug excretion (sometimes activation) – alcohol breakdown Manufactures Proteins – albumin – binding proteins Symptoms Early disease Cholestatic patients • • • • • • • • • • • asymptomatic fatigue, malaise anorexia, nausea jaundice pruritis easy bruising and bleeding • abdominal pain fatigue, malaise anorexia, nausea jaundice +++ pruritis +++ grey or claycoloured stools Disease Progression Acute Liver Failure Chronic Liver Disease • <6 weeks duration • >6 months • • • • • • • Cirrhosis leading to Jaundice Encephalopathy Cerebral Oedema Acute Renal Failure Acidosis Hypoglycaemia MOF • Recurrent decompensation – Ascites – Portal Hypertension (variceal bleeding) – Encephalopathy • • • • Low albumin/Malnutrition Hepatorenal syndrome Hyponatraemia Hepatoma Disease Progression 100% Liver function A B Cirrhosis C Liver Failure Years Causes of Chronic Liver disease • Viral • Hepatitis B • Hepatitis C • Inherited • Haemochromatosis • Wilsons Disease • -1 Antitrypsin Deficiency • Autoimmune Hepatitis • Biliary Disease • Metabolic • NASH • Amyloid • Alcoholic Cirrhosis • PBC • PSC • Secondary sclerosing cholangitis • Caroli’s syndrome Signs of Chronic Liver Disease • • • • • • • • • None Asterixis/Flap Relative hypotension Oedema Jaundice/No jaundice Large/Small liver Splenomegaly Gynecomastia Testicular atrophy-loss of secondary sexual characteristics Cirrhosis Expanded Portal Tracts (Blue) Decompensation in Cirrhosis Means the development ofAscites Hepatic Encephalopathy Portal hypertension (variceal haemorrhage) Decompensation in Cirrhosis Means the development ofAscites Hepatic Encephalopathy Portal hypertension (variceal haemorrhage) The Development of Ascites 50% of compensated cirrhotics develop ascites over 10yrs 50% of cirrhotics with ascites will die within 2 yrs (50% 2yr rule for OLTx assessment) The Development of Ascites Peripheral arterial dilatation Reduced effective blood volume Activation of renin-angiotensin-aldosterone system Sympathetic nervous system ADH NaCl Na retention & Water retention Ascites and Oedema Low urinary Na Dilutional hyponatraemia Plasma volume expansion Ascites Schrier et al Hepatol 1988 Decompensation in Cirrhosis Means the development ofAscites Hepatic Encephalopathy Portal hypertension (variceal haemorrhage) Encephalopathy • Grade 1 » » » » Constructional apraxia Poor memory – number connection test Agitation/ irritability Reversed sleep pattern • Grade 2 » Lethargy, disorientation » Asterixis • Grade 3 » Drowsy, reduced conscious level • Grade 4 » Coma Causes of Encephalopathy INCREASED AMMONIAGENESIS Increased substrate (protein) for ammoniagenesis – – – – Increased protein intake Gastrointestinal bleeding Constipation Dehydration Increased substrate (urea) for ammoniagenesis – Renal failure Increased catabolism of protein – Infection – Hypokalemia – Sepsis Causes of Encephalopathy DECREASED HEPATOCELLULAR FUNCTION – – – – – – – – – Worsened intrinsic liver disease Hypoxia Anaemia Development of hepatocellular carcinoma Dehydration Hypotension Sepsis Drug toxicity Superimposed viral hepatitis Causes of Encephalopathy INCREASED PORTOCAVAL SHUNTING – – – – Portal vein thrombosis Transjugular intrahepatic portosystemic shunt formation Surgical shunt formation Spontaneous shunt formation PSYCHOACTIVE DRUG USE – – – – – Benzodiazepines Ethanol Antiemetics Antihistamines Others Decompensation in Cirrhosis Means the development ofAscites Hepatic Encephalopathy Portal hypertension (variceal haemorrhage) Portal Circulation Oesophageal varices Prognosis 1 Year Survival – Child Pugh A – Child Pugh B – Child Pugh C 80 - 100% 60 - 80% 35 - 45% Management of Bleeding Varices • Prevention • Resuscitation • Endoscopy - Band Ligation Sclerotherapy • Pharmacotherapy- Terlipressin • Balloon Tamponade • TIPS Management of Bleeding Varices • Prevention • Resuscitation • Endoscopy - Band Ligation Sclerotherapy • Pharmacotherapy- Terlipressin • Balloon Tamponade • TIPS Fluid Management • • • • • • Crystalloid Colloid Blood Platelets FFP Vitamin K Management of Bleeding Varices • Prevention • Resuscitation • Endoscopy - Band Ligation Sclerotherapy • Pharmacotherapy- Terlipressin • Balloon Tamponade • TIPS Oesophageal varices Oesophageal varices Bleeding Gastric Varices Variceal Bander Variceal Band Ligation Management of Bleeding Varices • Resuscitation • Endoscopy - Band Ligation Sclerotherapy • Pharmacotherapy- Terlipressin • Balloon Tamponade • TIPS Pharmacotherapy Terlipressin vs. Balloon Tamponade Mortality Favours Terlipressin Favours Tamponade Terlipressin vs. Endoscopic Therapy Mortality Management of Bleeding Varices • Resuscitation • Endoscopy - Band Ligation Sclerotherapy • Pharmacotherapy- Terlipressin • Balloon Tamponade • TIPS Sengstaken-Blakemore Tube Complication of SBT Management of Bleeding Varices • Resuscitation • Endoscopy - Band Ligation Sclerotherapy • Pharmacotherapy- Terlipressin • Balloon Tamponade • TIPS The End “All right, let's not panic. I'll make the money by selling one of my livers. I can get by with one “ Doh!