Transcript Obstructive Jaundice - The Cabrini Code

A woman with
abdominal pain….
Michelle Papandony
Amanda Vo
Veronica Mezhov
Wei De Tee
Patient
• Mrs Wong
• 65 yo
• Migrated from China 5 years ago with her
family
HOPC
• Presented to ED with
– Pseudocolic
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RUQ pain 7/10, no radiation
Started 30 mins after dinner
No relieving/ aggravating factors
2-3 similar episodes over the last 2 months but each
lasting 10-15 mins
– Slightly nauseated, no vomiting
– Relevant negatives
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No abdominal distension
Denies change in appearance of stool or urine
No diarrhoea
No jaundice
No fever/ rigors
No recent travel
No sick contacts
No take-away food
No cough
No CV or resp symptoms
No urinary symptoms
PHx
• GORD
• Hyperlipidaemia (diet control)
• Salpingectomy and hysterectomy 15 years ago
due to peri-menopausal dysmenorrhea and
menorrhagia
Medications
• Omeprazole
• NKDA
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No relevant family history
No smoking history
Social drinker
Lives at home with her husband and two
daughters
• No financial/ other stressors
Examination
• Vital Signs (HR 90, BP 150/90, RR 18, Temp 36.9)
• Mild truncal obesity
• Slight scleral icterus, nil other peripheral stigmata
of liver disease
• Small xanthelasma bilaterally
• Nil scars or distension
of abdomen
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• No peritonism
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• Tender RUQ
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• Positive Murphy’s sign•
• Liver non palpable
due to pain
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• Liver span normal
• Bowel sounds present
• Kidneys not ballotable •
No hernia detected
PR not performed
Chest clear
S1S2 NAD, no
murmur
Peripheral
examinations
unremarkable
FWT: NAD
Ddx
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Cholecystitis ?Ascending cholangitis
Hepatitis
Pancreatitis
AMI
Lower lobe pneumonia
PID – not in this patient
Appendicitis – anatomical variant
Perforated peptic ulcer
Pyelonephritis – unlikely
Ix
• Bloods
– FBE + CRP
– U&E
– LFT + Coags
– Lipase/ Amylase
• Imaging
– Abdo USS
• Ix to rule out other dx if suspected eg. ECG
• While in ED, Mrs Wong became febrile (38.5)
and developed rigors. While her skin was not
jaundiced, her scleral icterus appeared to
worsen.
• Mx Plan
– IV Fluids
– Morphine + Metaclopramide
– NBM
– IV antibiotics (Ceftriaxone and Metronidazole)
Ix Results
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Mildly increased WCC
Raised CRP (250)
Markedly raised ALP and GGT
Mildly raised ALT and AST
Raised bilirubin
Coags NAD
Lipase NAD
U/S showed:
• Enlarged common bile duct of 10mm
• Gallbladder wall thickened
• Stones within the gallbladder and the common bile duct
• Mrs Wong was diagnosed with cholecystitis with
secondary ascending cholangitis (Charcot’s triad).
