Gallstone Disease and Acute Cholecystitis MAD

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Muhammad `Abdurrahman General Surgery

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Transcript of Gallstone Disease and Acute Cholecystitis MAD

Muhammad `AbdurrahmanGeneral Surgery

Types of gallstone Cholesterol stones (20%) Pigment stones (5%) Mixed (75%)

Epidemiology Fat, Fair, Female, Fertile, Fourty above 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

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 (very rare)

Gallstone disease (and its related complications)

Gastritis/duodenitis Peptic ulcer disease/perforated peptic ulcer Acute pancreatitis Right lower lobe pneumonia MI etc

Can differentiate between gallstone complications based on:

History Examination Blood tests

Full Blood Count Liver Function Test CRP Clotting Amylase Lipid profile Tumor marker

Complication History Examination Blood testsBiliary 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)

-WBC (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 (↑)

-WBC 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

-WBC 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)

-WBC 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

-WBC 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 ↓)

-WBC 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.

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◦ Become new gold standard therapy

Advantages: Less post-op pain Shorter hospital stay Quicker return to normal activities

Disadvantages: Limited vision

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