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
4
1
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)
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, Usually asymptomatic early on
jaundice, RUQ pain
Investigation See below. Biopsy Anti-HCV, HCV DNA. Biopsy.

% Chronic 5-10% 85%

Treatment Supportive. Chronic: antivirals (nucleoside Nucleoside analogues, protease inhibitors
analogues). Transplant (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 • Imaging
 Bedside
 Observations (BP, pyrexia, BM) • US Abdomen
 ECG • CT abdomen
 ABG • CT angiography
 GCS/West Haven
• CXR
 Bloods
• ERCP
 FBC (anaemia, WCC)
• Special
 U&Es (urea, creatinine)
 LFTs (all important) • Drugs e.g. paracetemol
 Clotting (intrinsic and extrinsic) • OGD (varices)
 CRP (infective) • Hepatitis screen/leptospirosis
 Cholesterol (fatty) • Ascitic tap
 HbA1c
• Liver biopsy (cancer, severity)
 Gamma GT (alcohol)
• PET scan (mets)
 Antibodies
• 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 • Hepatic encephlopathy –
 Alcohol abstinence laxatives, antibiotics, IV fluids
 Fluid restriction (avoid NaCl), mannitol
 10% dextrose infusion/sliding scale • SBP – antibiotics e.g. tazocin
 Raise head of bed Surgical
Medical • TIPSS
 Jaundice – urseodoexycholic acid , • Peritoneal lavage/ascitic tap
colystyramine reduces pruritus
 Alcohol complications - Pabrinex
(IV/PO), chlordiazepoxide
 Ascites – Diuretics, Paracentesis, NG
feeding
 Ulceration – omeprazole
 Bleeding – vitamin K/octaplex
 Wilsons’s - penicillamine
Chronic management
Personal Surgical
 Alcohol abstinence • TIPSS
 Optimise nutrition • Liver transplantation
 Low salt diet

Medical
 Jaundice – urseodoexycholic acid ,
 Ascites – Diuretics
 Hepatic encephlopathy – laxatives,
 Autoimmune – steroids
 Renal failure - Haemodialysis
 Rastionalise pharmacy
 Omeprazole
Prognosis
 5 year survival rate is 50%
 Post-transplant 5 year survival 65%
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?