Tim Badcock
FY1 Colorectal surgery
21/10/13
Plan
• Introduction to the liver
• Definition
• Clinical Scenario
• Presentation
• Aetiology
• Complications
• Investigations
• Management
• Prognosis
Introduction to the liver
 5 Functional
domains
 4 lobes
 3 vascular
 2 important
ligaments
 1 Biliary tree
5.Domains
• Synthetic
– Albumin
– Clotting factors (1972)
• Metabolism
– CYP350 drugs
– Gluconeogenesis/glycogenesis/glycogenolysis
– Homeostasis
– Iron, copper, vitamin K
• Vascular
• Immunological
– Kuppfer cells beside sinusoids
• Biliary tree
– Bilirubin
– Left/right hepatic = common hepatic duct
– Common hepatic + bile duct = common bile duct
– Common bile duct + pancreatic duct
4. Lobes
 Left
 Right
 Caudate
 Quadrate
3. Vascular structures
 Hepatic portal vein (80%)
 Hepatic artery (18%)
 Hepatic vein (2%)
2. Ligaments
 Falciform (developmental structure of liver, umbilical
vein)
 Venosum (ductus venosus)
1. Biliary tree
2
3
1
4
5
6
7
8
9
Definition
• Acute/chronic, organ system, key characteristics
• A chronic reduction in hepatic function characterised
by poor synthetic, metabolic, and immunological
functions and vascular compromise associated with
ascites and portal hypertension.
• Also associated with acute decompensation events
characterised by acute haemorrhage, severe abdominal
infection, neurological impairment and oedema
Timing
 Hyperacute (<1week)
 Acute liver failure (7-28 days)
 Fulminant liver failure
(1 month-6 months)
 Chronic (>6 months)
Clinical scenario
• 54 year old gentleman presents to his GP with
increasing swelling of his abdomen and feet over the
last 2 months. He has been increasing tired over this
time and feels nauseous and is off his food. His wife
has commented that his eye have turned yellow over
the last few days. He works in a warehouse and
smokes 10 cigarettes a day. He admits to drinking 4
cans of lager a night. His wife says he drinks at least 8
cans a night and a bottle of whiskey a week. He
noticed that he bled profusely when he cuaght himself
on a baked beans can
Case study
 On examination he has pale white nails and a slghtly
bent 4th finger. He has man boobs. He is jaundiced but
has no hepatic flap and is orientated in time, place and
person. His abdomen is distended but soft and nontender. There is no palpable organomegaly but there is
shifting dullness. A raised JVP is noted on hepatic
compression
Presentation
• Synthetic
– Albumin – ascites, infection
– Clotting - variceal bleed, haematemesis, meleana
• Metabolism
• Bilirubin – jaundice
• CYP450 drugs – variable INR, toxicity
•
•
•
•
•
•
ODEVICES = inhibitor
PCBRAS – inducer
Hepatic encephalopathy
Hypoglycaemic
Hormones – high oestrogen
Syndromes
Syndromes
 Autoantibodies against hepatocytes. Often young women with
other autoimmune conditions. RUQ pain and jaundice
 α1- antitrypsin deficiency (early severe fibrosis)
 Primary biliary cirrhosis (AMA, young women autoimmune)
 Primary sclerosing choloangitis (ANA,
 Haemochromatosis – early onset jaundice, bronze diabetes
 Wilson’s disease – Keyser-Flescher, serum caeruloplasmin
 Gilbert Syndrome (UDP glucoronyl transferase, early mild
jaundice)
 Crigler Nijjar syndrome (severe early, kernicterus)
