Mohammad Mobasheri

SpR General Surgery

Types of gallstone
Cholesterol stones (20%)
Pigment stones (5%)
Mixed (75%)

Epidemiology
Fat, Fair, Female, Fertile, Fourty inaccurate, but
reminder of the typical patient
F:M = 2:1
10% of British women in their 40s have gallstones
Genetic predisposition ask about family history

Composition of bile:
Bilirubin (by-product of haem degradation)
Cholesterol (kept soluble by bile salts and lecithin)
Bile salts/acids (cholic acid/chenodeoxycholic acid):
mostly reabsorbed in terminal ileum(entero-hepatic
circulation).
Lecithin (increases solubility of cholesterol)
Inorganic salts (sodium bicarbonate to keep bile
alkaline to neutralise gastric acid in duodenum)
Water (makes up 97% of bile)

Cholesterol
Imbalance between bile salts/lecithin and cholesterol allows
cholesterol to precipitate out of solution and form stones

Pigment
Occur due to excess of circulating bile pigment (e.g.
Heamolytic anaemia)

Mixed
Same pathophysiology as cholesterol stones

Other Factors
Stasis (e.g. Pregnancy)
Ileal dysfunction (prevents re-absorption of bile salts)
Obesity and hypercholesterolaemia

80% Asymptomatic
20% develop complications and do so on
recurrent basis

Biliary Colic
Acute Cholecystitis

Gallbladder Empyema
Gallbladder gangrene
Gallbladder perforation

Obstructive Jaundice
Ascending Cholangitis
Pancreatitis
Gallstone Ileus (rare)

Gallstone disease (and its related complications)

Gastritis/duodenitis
Peptic ulcer disease/perforated peptic ulcer
Acute pancreatitis
Right lower lobe pneumonia
MI
If presenting to A&E with RUQ pain all patients
should get
Blood tests
AXR/E-CXR (to exclude perforation/pneumonia)
ECG

Can differentiate between gallstone

complications based on:
History
Examination
Blood tests

FBC
LFT
CRP
Clotting
Amylase

Complication

History

Examination

Blood tests

Biliary Colic

- Intermittent RUQ/epigastric
pain (minutes/hours) into
back or right shoulder
- N&V

-Tender RUQ
-No peritonism
-Murphys
-Apyrexial, HR and BP (N)

-WCC (N) CRP (N)

- LFT (N)

Acute Cholecystitis

-Constant RUQ pain into back

or right shoulder
-N&V
-Feverish

-Tender

RUQ
RUQ
(guarding/rebound)
-Murphys +
-Pyrexia, HR ()

-WCC

-Periotnism

-LFT

-Constant RUQ pain into back

or right shoulder
-N&V
-Feverish

-Tender

RUQ
RUQ
-Murphys +
-Pyrexia, HR (), BP ( or )
-More septic than acute
cholecystitis

-WCC

-Peritonism

-LFT

-Yellow

discolouration
stool, dark urine
-painless or assocaited with
mild RUQ pain

-Jaundiced

-WCC

-Pale

-Non-tender

Becks triad
-RUQ pain (constant)
-Jaundice
-Rigors

-Jaundiced
-Tender RUQ
-Peritonism RUQ
-Spiking high pyrexia (38-39)
-HR (), BP ( or )
-Can develop septic shock

-WCC

Acute Pancreatitis

-Severe

upper abdominal
pain (constant) into back
-Profuse vomiting

-Tender upper abdomen

-Upper abdominal or
generalised peritonism
-Usually apyrexial, HR (), BP
( or )

-WCC and CRP ()

-LFT: (N) if passed stone or
obstructive pattern ifstone
still in CBD
-Amylase ()
-INR/APTT (N) or () if DIC

Gallstone Ileus

- 4 cardinal features of SBO

-distended tympanic abdomen

-hyperactive/tinkling bowel
sounds

Empyema

Obstructive Jaundice

Ascending Cholangitis

or minimally

tender RUQ
-No peritonism
-Murphys
-Apyrexial, HR and BP (N)

and CRP ()
(N or mildly ()

and CRP ()
(N or mildly ()

and CRP (N)

obstructive pattern bili
(), ALP (), GGT (),
ALT/AST ()
-INR ( or )
-LFT:

and CRP ()
: obstructive pattern
bili (), ALP (), GGT (),
ALT/AST ()
-INR ( or )
-LFT

Bloods (already discussed)

AXR (10% gallstones are radio-opaque)
E-CXR (to exclude perforation MUST!)
ECG (to exclude MI)
USS: first line investigation in gallstone disease

MRCP: To visualise biliary tree accurately (much more accurate than USS)

Diagnostic and therepeutic but invasive

Look for biliary tree dilatation and stones in biliary tree
Stones can be extracted to unobstruct the biliary tree and perform sphincterotomy
Risk of pancreatitis, duodenal perforation

PTC

Diagnostic only but non-invasive

Look for biliary dilatation and any stones in biliary tree

ERCP: Diagnostic and therepeutic in biliary obstruction

Confirms presence of gallstones

Gall bladder wall thickness (if thickened suggests cholecystitis)
Biliary tree calibre (CBD/extrahepatic/intrahepatic) if dilated suggests stone in CBD (normal CBD <8mm).
Sometimes CBD stone can be seen.

