Signature ✍️
Clinical ☠️
- Gallbladder: cystic duct obstruction (”calculous”) vs. gallbladder wall edema/inflammation (”acalculous”) → right upper quadrant/epigastric pain (”cholecystalgia”), right shoulder/back pain (referred T5-L2 pain), RLQ pain (inferior extension), non-specific abdominal pain (falsely-reassuring), sepsis-related GI dysfunction resulting in diarrhea
- Gallbladder neck compressing CBD (”Mirizzi syndrome”): mimics choledocholithiasis/cholangitis
↓ ↓ ↓ Rupture ↓ ↓ ↓
- Type 1 (acute): free peritoneal fluid, abdominal sepsis / death
- Type 2 (subacute): walled-off → focal peritonitis, surrounding abscess(es)
- Type 3 (chronic): gallbladder-__ fistula → enteric (gallstone ileus), pleural (pleural effusions), hepatic (liver abscesses, septic thrombophlebitis), abdominal wall (intramuscular abscess)
- Type 4 (chronic): gallbladder-biliary fistula → cholangitis
⚪ Note: patients with severe sensory neuropathy (e.g. diabetes) may have denervated gallbladder allowing acute presentation of fulminant sepsis without pain (i.e. gangrene, perforation), or progression to chronic gallbladder pathology (e.g. emphysematous cholecystitis, gallstone ileus). Advanced age, cognitive deficits, & immunocompromising conditions may also mask typical symptoms
⚪ Note: there are no reliable clinical nor laboratory features that can distinguish non-perforated from perforated cholecystitis, & a preop diagnosis of perforation is only made in ~3% of patients
⚪ Note: additionally, studies on diagnostic error in cholecystitis suggest the false ⊖ rate is ~30%, with the most common reasons for misdiagnosis attributed to diagnostic misdirection (e.g. post-stroke patient → aspiration pneumonia) & inconspicuous/underrecognized imaging findings (i.e. radiology limitations)
Laboratory ⚠️
- CBC: neutrophilic leukocytosis (”unexplained”)
- LFTs: normal AST/ALT/bili/ALP*
⚪ Note: in the absence of Mirizzi syndrome, ↑ AST/ALT/Bili is not expected, however a mild ↑ in AST/ALT/ALP can be generated by contiguous focal hepatitis, particularly in gallbladder rupture
Radiographic 🩻
- RUQ US: gallbladder wall edema & thickening, pericholecystic fluid, stones
- CT/MRCP: gallbladder wall edema & thickening, pericholecystic fat stranding → “decompressed” gallbladder & free fluid (rupture)
- HIDA: confirm active cholecystitis (⊖ uptake) vs. perforation (⊕ uptake → leak)
⚪ Note: the RUQ US report of "overlying bowel gas making adequate visualization of the gallbladder difficult” can suggest emphysematous cholecystitis due to air within the gallbladder wall
DDx 🏳️🌈
- Calculous Cholecystitis 🟢
- Direct Evidence
- Stone
- Indirect Evidence
- Acalculous Cholecystitis 🟢
- Ischemia, Occlusive
- Acute mesenteric ischemia
- Ischemia, Non-occlusive
- Post-shock
- Stasis (critical illness, TPN/fasting)
- Small → medium-vessel vasculitis
- Direct Infection 🟢
- Viral
- EBV
- CMV
- Bacterial
- Salmonella
- Legionella
- Leptospirosis
- Tuberculosis
- Rickettsia
- Brucella
- Q fever
- Parasitic
- Malaria
- Schistosoma
- Cyclospora, cystoisospora, microsporidia
- Fungal
- Invasive candidiasis
Principles ❗
Diagnostic Arc 🗻
Emphasis on Diagnosis of Calculous Cholecystitis 🔥 : if there is any concern at all for cholecystitis & the ultrasound/CT are not diagnostic, HIDA scan is best next step (sensitivity ~90-95%). The purpose of the HIDA scan is specifically to look for cystic duct obstruction, whether that be due to calculous plugging vs. acalculous obstruction. Cystic duct obstruction is the gallbladder correlate of other infections brewing within a high pressure system that won’t get better without relieving the obstruction (e.g. cholangitis 2/2 CBD stone, pyelo 2/2 nephrolithiasis). Some cholecystitis will resolve with antibiotics alone, but if you think of it as a source control issue, it makes sense that it should at least be investigated. (Note: the assumption that only calculous cholecystitis poses a source control issue is a faulty one, as ~50% of acalculous cholecystitis patients develop gangrene.)
❓ Role of CT Scan❓: the RUQ US & (confirmatory) HIDA scan are the workhorses for the diagnosis of calculous cholecystitis. However, if your patient w/ suspected cholecystitis has sepsis (gangrene), peritonitis (perforation), crepitus (emphysematous disease), or bowel obstruction (gallstone ileus), a CT scan w/ IV contrast is warranted for rapid rule-out of these highly morbid complications
HIDA Scan 🟢 : highly sensitive, but ultimately non-specific, as a ⊕ study simply denotes lack of flow through the cystic duct. Reasons for this include:
- Obstructed Cystic Duct ✅
- Gallstone w/o infection
- External compression (e.g. tumor)
- Non-Obstructed Cystic Duct ❌
- ↑ INR: severe liver disease (i.e. abnormal uptake & excretion of tracer)
- ↑ Bilirubin: ↓ hepatic clearance of tracer (although this is not issue if agent used is di-isopropyl & m-bromotrimetyl iminodiacetic acid)
- TPN/malnourished: ↓ gallbladder contraction stimulation → viscous bile that prevents tracer uptake
- Biliary sphincterotomy: ↓ resistance of bile flow facilitates tracer movement immediately down CBD rather than into cystic duct
Gallstones: Endpoint DDx 💭
After the diagnosis of calculous cholecystitis, some thought should be put into whether patient has reason for pathologic gallstone disease (e.g. young patient, no obesity, no hyperlipidemia)
↑ Substrate
- Pigment: chronic hemolysis, parasitic HPB infection
- Cholesterol: metabolic syndrome
- Antibiotic: fibrates, ceftriaxone
↑ Crystallization Rate (Gallbladder Stasis)
- Extreme dieting & malnutrition
- Prolonged immobility
- Estrogen therapy
- Functional gallbladder disorder
↓ Enterohepatic Recycling
- Disease of the ileum (e.g. Crohn’s, other infiltrative disease, ileal resection)
References 📚