Presentation
 Vascular
 Hepatomegaly (RUQ pain)
 Splenomegaly
 Haematesis (oesophageal varices)
 Meleana
 Immunological
 Spontaneous bacterial peritonitis
Biliary tree
 Jaundice
 Pre-hepatic (dark
stools)
 Hepatic (dark urine,
normal/pale stools)
 Obstructive (dark urine,
pale stools)
Urobilinogen/
stercobilinogen
Signs
Aetiology
• Alcoholic liver disease
• Non-alcoholic fatty liver disease
• Viral liver disease
• Primiary biliary sclerosis, Primary sclerosing
cholangitis, Wilson’s, HH etc
• Hepatocellular Carcinoma (rare, UC)
• Metastasis (common)/ Pancreatic cancer (rare)
• Cryptogenic Liver Cirrhosis
Pathophysiology
 Chronic inflammatory (swelling, fatty infiltraton,
cytoplasm granulation)
 Eosinophil and macrophage invasion
 Lytic necrosis
 Fibrosis and contracture
 Loss of liver architecture
 Sinusoids
 Acinii
 Portal triad
Alcoholic fatty liver disease
 High calorie intake in alcohol
 Fat droplets deposit in hepatocytes
 Ethanol directly affects cell membrane stability as does
aldehyde
 Chronic necrosis of cells with fibrosis
 Later becomes small cirrhotic liver
Non-alcoholic fatty liver disease
 5% population, asymptomatic
 Seen on US abdo/biopsy
 Diabetes Mellitus
 Metabolic syndrome (HTN, hypercholesteraemia,
diabetes)
 Pregnancy (high oestrogen)
 Idiopathic
 Oxidative stress and steatohepatitis
Hepatitis B & C
Hepatitis B
Hepatitis C
Virus
DNA
RNA
Spread
Blood, sexual
Blood
Presentation
Fever, malaise, anorexia, nausea, arthralgia,
jaundice, RUQ pain
Usually asymptomatic early on
Investigation
See below. Biopsy
Anti-HCV, HCV DNA. Biopsy.
% Chronic
5-10%
85%
Treatment
Supportive. Chronic: antivirals (nucleoside
analogues). Transplant
Nucleoside analogues, protease inhibitors
(anti-retroviral). Liver transplant
HbcAg = core antigen = replicating
HBeAg = pre-core antigen = current infection
HBsAg = surface antigen = acute/chronic
HBV DNA = infectious
Anti-HBc = active infection
Anti-HBe = latent infection if HBeAg +ve
vaccinated if HBeAg -ve
Complications
 Portal hypertension
 Diabetes
 Spontaneous bacterial peritoneal
 Hepatic encephalopathy
 Liver transplant
 Malnutrition
 Renal failure
Portal hypertension
 Oesophageal varices (azygous veins)
 Rectal varices (inferior rectal veins)
 Caput medusae (umbilical veins)
 Budd-Chiari syndrome (hepatic vein thrombosis)
 TIPSS (transjugular intrahepatic portosystemic shunt)
 OGD +/- Variceal banding, stent, sclerotherapy
 Massive haemorrhage protocol
Diabetes
 Poor glucose storage
 Bronze diabetes
 Diabetic therapy
 Dietary modification
Spontaneous bacterial peritoneal
 8% ascites
 Severe abdominal pain
 Severely unwell
 Ascitic tap
 Peritoneal lavage
 Intravenous antibiotics
 Liver transplant
Hepatic encephalopathy
 Increased ammonia from bacterial activity on protein in faeces
 Liver bypass (TIPSS)
 Haemorrhage
 Foetor hepaticus
 Hepatic flap (asterix)
 Decreased mental capacity e.g. Constructional apraxia
 West Haven Criteria
 Grade I altered mood/behaviour
 Grade II reduced consciousness
 Grade III Stupor
 Grade IV Coma
 Enemas, lactulose, niacin, IV fluids
Liver transplant
End stage liver failure
SBP
Congenital syndromes
Strict criteria for transplant