Mx
• Endoscopic Retrograde
Cholangiopancreatography (ERCP)
• Cholecystectomy 6 weeks after
Biliary Disease
Gallstone(s)
Defn: Solid crystal deposits that form within biliary
tract
Types:
1) Mixed (80%)
2)
Cholesterol
3)
Pigment stones
a) Black (2° haemolytic disease)
b) Brown (2° infection)
Normal bile
Bile salts
Phospholipids
(lecithin)
Cholesterol
Protein
Bilirubin
Definitions
• Cholestasis
=
Obstruction of bile flow
• Cholelithiasis
=
Gallstone(s) within the gallbladder
• Choledocholithiasis
=
Gallstone(s) within the CBD
*CBD = common bile duct
Overview of Biliary Disease
• Biliary colic
• Cholecystitis
– Acute
– Chronic
• Cholangitis
– Acute
– Primary Sclerosing (PSC)
cholangitis
• Primary Biliary Cirrhosis
(PBC)
Overview of Biliary Disease
• Biliary colic
Defn: Cystic duct obstruction
• Cholecystitis
Features
– Acute
– Chronic
• Cholangitis
– Acute
– Primary Sclerosing (PSC)
• Primary Biliary Cirrhosis
(PBC)
– 2° gallstone
• Epigastric / RUQ pain
– Resolves <6hrs
– Usu. constant
• Otherwise: colicky
– Intermittent pain 2° gallbladder
contractn
– Quality:
• Aching
• Tightness
– Location:
• Epigastric (usually)
• RUQ
± Referred pain: shoulder / scapula
Overview of Biliary Disease
• Biliary colic
Defn: Gallbladder inflammation
• Cholecystitis
Features
– Acute
– Chronic
• Cholangitis
– Acute
– Primary Sclerosing (PSC)
• Primary Biliary Cirrhosis
(PBC)
– 2° cholestasis from blocked cystic duct
• Epigastric / RUQ pain
– Persists >6hrs
– Usu. constant
• Otherwise: colicky
– Intermittent pain 2° gallbladder contractn
– Quality:
• Aching
• Tightness
– Location:
• Epigastric (usually)
• RUQ
± Referred pain: shoulder / scapula
Overview of Biliary Disease
• Biliary colic
• Cholecystitis
– Acute
– Chronic
• Cholangitis
– Acute
– Primary Sclerosing (PSC)
• Primary Biliary Cirrhosis
(PBC)
Defn: Infection & inflammation of CBD
Features
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RUQ pain
Jaundice
Fever
(CHARCOT’s TRIAD)
Cholecystitis
Aetiology
• 90% ‘Calculous cholecystitis’: gallstones
obstructing of cystic duct causing
inflammation of gallbladder
• 10% ‘Acalculous cholecystitis’: inflammation
of gallbladder without associated stones
• Bile cultures are positive for bacteria in 5075% of cases but bacterial proliferation may
be A RESULT of cholecystitis and not the
precipitating factor
Risk factors
Calculous Cholecystitis:
•Female sex
•Obesity or rapid weight loss
•Increasing age
•Pregnancy (elevated progesterone
levels cause biliary stasis)
•Drugs- especially hormonal therapy
in women
Acalculous Cholecystitis:
Conditions associated with biliary
stasis
• Critical illness
• Major surgery/severe burns or
trauma
• Sepsis
• Long-term total parenteral
nutrition (TPN)
• Prolonged fasting
Clinical Presentation-History
• Pain begins in epigastric region
• Localizes to RUQ, radiating to the scapula/right shoulder
• Pain described as colicky initially but usually becomes
constant
• Nausea and vomiting
• Fever
• History of biliary pain but differentiated from biliary colic
by persistence of severe constant pain >6hours
Clinical Presentation-Examination
• Fever, tachycardia
• Tenderness in RUQ often with guarding or
rebound tenderness
• ‘Murphy Sign’ tenderness and inspiratory
pause elicited during palpation of RUQ
• Palpable gallbladder in 30-40%
• Jaundice in 15%
Clinical Presentation
• Absence of findings does not rule out
cholecystitis, many present with diffuse
epigastric pain without localization to RUQ
• Elderly patients and patients with diabetes
have often atypical presentations including
absence of fever and localized tenderness
with only vague symptoms
Ix/Dx
Lab Tests
•Leukocytosis
•AST/ALT may be elevated in cholecystitis or common bile
duct obstruction
•Bilirubin and ALP are elevated in common duct
obstruction, ALP is raised in 25% of cholecystitis
•Amylase/Lipase used to evaluate for pancreatitis
•Urinalysis used to rule out pyelonephritis and renal
calculi
•All females of childbearing age should undergo
pregnancy testing
Ix/Dx
Abdo Xray:
