Biliary disease

Introduction

• Cholecystitis
  • Inflammation of gallbladder usually caused by obstructing gallstone
• Gallstones
  • 8% of men and 17% of women
  • Prevalence increases with age and increasing BMI
  • Bariatric surgery is a risk factor for development
  • Asymptomatic gallstones carry a 1-4% risk per year of symptoms or complications
• Biliary colic
  • Most common complication of gallstones
  • Recurrent attacks of steady upper abdominal pain lasting several hours and resolving spontaneously when gallstone moves from obstructing position
  • If stone remains obstructive, get acute cholecystitis
• Acute cholecystitis may develop into gangrenous cholecystitis
• Emphysematous cholecystitis develops when gas-producing bacteria infect the inflamed gallbladder
• Gallbladder perforation is uncommon but life-threatening

Introduction

• Choledocholithiasis
  • Gallstones within common bile duct
  • May be primary (from within bile ducts) or secondary (forming in gallbladder and descending into CBD)
  • Can result in cholangitis (infection of biliary tree)
• Chronic cholecystitis
  • Prolonged gallbladder inflammation due to recurrent cystic duct obstruction by gallstones
• Biliary sludge
  • Microlithiasis composed of cholesterol crystals, calcium bilirubinate pigment and other calcium salts
  • May resolve or progress to biliary colic, cholecystitis, cholangitis or pancreatitis
• Acute acalculous cholecystitis
  • Much less common but more likely to suffer complications
  • Seen in critical illness, old age, diabetes and immunosuppression

Jaundice

• Clinically evident at bilirubin >40mmol/L
• Visualised in tissues with high albumin concentration (sclera, skin)
• To get urobilinogen in urine, need non-obstructed biliary system as bilirubin must reach intestinal tract and be converted to urobilinogen by bacteria then reabsorbed to blood stream and filtered to urine

Pathophysiology

• Cholesterol stones (80%)
  • Radiolucent
• Pigment stones (20%)
  • Radioopaque
• Gallstones can then obstruct at gallbladder neck, cystic duct, or CBD
• Bile cultures are positive in 50% of cases of acute cholecystitis
  • Gram-negative organisms predominate (E. coli, Klebsiella)
  • Streptococcus (18%) and Enterococcus (17%) also seen
  • Anaerobes (Clostridia 14%, Bacteroides 3%)

Clinical presentation

• Pain in epigastrium or RUQ radiating to back occasionally
• Usually steady vs. colicky
• Often nausea and vomiting
• Fatty food intolerance is NOT a reliable predictor of stones
• Peak in symptoms around midnight
• If pain persists > 6 hours, complications such as acute cholecystitis or cholangitis must be considered

Clinical presentation

• Examination
  • Biliary colic – Mild RUQ tenderness without peritonism. Afebrile.
  • Acute cholecystitis – More significant RUQ tenderness and may have signs of localised peritonism
  • Murphy’s positive is 67% sensitive and 87% specific for acute cholecystitis
  • Fever evidence in 1/3 of acute cholecystitis
  • Jaundice implies CBD obstruction from choledocholithiasis or extrinsic compression of the bile duct by an impacted cystic duct or gallbladder stones or adjacent inflammation (Mirizzi’s syndrome)

Diagnostic criteria for acute cholecystitis

• Suspected: One local sign and one systemic sign
• Definite: One local sign, one systemic sign and imaging findings consistent with acute cholecystitis
• Local signs: Murphy’s positive, RUQ mass/pain/tenderness
• Systemic: Fever, raised CRP, raised WCC
• Sensitivity 91%, specificity 97% for definite diagnosis criteria

US findings of acute cholecystitis

• Sonographic Murphy’s
• Gallbladder wall >3mm (measure anterior wall as posterior wall obscured by artefact)
• Pericholecystic fluid
• Gallbladder distension: Short axis >40mm
• 81% sensitivity and 83% specific for acute cholecystitis
• Presence of gallstones + sonographic Murphy’s = 92% PPV for acute cholecystitis
• Absence of both = 95% NPV for acute cholecystitis
• CBD normally <6mm (>8mm = abnormal)

Cholangitis

• Charcot’s triad: Jaundice, fever, RUQ pain
  • Triad seen in >50% of cases
  • Jaundice is only in 2/3
• Reynold’s pentad: Charcot’s + ALOC and shock
  • Seen in <10% of cases
• Raised bilirubin strongly suggestive of cholangitis vs. biliary colic/acute cholecystitis

Lab tests

• Usually normal in biliary colic
• Acute cholecystitis
  • Usually leukocytosis but absence does not rule it out
  • WCC >10 has 63% sensitivity, 57% specificity, +LR 1.5 and –LR 0.6
  • Mean WCC 12.6
  • Elevation of CRP is associated but not specific
  • LFT’s usually normal
• Choledocholithiasis
  • LFT derangement
  • Abnormal GGT is the most sensitive and specific marker of choledocholithiasis
  • ALT or AST >1000 can occur in choledocholithiasis but are more suggestive of hepatocellular necrosis