Long term immunosuppresants (azathioprine,
ciclosporin)
Avoid alcohol
Malnutrition
 Encourage highest possible protein intake
 High calorie intake
 Avoid alcohol
 Chlordiazepoxide
 Acamprosate
 Disulfiram
Renal failure
 Increased vascular pressure from portal hypertension
into splenic and renal veins
 Diabetic nephrotic syndrome – minimal change
 Hepatorenal syndrome – low oncotic pressure triggers
peripheral hypovolaemia, neuropepetide Y and RAAS
activation leads to constriction of afferent and
dilatation of efferent arterioles leading to renal
hypoperfusion
Investigations
 Biological
 Bedside
 Bloods
 Imaging
 Special
 Psychological
 Alcohol addiction
 Depression
 Social
 Unemployment
 Supportive housing
Biological
 Bedside
•
 Observations (BP, pyrexia, BM)
 ECG
 ABG
 GCS/West Haven
 Bloods
 FBC (anaemia, WCC)
 U&Es (urea, creatinine)
 LFTs (all important)
 Clotting (intrinsic and extrinsic)
 CRP (infective)
 Cholesterol (fatty)
 HbA1c
 Gamma GT (alcohol)
 Antibodies
•
Imaging
• US Abdomen
• CT abdomen
• CT angiography
• CXR
• ERCP
Special
• Drugs e.g. paracetemol
• OGD (varices)
• Hepatitis screen/leptospirosis
• Ascitic tap
• Liver biopsy (cancer, severity)
• PET scan (mets)
• Colnoscopy (ulcerative colitis)
Liver function tests
 Total protein = albumin + globins
 Albumin – long term synthetic
 Bilirubin – bile production/retention, Gilberts/Crigler
Nijjar, Sickle cell, Iatrogenic - carbimazole
 ALP – bile duct inflammation + bone + hyperoestrogenic
states, drugs
 ALT – hepatocyte inflammaion + thyroid dysregulation +
coeliac + exercise
 Clotting – INR, APTT
 Extras – amylase, gGT, paracetemol (NAC)
Acute Management
Personal
 Alcohol abstinence
 Fluid restriction
 10% dextrose infusion/sliding scale
 Raise head of bed
Medical
 Jaundice – urseodoexycholic acid ,
colystyramine reduces pruritus
 Alcohol complications - Pabrinex
(IV/PO), chlordiazepoxide
 Ascites – Diuretics, Paracentesis, NG
feeding
 Ulceration – omeprazole
 Bleeding – vitamin K/octaplex
 Wilsons’s - penicillamine
• Hepatic encephlopathy –
laxatives, antibiotics, IV fluids
(avoid NaCl), mannitol
• SBP – antibiotics e.g. tazocin
Surgical
• TIPSS
• Peritoneal lavage/ascitic tap
Chronic management
Personal
 Alcohol abstinence
 Optimise nutrition
 Low salt diet
Medical
 Jaundice – urseodoexycholic acid ,
 Ascites – Diuretics
 Hepatic encephlopathy – laxatives,
 Autoimmune – steroids
 Renal failure - Haemodialysis
 Rastionalise pharmacy
 Omeprazole
Surgical
• TIPSS
• Liver transplantation
Multidisciplinerary Team
• GP
• Psychiatrist
• Gastroenterology
• Social services
• Physiotherapy
• Dietician
• Specialist nurses
Prognosis
 5 year survival rate is 50%
 Post-transplant 5 year survival 65%
Prognosis
References
 Kumar and Clarke, Clinical Medicine
 Oxford Clinical Handbook of Medicine
 Washington Hepatitis Study
 NICE guidelines albumen dialysis
 NICE guidance living donor liver transplant
 Review article: the modern management of hepatic encephalopathy by Bhajaj
 Netters anatomy
 Child-Pugh scoring article by Child and Pugh
 BMJ learning – liver disease module
 Doctors
 Consultant S Ramcharan, M Osborne, Dr Gelsthorpe
 Reg. K McArdle, J. Barnes
 SHO T. Nash
THANK YOU
 Any questions?