•Gallstones visualized in 10-15% of cases
Abdo US:
•First line investigation
•90-95% sensitive and 80% specific for cholecystitis
CT/MRI:
•Sensitivity and specificity are >95%
•Unlike ERCP, both are non-invasive but not therapeutic
Ix/Dx
Hepatobiliary Scintigraphy (HBS):
•Isotopes are taken up by hepatocytes and secreted into bile,
delineating the biliary tree
•If the cystic duct and gallbladder do not take up the isotope, it
indicates acute cholecystitis
Endoscopic Retrograde Cholangiopancreatography (ERCP):
•Endoscope passed through duodenum, catheter into ampulla of Vater
and contrast medium injected
•Allows direct visualization of biliary tree and pancreatic ducts and can
perform therapeutic interventions including stone extraction
•Better for biliary obstructive jaundice
Ix/Dx
Management
• Gallstones that are not symptomatic do not
need treatment
• Some people are able to manage mild
symptoms with a combination of low fat diet
and painkillers
Alternatives to Surgery
• Dissolution Agent: Ursodeoxycholic Acid (Urdox tablets)
– Medication used to dissolve the gallstones
– Not effective – takes too long to dissolve gallstone and recurs post
treatment cessation
– Suitable gallstones
• Small
• Radiolucent (do not show up on xray)
• Gallbladder needs to have the ability to contract
• Lithotripsy: using a beam of sound energy to blast the stone
– The gallbladder is diseased  blasting the stone is not treating
– Fragments of the shattered stone will still need to be removed by
ERCP
– Commonly used for kidney stones
Surgery
• Laparoscopic
cholecystectomy
– Removal of the gallbladder
and gallstones together (if
gallbladder left behind,
likely that further stones
will develop)
– In under 5% of cases 
convert to open surgery
Indications for Cholecystectomy
Conditions
When to perform surgery
Biliary pain
First open operative day
Biliary dyskinesia
First open operative day
Calcified gallbladder
First open operative day
Acute cholecystitis
Urgent (within 72 hours)
Choledocholithiasis
After the common bile duct is
cleared
Before discharge but after
pancreatitis resolves
Gallstone pancreatitis
Cholecystitis
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Nil orally
IV fluids
Pain relief: Pethidine
Surgery
Complications of surgery
• General
– DVT
– Anaesthetic complications
• Specific
– Infection of the wound
– Bleeding  Cystic artery
– Damage to the common bile duct
– Damage to abdominal visci
Complications: Gallbladder
• Biliary colic
– Colic: intermittent pain that increases in intensity
and them completely disappears
– In this case, the pain is PSEUDO-Colic: pain never
completely disappears
• Chemical cholecystitis
– Laceration of gallbladder wall by a stone
– Bile to leak into the submucosa  Infection
• Empyema of the gallbladder
Continued inflammation  pus  Empyema
(collection of pus in organ)
• Gangrene and necrosis
– Inflammation  swelling  increase in
interstitial pressure  interstitial pressure =
arterial pressure (Cystic artery that supplies
gallbladder)  stop in arterial flow  gangrene
and necrosis of gallbladder wall
• Perforation (Peritonitis)
– Gangrene and necrosis of the gallbladder wall 
perforation  contents seep into peritoneum 
peritonitis
Complications: Other
• Obstructive jaundice (stone in common bile
duct)
– Bile from the liver cannot flow into duodenum
– Ascending cholangitis: inflammation of common
bile duct
• Liver abscess
– Infection spread to the liver
• Pancreatitis
• Gallstone ileus
– Impaction of a
gallstone in the
terminal ileum by
passing through a
biliary-enteric fistula
(often from
duodenum)
LFT’s
ALT
Produced
by:
Elevation
Liver
AST
Liver
Cardiac
muscle
Sk muscle
Kidneys
Brain
Pancreas
Lungs
RBC and
WBC
Intra-hepatic pathology
- Acute viral
- Drug/toxins
- Ischaemic liver injury
ALP
GGT
Liver
Bone
Placenta
Liver
Biliary
epithelium
Biliary
obstruction
Bony
disease
Biliary
obstruction
EtOH abuse
Warfarin
Drugs
Normal LFTs
Alb
Bilirubi
n
ALP
GGT
ALT
AST
>35
<20
Total serum is given. Must ask for
conjugated and unconjugated.