To unobstruct biliary tree when ERCP has failed

Invasive higher complication rate than ERCP

CT: Not first line investigation. Mainly used if suspicion of gallbladder empyema, gangrene,
or perforation and in acute pancreatitis (USS not good for looking at pancreas)

Pathogenesis
Stone intermittently obstructing cystic duct
(causing pain) and then dropping back into
gallbladder (pain subsides)
USS confirms presence of gallstones
Treatment
Analgesia
Fluid resuscitation if vomiting
If pain and vomiting subside does not need
admitting

Pathogenesis:

Due to obstruction of cystic duct by gallstone:

Cystic duct blockage by gallstone

Obstruction to secretion of bile from gallbladder
Bile becomes concentrated
Chemical inflammation initially
Secondarily infected by organisms released by liver into bile stream

USS confirms diagnosis (gallstones, thickened gallbladder wall, peri-cholecystic fluid)

Complications of acute cholecystitis

Empyema of gallbaldder
Gangrene of gallbladder (rare)
Perforation ofgallbaldder (rare)

Treatment

Admit for monitoring

Analgesia
Clear fluids initially, then build up oral intake as cholecystitis settles
IVF
Antibiotics
95% settle with above management
If do not settle then for CT scan

Empyema percutaneous drainage

Gangrene/perforation with generalised peritonitis emergency surgery

Pathogenesis:
Stone obstructing CBD (bear in mind there are other causes for obstructive
jaundice) danger is progression to ascending cholangitis.

USS

MRCP

Will confirm gallstones in the gallbladder

CBD dilatation i.e. >8mm (not always!)
May visualise stone in CBD (most often does not)
In cases where suspect stone in CBD but USS indeterminate
E.g.1 obstructive LFTs but USS shows no biliary dilatation and no stone in CBD
E.g. 2 normal LFTS but USS shows biliary dilatation

ERCP

If confirmed stone in CBD on USS or MRCP proceed to ERCP which will confirm this
(diagnostic) and allow extraction of stones and sphincterotomy (therepeutic)

Treatment
Must unobstruct biliary tree with ERCP to prevent progression to ascending
cholangitis
Whilst awaiting ERCP monitor for signs of sepsis suggestive of cholangitis

Pathogenesis:
Stone obstructing CBD with infection/pus
proximal to the blockage
Treatment
ABC
Fluid resuscitation (clear fuids and IVF, catheter)
Antibiotics (Augmentin)
HDU/ITU if unwell/septic shock
Pus must be drained* - this is done by
decompressing the biliary tree
Urgent ERCP
Urgent PTC if ERCP unavailable or unsuccesful

Pathogenesis
Obstruction of pancreatic outflow

Pancreatic enzymes activated within pancreas

Pancreatic auto-digestion

USS: to confirm gallstones as cause of pancreatitis

USS not good for visualising pancreas
CT: gold standard for assessing pancreas.
Performed if failing to settle with conservative management to look for complications
such as pancreatic necrosis
Treatment
Analgesia
Fluid resuscitation
Pancreatic rest clear fluids initially
Identify underlying cause of pancreatitis

95% settle with above conservative management

5% who do no settle or deteriorate need CT scan to look for pancreatic necrosis

Pathogenesis:
Gallstone causing small bowel obstruction (usually obstructs in terminal
ileum)
Gallstone enters small bowel via cholecysto-duodenal fistula (not via CBD)
AXR dilated small bowel loops
May see stone if radio-opaque
Treatment
NBM
Fluid resuscitation + catheter
NG tube
Analgesia
Surgery (will not settle with conservative management) enterotomy +
removal of stone
Diagnosis of gallstone ileus usually made at the time of surgery.

Asymptomatic gallstones do not require operation

Indications
A single complication of gallstones is an indication for
cholecystectomy (this includes biliary colic)
After a single complication risk of recurrent
complications is high (and some of these can be life
threatening e.g. cholangitis, pancreatitis)

Whilst awaiting laparoscopic cholecystectomy

Low fat diet
Dissolution therapy (ursodeoxycholic acid) generally
useless

All performed laparoscopically

Advantages:
Less post-op pain
Shorter hospital stay
Quicker return to normal activities

Disadvantages:
Learning curve
Inexperience at performing open cholecystectomies

After acute cholecystitis, cholecystectomy traditionally

performed after 6 weeks

Arguments for 6 weeks later

Laparoscopic dissection more difficult when acutely inflammed
Surgery not optimal when patient septic/dehydrated
Logistical difficulties (theatre space, lack of surgeons)

Arguments for same admission

Research suggests same admission lap chole as safe as elective chole
(conversion to open maybe higher)
Waiting increases risk of further attacks/complications which can be life
threatening
Risk of failure of conservative management and development of
dangerous complication such as empyema, gangrene and perforation can
be avoided

National guidelines state any patient with attack of gallstone

pancreatitis should have lap chole within 3 weeks of the attack

Questions?