Transcript Slide 1

How to manage a
case of jaundice in
General Practice
Andrew M Smith
Nov 2007
Jaundice
"it looks like there's something wrong…
….with your television set.“
Matt Groenig, creator of
The Simpsons
Jaundice
• An elevation of serum bilirubin above
normal limit (>40 umol/l)
• Clinically evident at x2 normal level
Learning Objectives
By the end of this talk participants will be able to:
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understand normal liver anatomy and physiology
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Recognise the COMMON causes of jaundice and their
classification
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take a history and perform an examination pertinent for
jaundiced patients
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Select the appropriate investigations and understand who
and when to refer
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opportunity to apply the above in selected case histories
Gross Hepatic Anatomy
Gross Hepatic Anatomy
Liver Histological Structure
Liver Histological Structure
Functions of the Liver
1.Metabolism
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Fats
Proteins
Carbohydrates
Hormones
2.Storage
3.Metabolism and excretion bilirubin
4. Drug metabolism and excretion
Normal Bile Physiology
• 1500ml bile/day
2 roles: 1. excretion
2. emulsification of fat
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Water (98%)
Bile Salts
Bile pigments (Bilirubin)
Fatty Acids
Lecithin
Cholesterol
Normal Bilirubin Metabolism
RBC
Hb Degraded to
Globin + Fe + Bilirubin
Hepatocyte
Bilirubin bound to
albumin
Conjugated
Bilirubin Diglucuronide
Kidney
Portal Vein
Intestine
Urobilinogen
Urobilinogen
Bilirubin
Urobilinogen
Stercobilin
Major Causes of Jaundice
Pre-hepatic
Haemolysis
Ineffective erythropoiesis
Hepatic
Prematurity
Gilberts
Drugs
Hepatitis: viral, NASH
Alcohol / cirrhosis
Tumours
Extrahepatic sepsis
Post-hepatic
‘Obstructive’
Gallstones (in the lumen)
Bile duct stricture ( in the wall)
Ca pancreas (extrinsic)
Investigation Of A Jaundiced
Patient
• History
• Examination
• Tests
– Blood
– Urine
– Imaging
History
‘most important part of the evaluation of the
patient with jaundice’
History
1. Jaundice
2. Pale stools, dark urine?
YES = POST HEPATIC
PAIN?
YES
Colicky
Fatty food
intolerant
NO
Wt loss
Back Pain
Non-specific
symptoms
GALLSTONES
MALIGNANCY
ASSOCIATED FEVERS / RIGORS?
Gram –ve Septicaemia
ADMIT
NO = PRE & HEPATIC
Pre-hepatic:
Family history of bleeding
disorders, tendency to bleed
Hepatic:
IV Drug abuse
blood transfusions
Travel
flu-like illness
Hepatitis
Excess alcohol intake
(AUDIT & CAGE)
Obesity
Drug History
Cirrhosis/
NASH
Examination
• Stigmata Chronic Liver disease
• Hepatomegaly – texture,edge,
nodules
• Hepatosplenomegaly
• Ascites –shifting dullness
• Portal hypertesion
• Obvious iv drug use
Examination – obstructive
jaundice
• Temp
• Tachycardic +/- hypotensive
• Cachexia, Virchow’s
node,clubbing
• Murphy’s sign
• Courvoisier’s law ‘If in the presence
of jaundice the gallbladder is palpable then the
cause of the jaundice is unlikely to be gallstones’
• Urine
cholangitis
Investigations for jaundice
• Bloods
– General – Liver Function Tests
- Albumin, INR (give more info on function!)