<120 Raised in post- hepatic pathology
<80
<50 Raised in intra- hepatic pathology
<50 - Acute viral
- Drug/ toxins
- Ischaemic liver injury
Interpreting LFTs 1
Alb
33
↓
Bilirubin
90
↑
ALP
160
↑
GGT
120
↑
ALT
2100
↑↑
AST
1985
↑↑
Jaundice, viral prodrome
(lethargy, nausea, vague
abdominal discomfort)
Acute hepatitis
Alb
33
↓
Bilirubin
90
↑
ALP
160
↑
GGT
120
↑
ALT
2100
↑↑
AST
1985
↑↑
Jaundice, viral prodrome
(lethargy, nausea, vague
abdominal discomfort)
ACUTE HEPATITIS (acute inflammation) e.g. OD on
paracetamol, viral hep, EBM/ CMV, autoimmune
hepatitis
Interpreting LFTs 2
Alb
30
↓
Bilirubin
400
↑
ALP
900
↑↑
GGT
915
↑↑
ALT
60
↑
AST
55
↑
Obstructive jaundice
Alb
30
↓
Bilirubin
400
↑
ALP
900
↑↑
GGT
915
↑↑
ALT
60
↑
AST
55
↑
OBSTRUCTIVE JAUNDICE
Pain  cholangitis (sudden dilatation)
Painless  pancreatic tumour (gradual increase
in pressure)
Interpreting LFTs 3
Alb
Bilirubin
ALP
GGT
>35
50
250
120
+ Increased WCC
↑
↑↑
↑↑ (variable)
ALT
AST
80
80
↑
↑
Cholangitis
Alb
Bilirubin
ALP
GGT
>35
50
250
120
↑
↑↑
↑↑
ALT
AST
80
80
↑
↑
+ Increased WCC
CHOLANGITIS – infection of the biliary tree.
Increase in ALT/ AST as there is a dilatation of tight junctions in liver due
to biliary obstruction and increased intraluminal pressure.
Due to stasis (blockage), the bile is often infected, and enters the blood
stream  risk of sepsis, thus EMERGENCY
Histology: yellow because of bile
Interpreting LFTs 4
Alb
30
↓
Bilirubin
60
↑
ALP
160
↑↑
GGT
300
↑↑
ALT
70
↑
AST
150
↑
Alcoholic hepatitis or cirrhosis
Alb
30
↓
Bilirubin
60
↑
ALP
160
↑↑
GGT
300
↑↑
ALT
70
↑
AST
150
↑
ALCOHOLIC HEPATITIS OR CIRRHOSIS
Usually ALT mirrors AST,
but in alcoholic
hepatitis, there is:
2:1 ratio of AST: ALT
Isolated increase in GGT
- Alcohol (not alcoholic
hepatitis)
- Phenytoin
Bilirubin 1
1) Fragile RBCs
phagocytosed by
macrophages
• Aka Reticulendothelial
system
• Within macrophages:
• Haemoglobin split  globin &
heme
• Heme breakdown products 
Biliverdin  Bilirubin
2) Free bilirubin
– Transported through
blood plasma bound
• With albumin
– Transported to liver
Bilirubin 2
3) Liver conjugates free
bilirubin  conjugated
bilirubin
– With glucuronic acid
• Makes bilirubin H2O soluble
4) In intestines: Conjugated
bilirubin  urobilinogen
– By bacterial action
5) Urobilinogen
– Reabsorbed into plasma
(5%)
• Excreted by kidneys
– Oxidised in intestines 
stercobilin
• Excreted in faeces
Jaundice
• Definition = yellow discolouration of tissue
due to increased bilirubin concentration in
blood
Types
• Prehepatic (haemolytic)
• Intrahepatic
• Post-hepatic (obstructive)
Pre-hepatic jaundice
• Excessive haemolysis (destruction of RBC) 
increased bilirubin
• Liver cannot conjugate the bilirubin as rapidly
as it is formed
• Increased free unconjugated bilirubin bound
to albumin in blood plasma
• ↑ urobilinogen excreted in urine
Intra-hepatic jaundice
• Poor hepatocyte function  impaired uptake,
transport and conjugation of bilirubin
(unconjugated and conjugated)
Conjugated
bilirubin
AST or ALT
Prehepatic
Intrahepatic
Posthepatic
Absent
↑
↑
↑
↑
ALP
Urine Bilirubin
Absent
Present
Present
Urine
Urobilinogen
Present
Present
Absent
Post-hepatic jaundice
• Due to cholestasis (obstruction of bile ducts) 
gallstones or pancreatic tumour
• Causes impaired excretion of conjugated bilirubin
into intestine, HENCE conjugated bilirubin reflux
to blood
– Increased conjugated bilirubin (H20 soluble) 
increased bilirubin and bilirubinuria
– No conjugated bilirubin into intestine  no oxidation
into stercobilin
• CLINICAL PICTURE= jaundice, dark urine, pale
stools