ACUTE CHOLANGITIS

DEFINITION
Acute Cholangitis is an ascending bacterial infection superimposed in partial or complete
obstruction of the bile ducts. Patients may present with mild, self-limited episodes to a fulminant,
potentially life-threatening septicemia. The classic symptoms experienced by 2/3 of patients is
the Charcot’s triad, a progression of symptoms from RUQ abdominal pain, fever >39degC, and
jaundice (P 90%, F 95%, J 80%). This can rapidly progress to septicemia with accompanying
hypotension and altered mental status, known as the Reynold’s pentad. In the elderly, it may be
atypical in presentation with unremarkable symptoms until the disease is already advanced.

PATHOPHYSIOLOGY
Normally, bile salts, biliary epithelium, Kupffer cells, tight junctions between the cholangiocytes,
and the sphincter of oddi are protective mechanisms to prevent cholangitis. However, in the
onset of biliary obstruction, bile becomes stagnant in the biliary system, increasing susceptibility
of bacterial colonization to the extent where Kupffer cell’s activity of bacterial phagocytis is
overwhelmed. Long-standing bile stagnancy may raise intraductal pressure, causing widening of
the tight junctions between cholangiocytes allowing translocation of bacteria from the
hepatobiliary system into the systemic circulation resulting in septicemia.

ETIOLOGY + EPIDEMIOLOGY
Gallstones remain one of the main causes of biliary obstruction in Acute cholangitis (85%), the
remaining 15% is caused by neoplasms, and very rarely, stents causing a nidus of infection. 10-
15% of cases are Caucasians, usually affecting the 50-60 age group, and there’s no specific sex
predilection. The usual bacteria isolated in specimens are gram negatives such as E. coli,
klebsiella, pseudomonas. Occasionally, anaerobes and enterococci may co-infect.

DIAGNOSTICS
The diagnostic test requested is first a Complete Blood count where we would expect
leukocytosis that is seen in 80% of patients with acute cholangitis. Total Bilirubin is also requested
and is expected in ³ 80% of patients where we would expect ³2mg/dL. AST, ALT, ALP is also
requested and as well as CRP, a marker for systemic inflammation which are all be expected to
be elevated.

Imaging Studies are also requested. First for initial screening is a Whole Abdominal Ultrasound
for the detection of biliary stones. Another is the Abdominal CT Scan that may help exclude
gallstone complications (acute pancreatitis, abscesses, other organ affectations). ERCP may also
be requested for definitive imaging for bile duct stones and cholangitis. This also allows direct
visualization of the biliary tree and also therapeutic in allowing decompression and biliary
drainage
The 2013 Tokyo Guidelines suggest 3 parameters on suspected or definitive diagnosis for acute
cholangitis. First is presence of systemic inflammation proven clinically be fever and chills; and
from laboratory data of abnormal levels of WBC (<4000 or >10 000) and elevated CRP (³ 1mg/dL).
Presence of Cholestasis is another parameter, proven clinically with jaundice and Total Bilirubin
levels ³ 2mg/dL, and elevated ALP, AST, and ALT 1.5 x the ULN. Third is the presence of imaging
evidence of biliary dilatation and as well as its etiology. Suspected diagnosis is presence of
systemic inflammation and either cholestasis and imaging; while Confirmatory for the diagnosis
is clinical, laboratory, or imaging for all parameters.

Acute Cholecystitis can be further graded into Grade III, if there’s presence of organ dysfunction,
Grade II if there’s leukocytosis or leukopenia, high-grade fever, hyperbilirubinemia,
hypoalbuminemia, or if the patient is ³75 years old. Any two of the following can be fit as Grade
II. Grade I if it cannot be fit into any of the criteria and the presentation is non-toxic.

MANAGEMENT + PROGNOSIS
Cholecystectomy or biliary decompression is the cornerstone of management that improves
survival dramatically.

Cefazolin +/- Metronidazole that covers for Gram +, -, and anaerobes with elective stone removal
will suffice for mild cases. Severe Cases constitute more intensive therapy with gentamicin,
ampicillin, and metronidazole. Suspected ESBL organisms indicate meropenem use. Patients
generally improve within 6-12 hours of therapy and may planned on elective stone removal with
ERCP. Antimicrobial therapy may be discontinued within 24 hours s/p cholecystectomy.
Extension of therapy is indicated in patients with perforation, emphysema, and necrosis.
Emergency ERCP should be done in patients with declining clinical status for immediate stone
extraction and decompression. High mortality rate is seen once septicemia sets in.