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 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 -Tender RUQ -WCC (N) CRP (N)
pain (minutes/hours) into -No peritonism - LFT (N)
back or right shoulder -Murphy’s –
- N&V -Apyrexial, HR and BP (N)
Acute Cholecystitis -Constant RUQ pain into back -Tender RUQ -WCC and CRP (↑)
or right shoulder -Periotnism RUQ -LFT (N or mildly (↑)
-N&V (guarding/rebound)
-Feverish -Murphy’s +
-Pyrexia, HR (↑)
Empyema -Constant RUQ pain into back -Tender RUQ -WCC and CRP (↑)
or right shoulder -Peritonism RUQ -LFT (N or mildly (↑)
-N&V -Murphy’s +
-Feverish -Pyrexia, HR (↑), BP (↔ or ↓)
-More septic than acute
cholecystitis
Obstructive Jaundice -Yellow discolouration -Jaundiced -WCC and CRP (N)
-Pale stool, dark urine -Non-tender or minimally -LFT: obstructive pattern bili
-painless or assocaited with tender RUQ (↑), ALP (↑), GGT (↑),
mild RUQ pain -No peritonism ALT/AST (↔)
-Murphy’s – -INR (↔ or ↑)
-Apyrexial, HR and BP (N)
Ascending Cholangitis Becks triad -Jaundiced -WCC and CRP (↑)
-RUQ pain (constant) -Tender RUQ -LFT : obstructive pattern
-Jaundice -Peritonism RUQ bili (↑), ALP (↑), GGT (↑),
-Rigors -Spiking high pyrexia (38-39) ALT/AST (↔)
-HR (↑), BP (↔ or ↓) -INR (↔ or ↑)
-Can develop septic shock

Acute Pancreatitis -Severe upper abdominal pain -Tender upper abdomen -WCC and CRP (↑)
(constant) into back -Upper abdominal or -LFT: (N) if passed stone or
-Profuse vomiting generalised peritonism obstructive pattern ifstone
-Usually apyrexial, HR (↑), BP still in CBD
(↔ or ↓) -Amylase (↑)
-INR/APTT (N) or (↑) if DIC
Gallstone Ileus - 4 cardinal features of SBO -distended tympanic abdomen
-hyperactive/tinkling bowel
sounds
 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.
 MRCP: To visualise biliary tree accurately (much more accurate than USS)
 Diagnostic only but non-invasive
 Look for biliary dilatation and any stones in biliary tree
 ERCP: Diagnostic and therepeutic in biliary obstruction
 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
 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
 Will confirm gallstones in the gallbladder
 CBD dilatation i.e. >8mm (not always!)
 May visualise stone in CBD (most often does not)
 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 (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?

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