Transcript Gallstones

Gallstones
Mrs. Kirsty Cattle MRCS
SHO
General
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Ian Aird said “Good pathology makes mighty surgeons
proud.”
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Incidence – common (17% at time of death)
Age – any age, mostly 40s
Aetiology – bile constituents, infective, bile stasis
Sex ratio – female>male
Geography – Western diet
Predisposing factors – “fat, fair, fertile, flatulant, forties”
Macroscopy – cholesterol, mixed (90%), pigment
Microscopy – histology of gallbladder wall
Spread
Prognosis
Anatomy
Presentation
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Asymptomatic (85-90%)
Biliary colic
Cholecystitis
Obstructive jaundice
Ascending cholangitis
Pancreatitis
Rarities:
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Gallstone ileus, Mucocoele, Perforation, Mirizzi’s syndrome,
Carcinoma
Biliary colic
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Definition: colicky abdominal pain due to the
presence of gallstones in gall bladder
Investigations
Normal blood results
 USS: gallstones within thin-walled gall bladder, no
CBD dilatation
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Management
Symptomatic
 Cholecystectomy
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Cholecystitis
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Definition: constant abdominal pain and
tenderness due to an infected gall bladder
Investigations
Raised WBC, Normal LFTs
 USS: gallstones within thick-walled gall bladder, no
CBD dilatation
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Management
Symptomatic
 Cholecystectomy
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Jaundice
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Definition: obstructive jaundice due to CBD
stone
Investigations
Raised LFTs: Alk Phos > ALT,
 USS: gallstones, CBD dilatation ± CBD stone
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Management
ERCP
 Cholecystectomy
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Ascending cholangitis
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Surgical emergency
Definition: jaundice, rigors, RUQ tenderness
Investigations
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Raised WBC, raised LFTs
USS: gallstones, CBD dilatation ± CBD stone
Management
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Urgent resuscitation, iv Antibiotics (e.g. Ciprofloxacin)
Urgent ERCP
Cholecystectomy
Acute Pancreatitis
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Definition
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Presentation
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acute inflammation of the pancreas, primarily due to
intracellular activation of trypsinogen to trypsin.
Epigastric pain, radiating to back, nausea ±
vomiting, dehydration, renal failure
Investigations
Amylase >3x normal range
 Scoring of severity
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Causes of Acute Pancreatitis
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Obstruction:
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Gallstones (30-70%)
Ampullary or pancreatic
tumours (3%)
Congenital abnormalities (5%)
Sphincter of Oddi
hypertension (1-2%)
Ascariasis
Drugs/Toxins:
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Alcohol (30-70%)
Azathioprine, 6mercaptopurine, some
antibiotics (metronidazole,
tetracycline), H2 blockers,
others
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Iatrogenic/Trauma:
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Metabolic:
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Hypertriglyceridaemia (2%)
Hypercalcaemia,
hyperparathyroidism (rare)
Infection:
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ERCP
Cardiopulmonary bypass
Blunt abdominal trauma
AIDS, secondary infection
Mumps, Coxsackie virus,
hepatitis A, B and C
Idiopathic (10%)
Modified Glasgow Score
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Indication of severity of pancreatitis
Factors:
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Age > 55
WBC > 15
Glucose > 10
Urea > 16
PaO2 < 8.0 kPa
Calcium < 2 mmol/l
Albumin < 32
LDH > 600
A score of 3 or more indicates severe pancreatitis and
requires anaesthetic input regarding HDU care
Compete score on admission and 48 hours later
Management
Supportive – analgesia, iv rehydration, catheterise,
fluid balance, NBM (± NG tube). Consider
Antibiotics.
 Observe for complications:
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Systemic: cardiovascular, pulmonary, renal,
haematological, metabolic, neurological, gastrointestinal
 Local: fluid collections, pseudocyst, necrosis, ascites,
infection, pseudoaneurysm
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Establish and remove cause:
ERCP, Cholecystectomy
 Strongly advise patient to stop drinking alcohol
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Rarities
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Gallstone ileus:
Large gallstone erodes through gall bladder wall into
neighbouring duodenum, passes along small bowel
until it lodges and causes small bowel obstruction
 AXR: distended loops of small bowel, typically to
terminal ileum, with air in biliary tree
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Rarities
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Mucocoele:
Gallstone lodges in neck of gall bladder, preventing
drainage of mucous.
 May become infected, causing empyema
 Require drainage and later cholecystectomy
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Perforation
Carcinoma
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Mirizzi’s syndrome:
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In 1948, P. L. Mirizzi described an unusual presentation of gallstones
which, when lodged in either the cystic duct or the Hartmann pouch of
the gallbladder, externally compressed the common hepatic duct (CHD),
causing symptoms of obstructive jaundice (Mirizzi, 1948).
Pathophysiology: Impaction of a large gallstone (or multiple small
gallstones) in the Hartmann pouch or cystic duct results in the Mirizzi
syndrome in 2 ways: (1) Chronic and/or acute inflammatory changes lead
to contraction of the gallbladder, which then fuses with and causes
secondary stenosis of the CHD, or (2) large impacted stones lead to
cholecystocholedochal fistula formation secondary to direct pressure
necrosis of the adjacent duct walls. Increasingly, these phenomena are
seen not as distinct and separate steps but as part of a continuum
(Pemberton, 1997; Hazzan, 1999).
Laparoscopic cholecystectomy
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This is a case of a 42 year old male with a previous history of abdominal pain
for 6 months. He was admitted to the hospital with nausea but vomiting or
fever. An ultrasound study showed gallstones with some thickening of the
gallbladder wall. The diagnosis of cholecystitis was made and the patient was
scheduled to undergo a laparoscopic cholecystectomy. This picture shows the
omentum partially covering the gallbladder in its normal position.
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Due to significant distention of the gallbladder, a needle is used
to drain some bile so grasper clamps can be applied for
dissection and manipulation.
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The Hartmann'a pouch is rectracted laterally and upward,
exposing the triangle of Calot where the cystic artery can be
identified branching off the right hepatic artery.
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A short cystic duct is dissected free using a "right angle" clamp.
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Clips are applied to the cystic duct away from the common bile
duct.
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The cystic duct is transected using scissors.
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Same technique is used with the cystic artery which is dissected
free using a "right angle" clamp and will be divided between
clips.
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Hook electrocautery is used to dissect the gallbladder off the
liver bed.
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The gallbladder is now free and will be placed into a Pleatman
sac for retreival.
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This picture shows the body of the gallbladder, that becomes
distended during removal. Caution must be used to avoid rupture
while pulling.
Thank you
Questions?