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 -Murphy’s – -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 -Periotnism RUQ (guarding/rebound) -Murphy’s + -Pyrexia, HR (↑) -WCC and CRP (↑) -LFT (N or mildly (↑) Empyema -Constant RUQ pain into back or right shoulder -N&V -Feverish -Tender RUQ -Peritonism RUQ -Murphy’s + -Pyrexia, HR (↑), BP (↔ or ↓) -More septic than acute cholecystitis -WCC and CRP (↑) -LFT (N or mildly (↑) Obstructive Jaundice -Yellow discolouration -Pale stool, dark urine -painless or assocaited with mild RUQ pain -Jaundiced -Non-tender or minimally tender RUQ -No peritonism -Murphy’s – -Apyrexial, HR and BP (N) -WCC and CRP (N) -LFT: obstructive pattern bili (↑), ALP (↑), GGT (↑), ALT/AST (↔) -INR (↔ or ↑) Ascending Cholangitis 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 and CRP (↑) -LFT : obstructive pattern bili (↑), ALP (↑), GGT (↑), ALT/AST (↔) -INR (↔ or ↑) 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 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. Diagnostic only but non-invasive Look for biliary dilatation and any stones in biliary tree 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 To unobstruct biliary tree when ERCP has failed Invasive – higher complication rate than ERCP MRCP: To visualise biliary tree accurately (much more accurate than USS) ERCP: Diagnostic and therepeutic in biliary obstruction PTC 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) 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 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) MRCP ERCP 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?