Gallstone Disease And

Acute Cholecystitis
 GALL STONES

• Types of gall stone

• Cholesterol stones (20%)
• Pigment stones (5%)
• Mixed (75%)

• Epidemiology
• F:M = 2:1
• 10% of British women in their 40s have gallstones
• Genetic predisposition – ask about family history
 PATHOGENESIS

• 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)
 PATHOGENESIS

 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
COMPLICATIONS OF GALLSTONES

• 80% Asymptomatic
• 20% develop complications and do so on
recurrent basis
COMPLICATIONS OF GALLSTONES

• Biliary Colic
• Acute Cholecystitis
• Gallbladder Empyema
• Gallbladder gangrene
• Gallbladder perforation

• Obstructive Jaundice
• Ascending Cholangitis
• Pancreatitis
• Gallstone Ileus (rare)
BILIARY COLIC

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
 ACUTE CHOLECYSTITIS

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)
 ACUTE CHOLECYSTITIS

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
 OBSTRUCTIVE JAUNDICE

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

• USS
• Will confirm gallstones in the gallbladder
• CBD dilatation i.e. >8mm (not always!)
• May visualise stone in CBD (most often
does not)
 OBSTRUCTIVE JAUNDICE

• MRCP
• 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 (therapeutic)

Treatment
• Must drain the obstructed biliary tree with ERCP to prevent
progression to ascending cholangitis
• Whilst awaiting ERCP monitor for signs of sepsis suggestive of
cholangitis
 ASCENDING CHOLANGITIS

Pathogenesis:
• Stone obstructing CBD with infection/pus proximal to
the blockage

Treatment
• Fluid resuscitation (clear fuids and IVF, catheter)
• Antibiotics
• Pus must be drained* - this is done by decompressing
the biliary tree
• Urgent ERCP
• Urgent PTC – if ERCP unavailable or unsuccesful
 ACUTE PANCREATITIS
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
 ACUTE PANCREATITIS

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
 GALLSTONE ILEUS

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
 GALLSTONE ILEUS

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.
WHICH GALLSTONE COMPLICATION?

• Can differentiate between gallstone

complications based on:
• History
• Examination
• Blood tests
• FBC
• Liver function test
• CRP
• Clotting
• Amylase
INVESTIGATIONS FOR GALLSTONE
DISEASE
• 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
• 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.
• 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)
DIFFERENTIAL DIAGNOSIS OF RUQ PAIN

 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
Complication History Examination Blood tests
- Intermittent RUQ/epigastric -Tender RUQ -WCC (N) CRP (N)
Biliary Colic pain (minutes/hours) into -No peritonism - LFT (N)
-Murphy’s –
back or right shoulder -Apyrexial, HR and BP (N)
- N&V
-Constant RUQ pain into -Tender RUQ -WCC and CRP (↑)
Acute back or right shoulder -Periotnism RUQ (guarding/rebound) -LFT (N or mildly (↑)
-Murphy’s +
Cholecystitis -N&V -Pyrexia, HR (↑)
-Feverish

-Constant RUQ pain into -Tender RUQ -WCC and CRP (↑)
Empyema back or right shoulder -Peritonism RUQ -LFT (N or mildly (↑)
-Murphy’s +
-N&V -Pyrexia, HR (↑), BP (↔ or ↓)
-Feverish -More septic than acute cholecystitis

-Yellow discolouration -Jaundiced -WCC and CRP (N)

Obstructive -Pale stool, dark urine -Non-tender or minimally tender -LFT: obstructive pattern bili (↑),
RUQ ALP (↑), GGT (↑), ALT/AST (↔)
Jaundice -painless or assocaited with -No peritonism -INR (↔ or ↑)
mild RUQ pain -Murphy’s –
-Apyrexial, HR and BP (N)

Becks triad -Jaundiced -WCC and CRP (↑)

Ascending -RUQ pain (constant) -Tender RUQ -LFT : obstructive pattern bili (↑),
-Peritonism RUQ ALP (↑), GGT (↑), ALT/AST (↔)
Cholangitis -Jaundice -Spiking high pyrexia (38-39) -INR (↔ or ↑)
-Rigors -HR (↑), BP (↔ or ↓)
-Can develop septic shock

-Severe upper abdominal pain -Tender upper abdomen -WCC and CRP (↑)
Acute (constant) into back -Upper abdominal or generalised -LFT: (N) if passed stone or
peritonism obstructive pattern ifstone still in
Pancreatitis -Profuse vomiting -Usually apyrexial, HR (↑), BP (↔ or CBD
↓) -Amylase (↑)
-INR/APTT (N) or (↑) if DIC

- 4 cardinal features of SBO -distended tympanic abdomen

Gallstone Ileus -hyperactive/tinkling bowel sounds
COMPLICATIONS OF GALLSTONES

• https://fb.watch/jdwJhd6TKG/
 Cholecystectomy

• Asymptomatic gallstones 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
 CHOLECYSTECTOMY

• All performed laparoscopically

• Advantages:
• Less post-op pain
• Shorter hospital stay
• Quicker return to normal activities
 Cholecystectomy ….When To Perform?

• Arguments for 6 weeks later

• Laparoscopic dissection more difficult when acutely
inflamed
• 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
THANK YOU !!