– Specific
• Urine
• Imaging
• Histology
Ix Jaundice – Bloods
• Liver Function Tests
- really a test of hepatocyte damage
Alanine Transaminase ALT range <40iu/L
elevated cellular damage
AlkalinePhosphatase ALP range 70-300iu/KL
elevation post hepatic obstruction
Bilirubin range 5- 40 umol/L
Prehepatic
• Unconguated Bil ↑
• LFT’s N
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haptoglobins ↓
Reticulocytes ↑
Coombs test +ve
Clotting screen
• Urine urobilinogen
Hepatic
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ALT ↑ ↑ ↑
ALP N or ↑
Bil ↑
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Albumin ↓
INR ↑
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Hepatitis serology
Autoantibodies
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Caeruloplasmin ↑
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Anti-mitochondrial PBC
Anti-nuclear & antimicrosomal, Autoimmune
hepatitis
Wilson’s
γ-Globulins ↑
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Cirrhosis esp autoimmune
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Transferrin ↑ ↑
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α-foetoprotein, αFP ↑
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Haemochromatosis ↑
HCC in cirrhosis
Post - hepatic
• ALT N or ↑
• ALP ↑ ↑ ↑
• Bil ↑
• INR ↑
• CEA, Ca19.9 ↑
• Panc & cholangio Ca
LFTs and urine summary
Blood
Urine
ALT
ALP
Bil
Urobilinogen
Bilirubin
Prehepatic
N
N
↑↑
Present
absent
Hepatic
↑↑↑
N or ↑
↑↑
N
Present
Posthepatic
N or ↑
↑↑↑
↑↑
absent
Present
Imaging - Ultrasound
• Key investigation
• Distinguish obstruction
from hepatic cause
• Identify gallstones
Imaging - Ultrasound
Key information from report
Duct size
CBD normally < 7mm
Are both intrahepatic and extrahepatic ducts dilated?
If duct increased are calculi present?
Gallstones present none seen in CBD but Gallbaldder abnomalities ie
GB stones, SLUDGE, increased GB wall thickness
No gallstones, but CBD ↑ ? Pancreatic malignancy
No calculi
Texture of liver eg normal, fatty, micronodular
Dioscrete Lesions present
Imaging - CT Scan
Imaging MRCP + MRI
Imaging ERCP
Imaging PET scan
Management
• Good history, drives rest of management
• Investigations
– General: LFT’s and USS, Urine dipstix
– Determine obstruction or not
– Specific: Directed at underlying cause
Who to treat? Who to refer?
Determining who to refer is easier
Pragmatic approach
1. EMERGENCY
1. Any patient with evidence of ascending cholangitis
2. Unwell eg fulminant hepatic failure, paracetamol OD,
Decompensated cirrhosis
1. Failure to cope/thrive
2. 2 WEEK WAIT
1. Evidence or suspicion of cancer
QUESTIONS
Case 1
• An 18 year old first year med student
comes to see you and confides that his
mates take the mickey out of him as he
intermittently appears to have yellow
eyes?
• What do you do?
Gilbert’s disease
• Diagnosis of exclusion
• Good Hx. No family hx of sickle/G6PD defficiency
• no other risk factors
• Notes jaundice worsens on fasting
• Unconguated Bil ↑ and LFT’s N
• haptoglobins Reticulocytes both normal, Coombs test ve
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5 -7 % population, normal lifespan, reasssure.
Case 2
• One of your known recidivists attends,
complaining of a distended abdomen
which is becoming painful?
• Diagnosis?
• Management?
Decompensated alcoholic
cirrhosis
History – confirms 100+ unit intake for 20 yrs
Examination – stigmata chronic liver disease
abdo, palpable liver and spleen
shifting dullness
Ix -
LFTs Bil ↑ , ALT ↑ ↑ ↑, ALP ↑
INR ↑
Albumin low
USS , cirrhosis, splenomegaly and ascites
Treatment – Cessation of alcohol
- treatment of withdrawal
- thiamine, folic acid
- Nutritional support
- low salt diet, spironolactone
- Ix portal HTN, OGD, banding, B –blocker, TIPs
- If abstains, HCC surveillance
- contiuned abstinence, consider transplant
Survival with Alcoholic Liver
Disease
Case 3
• You are asked to make a home visit to see a 53 yr old
man with severe abdominal pain . His notes show that
he had an episode of pancreatitis on holiday in Spain a
year ago.
• He tells you that the has had upper tummy pain, can’t
get comfortable and has had shakes and feels cold?
• What is the diagnosis?
• What action do you take?
