Gallstone Disease and Acute Cholecystitis

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Gallstone Disease and Acute Cholecystitis

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

3. 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

4. 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 Pathogenesis

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

6. Complications of Gallstones

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

8. 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 Differential Diagnosis of RUQ pain

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

11. 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) Investigations for gallstone disease

12. 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 Biliary Colic

13. 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 Acute Cholecystitis

14. 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 Obstructive Jaundice

15. 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 Ascending Cholangitis

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. 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 Cholecystectomy

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. 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 Cholecystectomy when to perform?

21. The End Questions?

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