Tokyo Guidelines 2018: The Tokyo guidelines provide diagnostic criteria, severity grading, and management strategies for acute cholecystitis and acute cholangitis. They were produced on the basis of the consensus achieved during discussions by global experts at the Tokyo Consensus Meeting originally held in 2007, updated in 2013, and again in 2018.
Acute Cholecystitis
Pathogenesis
Persistent GB neck occlusion 2/2 stones/sludge
Clinical
Same symptoms as biliary colic but duration > 6 h
Diagnosis: The Tokyo guidelines outline three criteria for diagnosis. A suspected diagnosis is made when ≥ 1 component of both criteria A and B are met. A definite diagnosis is made when ≥ 1 component of all three (A, B, and C) are met.
A. local signs of inflammation
Murphy sign (inspiratory pause during GB fossa palpation)
RUQ mass, pain, or tenderness
B. systemic signs of inflammation
fever
↑CRP
↑WBC
C. imaging
RUQUS: The 2 most important features are the presence of gallstones and the sonographic Murphy sign, which together are highly specific (93.6%) for acute cholecystitis.
mobile hyperechoic foci that cast posterior acoustic shadowing (ie gallstones)
sonographic Murphy sign (maximal abdominal tenderness from pressure of the ultrasound probe over the visualized gallbladder)
GB wall thickening ≥ 3-4 mm
pericholecystic fluid
GB distension ≥ 9 x ≥ 4 cm (41%)
CT (venous-phased): CT is not the primary imaging modality because of its low sensitivity for gallstones. It is, however, of good value in imaging possible complications (ie gangrenous cholecystitis, perforation, Mirizzi syndrome, etc.)
generally same findings as on RUQUS
pericholecystic fat stranding
GB mucosal enhancement
transient focal liver enhancement adjacent to GB
HIDA: Cholescintigraphy using 99mTc-hepatic iminodiacetic acid (HIDA) may be indicated if the diagnosis remains uncertain following ultrasonography. The radiotracer is administered IV, selectively uptaken by hepatocytes, and excreted into bile ducts. HIDA has 100% negative predictive value, 90-97% sensitivity, & 71-90% specificity.
positive HIDA = failure to visualize gallbladder (but visualization of CBD/duodenum) w/in 1 h
false-positives may be seen in alcoholic liver disease, functional disorders, or pts on TPN
Severity: Higher severity grade is associated with increased mortality (despite an overall mortality of ~1%), length of hospital stay, conversion from laparoscopic to open, complications esp. bile duct injuries, & higher medical costs.
grade 1 (mild)
not grade 2 or 3
grade 2 (moderate): ≥ 1 of
WBC > 18
palpable RUQ mass
duration > 72 h
gangrenous cholecystitis
pericholecystic abscess
hepatic abscess
biliary peritonitis
emphysematous cholecystitis
grade 3 (severe): ≥ 1 of
hypotension requiring dopamine ≥ 5 mcg/kg/min or any norepinephrine
AMS
P/F ratio < 300
oliguria or Cr > 2.0
INR > 1.5
Plt < 100
Antibiotics
grade 1: any of the following
Unasyn (not recommended if > 20% local resistance)
ertapenem
cefazolin + metronidazole
ciprofloxacin + metronidazole
grade 2: any of the following
Zosyn 3.375 mg Q8H
ertapenem
ceftriaxone + metronidazole
ciprofloxacin + metronidazole
grade 3: any of the following
Zosyn 4.5 mg Q8H
meropenem
cefepime + metronidazole
therapy: guided by Charlson Comorbidity Index (CCI) and ASA class
grade 1
CCI ≤ 5 and/or ASA ≤ 2: early lap chole
CCI > 5 and/or ASA > 2: abx f/b delayed lap chole
grade 2
if abx/supportive tx succeeds
CCI ≤ 5 and/or ASA ≤ 2: early lap chole
CCI > 5 and/or ASA > 2: delayed lap chole
if abx/supportive tx fails: urgent GB drainage
grade 3
early lap chole only for select pts
no jaundice, TBili < 2, no AMS, P/F > 300
CV/renal failure rapidly reversed after admission
all other pts undergo urgent GB drainage
delayed lap chole if CCI < 4 and/or ASA < 3
continued obs if CCI ≥ 4 and/or ASA ≥ 3
complications
gangrenous cholecystitis (up to 20%)
pathogenesis: GB necrosis
clinical: ↑age, DM, delayed presentation
diagnosis
IV-contrasted CT: 73% SN vs 95% NPV
IV-contrasted MRI: 80% accuracy
irregular GB wall thickening
poor GB wall enhancement (interrupted rim sign)
pericholecystic fat stranding
gas in GB lumen or wall
membranes w/in lumen (intraluminal flap)
pericholecystic abscess
emphysematous cholecystitis
pathogenesis: GB wall infection w/aerogenic bacteria
risk factors: DM
microbiology: Clostridium welchii > E. coli
clinical: RUQ crepitus (rare but unique sign)
diagnosis: non-contrasted CT (gas in GB wall)
GB perforation (10%)
usually localized as pericholecystic abscess
rarely disseminates as biliary peritonitis
abscess (intra-abdominal, pericholecystic)
biliary peritonitis & sepsis
abdominal wall gas gangrene