Ascending Cholangitis
• Examination reveals fever, jaundice and a
tachycardia.
• He has Charcot’s triad – pain, jaundice,
fever, ie ascending cholangitis
• He needs an emergency admission,
significant morbidity and mortality
• If possible iv access, fluid, antibiotic,
analgesia
Ascending Cholangitis
At hospital, continue resuscitation, antibiotics, check and correct INR
Emergency ERCP and duct clearance
Laparoscopic Cholecystectomy, same admission
Gallstones
• Previous pancreatitis due to gallstones.
20% incidence of further complications
within 6 months once symptomatic
• In elective situation can avoid ERCP, by
performing a duct exploration at the time of
laparoscopic cholecystectomy
• On horizon of further sea change with
advent of NOTES (natural orifice
transluminal endoscopic surgery)
Case 4
• A 37 year old Chinese refugee who has just
settled in Leeds, presents frankly jaundiced with
a history of abdominal pain and weight loss. On
examination he is clearly jaundiced.
• Can we make an educated guess as to the
aetiology from the history?
• What do we do next?
Hep C and HCC
• LFT’s and USS – ALT, ALP and Bilirubin
grossly elevated.
• USS cirrhosis and multiple lesions.
Referred.
• CT and Hep C, aFP
Beyond transplant or resection
Rx Chemoembolisation
HCV
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Persistent infection in 85% individuals
170 million worldwide, 4 million USA
Acute HCV hepatitis, rarely seen
Progression of HCV is silent
• 20-30% cirrhosis, 2-3% HCC
• Treatment Interferon (Peg interferon and
Ribavirin)
Case 5
Your senior partner has been seeing for over a
year a previously fit 43yr old man with non
specific symptoms of fatigue. Two consecutive
ALT’s six months apart were elevated at 120,
and 107 ( normal < 40iu). The rest of his blood
work was normal.
Do you act on this result?
Investigation isolated abnormal
LFT
Investigation isolated raised ALT
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Present > 6 months should investigate
Good Hx and Exam
FIRST WAVE TESTS
1 .Exclude drugs NSAIDs, antibiotics, statins, antiepileptic drugs anti-TB.
Herbal remedies. Paracetamol
2. Assess Alcohol excess
3. Hep B and C
4. Hereditary Haemochromotosis
5. NASH and steatosis
SECOND WAVE TESTS Refer
6. Thyroid/Coeliac/muscle disorders
THIRD WAVE – Definitely refer
Hep B
• Send hepatitis serlogy .
• Will assess status to determine whether
immune/carrier or chronic infection
• HepBsAg, HepBsAb, HepBcAb
• chronic infection HepBsAG +ve + HepBcAb +ve
• immune
• HBV DNA
HepBsAb +ve , HepBcAb +ve
Hep C
• Hep C Antibody
• Then Hep C RNA, Hep C genotype and
liver biopsy
Haemochromotosis
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Frequency 5/1000
Fe and TIBC,
Fe saturation > 45% then ferritin
Ferritin > 400ng/ml
Liver biopsy
NASH
• NASH more common women and type 2
Diabetes
• Hep B/C/HCC negative USS to look for
steatosis
• Bx if stigmata chronic liver disese
Isolated Hyperbilirubinaemia
• Occurs – excess production or impaired uptake
• Check conjugated vs unconjugated
• Assess Haemolysis
• No haemolysis, fluctuating bilirubin – gilberts
disease.
Isolated Alkaline Phosphatase
• Source – liver and bone
• Increased 3rd trimester and in women between
30 and 50 yrs
• Determine source, gGT and 5’nucleosidase
increases in liver disease
• Gel electrophoresis
• If Hepatic – USS, if no obstruction then AMA for
PBC
What is the most likely cause of
jaundice that I will see?
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South Wales, Gut 2002
Glasgow, Gut, 2002
Alcoholic liver disease
Gallstones
Malignacy
Summary
• Good history will direct rest of care
• LFTs and USS initially
• Move to specific tests
• Admit ‘unwell’ ie cholangitis
• Always available to discuss
QUESTIONS