Gallstone Disease and Acute Cholecystitis

1. Gallstone Disease and Acute Cholecystitis Mohammad Mobasheri SpR General Surgery

2. Gallstones • 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

3. 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)

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

5. Complications of Gallstones • 80% Asymptomatic • 20% develop complications and do so on recurrent basis

6. Complications of Gallstones

7. Complications of Gallstones • Biliary Colic • Acute Cholecystitis • Gallbladder Empyema • Gallbladder gangrene • Gallbladder perforation • Obstructive Jaundice • Ascending Cholangitis • Pancreatitis • Gallstone Ileus (rare)

8. 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

9. Which Gallstone Complication? • Can differentiate between gallstone complications based on: • History • Examination • Blood tests • FBC • LFT • CRP • Clotting • Amylase

11. 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. • 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)

12. 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

13. 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) 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

14. 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) • 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

15. Ascending 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

16. 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 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

17. 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 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.

18. Cholecystectomy • 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

19. Cholecystectomy • All performed laparoscopically • Advantages: • Less post-op pain • Shorter hospital stay • Quicker return to normal activities • Disadvantages: • Learning curve • Inexperience at performing open cholecystectomies

20. Cholecystectomy when to perform? • 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

21. The End Questions?