Transcript Gallstones
Gallstones
Mrs. Kirsty Cattle MRCS
SHO
General
Ian Aird said “Good pathology makes mighty surgeons
proud.”
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
Asymptomatic (85-90%)
Biliary colic
Cholecystitis
Obstructive jaundice
Ascending cholangitis
Pancreatitis
Rarities:
Gallstone ileus, Mucocoele, Perforation, Mirizzi’s syndrome,
Carcinoma
Biliary colic
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
Management
Symptomatic
Cholecystectomy
Cholecystitis
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
Management
Symptomatic
Cholecystectomy
Jaundice
Definition: obstructive jaundice due to CBD
stone
Investigations
Raised LFTs: Alk Phos > ALT,
USS: gallstones, CBD dilatation ± CBD stone
Management
ERCP
Cholecystectomy
Ascending cholangitis
Surgical emergency
Definition: jaundice, rigors, RUQ tenderness
Investigations
Raised WBC, raised LFTs
USS: gallstones, CBD dilatation ± CBD stone
Management
Urgent resuscitation, iv Antibiotics (e.g. Ciprofloxacin)
Urgent ERCP
Cholecystectomy
Acute Pancreatitis
Definition
Presentation
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
Causes of Acute Pancreatitis
Obstruction:
Gallstones (30-70%)
Ampullary or pancreatic
tumours (3%)
Congenital abnormalities (5%)
Sphincter of Oddi
hypertension (1-2%)
Ascariasis
Drugs/Toxins:
Alcohol (30-70%)
Azathioprine, 6mercaptopurine, some
antibiotics (metronidazole,
tetracycline), H2 blockers,
others
Iatrogenic/Trauma:
Metabolic:
Hypertriglyceridaemia (2%)
Hypercalcaemia,
hyperparathyroidism (rare)
Infection:
ERCP
Cardiopulmonary bypass
Blunt abdominal trauma
AIDS, secondary infection
Mumps, Coxsackie virus,
hepatitis A, B and C
Idiopathic (10%)
Modified Glasgow Score
Indication of severity of pancreatitis
Factors:
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:
Systemic: cardiovascular, pulmonary, renal,
haematological, metabolic, neurological, gastrointestinal
Local: fluid collections, pseudocyst, necrosis, ascites,
infection, pseudoaneurysm
Establish and remove cause:
ERCP, Cholecystectomy
Strongly advise patient to stop drinking alcohol
Rarities
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
Rarities
Mucocoele:
Gallstone lodges in neck of gall bladder, preventing
drainage of mucous.
May become infected, causing empyema
Require drainage and later cholecystectomy
Perforation
Carcinoma
Mirizzi’s syndrome:
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
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.
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.
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.
A short cystic duct is dissected free using a "right angle" clamp.
Clips are applied to the cystic duct away from the common bile
duct.
The cystic duct is transected using scissors.
Same technique is used with the cystic artery which is dissected
free using a "right angle" clamp and will be divided between
clips.
Hook electrocautery is used to dissect the gallbladder off the
liver bed.
The gallbladder is now free and will be placed into a Pleatman
sac for retreival.
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?