CT

• Sensitivity for gallstones of around 75%
• Inability to detect Murphy’s sign
• May show complications such as gangrenous cholecystitis, emphysematous cholecystitis, gallstone ileus and gallbladder perforation
• Gangrenous cholecystitis appears as patchy enhancement/non-enhancement of the gall bladder wall
• Perforation appears as a deflated gallbag with heaps of fluid around it (bile)
• Better than USS for visualising stone in CBD (choledocholithiasis)

Imaging for choledocholithiasis

• Difficult to exclude with USS or CT
• US often fails to visualise the entire extrahepatic biliary tree
  • Sensitivity of only 60% for choledocholithiasis
• CT performs somewhat better than USS in this context
  • Highly specific if seen
  • Sensitivity up to 93% if contrast + helical cholangiography protocol
• Stones + CBD dilation provide indirect evidence of choledocholithiasis on either US or CT
  • Normal cut-off of 6mm but specificity increases with higher cut-offs
  • Dilates with age
• MRCP, endoscopic US or ERCP are all useful alternatives

Choledocholithiasis

• 5-20% of patients at the time of cholecystectomy
• Mostly secondary to cholelithiasis
• Primary choledocholithiasis (formation in CBD) is less common
  • Typically seen in bile stasis e.g. CF
• Usually present with biliary tree pain, early transaminitis and later cholestatic liver enzymosis
  • GGT/serum bilirubin are most sensitive and specific
  • Pain often more prolonged (>6 hours) than biliary colic
  • Pain may be transient if ball-valve effect
• Complications
  • Ascending cholangitis
  • Pancreatitis

Eponyms

• Courvoisier’s sign = Palpable gall bladder with jaundice = malignancy
• Charcot’s triad = RUQ pain, fever, jaundice = Cholangitis
• Reynaud’s pentad = Hypotension, ALOC = Severe cholangitis

Treatment

• Asymptomatic gallstones
  • No treatment
  • Elective cholecystectomy for those with high risk of complications such as sickle cell disease, planned organ transplant or those with ethnicity that is high risk for gallbladder cancer
• Biliary colic
  • Symptom control and referral to outpatients for lap chole
  • NSAID’s are first-line analgesics (parenteral NSAID = opioid), then opioids
  • NSAID’s decrease frequency of short-term cholecystitis
  • No evidence for one opioid over another and Sphincter of Oddi spasm is of unclear significance
  • Anticholinergics do not improve biliary colic pain

Treatment

• Acute cholecystitis
  • Early lap chole is the treatment of choice
  • Analgesia, antiemetics, NBM and antibiotics
    • Triples or Cef + Metronidazole
  • Value of antibiotics in mild acute cholecystitis has been questioned
• Cholangitis
  • Aggressive resuscitation, timely triple Ab’s and early biliary decompression
  • ERCP is the decompression procedure of choice
  • Percutaneous or surgical drainage is an alternative if ERCP is not thought to be feasible or is unsuccessful

Emphysematous cholecystitis

• Gas in gallbladder wall or lumen due to Clostridia, E. coli or Klebsiella
• Associated with DM and is more common in older patients
• Associated with gallstones sometimes
• 15% mortality rate
• Broad-spectrum Ab’s and urgent lap chole OR percutaneous cholecystotomy in severely ill patients

Gallstone ileus

• Mechanical small bowel obstruction due to ectopic gallstone that has reached intestinal lumen via a biliary-enteric fistula
• Rare
• Impacts at terminal ileum causing SBO usually
• Can occur secondary to cholecystitis
• Rigler’s triad is classic radiographic finding
  • SBO, pneumobilia and ectopic gallstone
• 15-18% mortality rate
• Mostly seen in the elderly

Acalculous cholecystitis

• Diagnosis is challenging as no test is diagnostic
• More fulminant course than cholecystitis and complications are common with high mortality
• US, IV CT abdo/pelvis and cholescintigraphy can all be helpful

Post-cholecystectomy syndrome

• Persistent abdominal symptoms post-cholecystectomy
• Bile leak is the principal concern early on
• Choledocholithiasis is a common cause
  • May be retained stones present at the time of surgery OR
  • May develop stones post-operatively due to bile stasis
• May also be non-biliary pain attributed to gallstones prior to operation
• Can be difficult to diagnose as CBD dilatation up to 10mm is seen normally after cholecystectomy
• CT, then MRCP +- ERCP is most common diagnostic approach

Last Updated on March 27, 2024 by Andrew Crofton