Cholecystitis :

Vascular congestion and oedema

Definition:
Inflammation of the gallbladder may be acute,
chronic, or acute superimposed on chronic. It
almost always occurs in association with
gallstones
Epidemiology:
United States cholecystitis is one of the most
common indications for abdominal surgery.
distribution closely parallels that of gallstones.
Types:

Acute cholesystitis:
o

Acute inflammation of the gallbladder,

precipitated 90% of the time by
obstruction of the neck or cystic duct.
It is the primary complication of
gallstones and the most common reason
for emergency cholecystectomy.
Cholecystitis without gallstones called
acalculous cholecystitis may occur in
severely ill patients and accounts for
about 10% of patients with cholecystitis.

Necrosis of wall, bacterial proliferation

Complications eg. gangrene, perforation, liver abscess,

cholangitis, bacteraemia etc.

Acute calculous cholecystitis:

o Results from chemical and inflammation
of obstructed gall bladder.
o Normal protective glycoprotein layer is
disrupt exposed epithelium to direct
action detergent of bile salts.
o Prostaglandin released from distended
gall bladder inflammation.
o Gallbladder dysmotility; distension &
increased intraluminal pressure
compromise blood flow to mucosa
o Occur in absences of bacterial infections.
Acute acalculous cholecystitis

Pathogenesis:
Impaction of gallstones in the cystic duct (>90%
cases)

Obstruction and dilatation of gallbladder

o
o

Results from inflammation

Due to inflammation & edema of wall that
compromise blood flow gallbladder
statisaccumulation of microcrystal of
cholesterol viscious bile gall bladder
mucus cystic duct obstruction
MH

Risk factors:
Sepsis with hypotension & multisystem
failure
Immuno-suppression
Major trauma & burns
infections
Morphology:
o Tense & Enlarged gall bladder
o Bright red or blotchy, violaceous to green
black discolouration subserosal
haemorrhage
o Serosal layered by fibrin, if severe
suppurative& coagulated exudates
o Acalculous absences of macroscopic
stones
o Calculous stone usually in neck of
gallbladder
o Empyema of gallbladder exudates
virtually with pus
o Thickened gallbladder wall
o Edematous & hyperemic
o Gangrenous cholecystistis
o

Clinical features;
o Progressive RUQ/ epigastric pain
o Associated : Mild fever, anorexia,
tachycardia, sweating, nausea, vomiting
o Jaundice if obstruct CBD
o Acute calculous sudden pain or acute
emergency needed, wout intervention
subsides in 7- 10 days.
o Acute acalculous insidious in onset, ,
higher incidence of gangrene and
perforation.

Chronic cholecystitis;
o
o

Sequel to repeated bout of acute

cholecystitis
Associated with cholelithiasis in >90% of
cases.

Pathogenesis:
Not clear
Supersaturation predisposed to both chronic
inflammation & stone formation.
E.coli & Enterococci found in 1/3rd cases.
Obstruction of outflow is not main for chronic
cholecystitis
Morphology:
Serosa smooth & glistening / dulled by
serosal fibrous.
Dense fibrous adhesion as sequel of
preexisting reapted acute cholecystitis.
Wall thickened, opaque-grey white
appearance.
Lumen fairly clear, green-yellow, mucoid bile
& usually stones.
Histology :
o Mild lymphocytes, plasma cells,
macrophages, in mucosa & subserosal
fibrous.
o Severe fibrous,mononuclear cell
infiltration, buried crypts ( reactive
proliferation mucosa + mucosal folds) ,
Rokitansky Aschoff sinuses (outpouch
of epithelium through wall),
o Rare porcelain gall bladder ( dystrophic
calcification), xanthogranulomatous
MH

cholecystitis ( massive thickened gall

bladder + shrunken nodular + chronic
inflamed with foci necrosis), Atrophic
( hydrops of gall bladder)

Clinical features:
o Recurrent attack of colicky pain
o RUQ pain
o Nausea & vomiting frequent associated
symptoms
o Intolerance for fatty foods.
Complications:
Bacterial superinfections with cholangitis /
sepsis
Gallbladder perforation & local abcess
formation.
Biliary enteric fistula W draining of bile into
adjacent organ
Aggravating of preexisting medical illness with
cardiac, pulmonary renal or liver
decompensation.

Investigation:

FBC
TWBC : leukocytosis elevated mild to moderate
Serum bilirubin : slightly elevated
USG ; calculi in 90- 95% of cases
Cholesyntigraphy : abnormal CCK gall bladder
ejection fraction <40%

Treatment:
Usually surgical as main choices.

MH

 Medical therapy
o Pre cholecystectomy:
Oral intake is eliminated
nasogastric suction may be
indicated
extracellular volume depletion and
electrolyte abnormalities are
repaired.
Meperidine / NSAIDS used due to
produced less spasm to the
sphincter of Oddi than morphine.
I.V antibiotics given: piperacillin or
mezlocillin, ampicillin sulbactam,
and third-generation
cephalosporins. Anaerobic
coverage by a drug such as
metronidazole should be added if
gangrenous or emphysematous
cholecystitis is suspected.

unacceptable risk for early

surgery .
pt in whom the diagnosis of acute
cholecystitis is in doubt

Extrahepatics bile ducts:

Ascending Cholangitis:
Definition:
Term used for bacterial infection of the bile
ducts
Causes :
Due to any obstruction to bile flow E.g.:
choledocolithiasis
Types :

Surgical therapy:
o Optimal timing depend on pt.
stabilizations.
o Urgent (emergency) cholecystectomy or
cholecystostomy is probably appropriate
in most patients in whom a complication
of acute cholecystitis such as empyema,
emphysematous cholecystitis, or
perforation is suspected or confirmed
o Delayed if:
patients in whom the overall
medical condition imposes an

Ascending cholangitis
Primary sclerosing cholangitis
Recurrent pyogenic cholangitis
AIDS-related cholangitis

Etiology :
Obstruction of the common bile duct due to
gallstones
Benign strictures
Malignant strictures
Sclerosing cholangitis
Parasites
MH

Pathophysiology :

Risk factors:

Age > 50 years

Cholelithiasis (formation of gallstones)

Benign strictures

Malignant strictures

Postprocedure injury of bile ducts

History of sclerosing cholangitis

Sign & Symptoms :

Bile is normally sterile. Biliary tree normally

protected because there is normal flow of bile to
flush, the sphincter of oddi prevents backflow
from the small intestine (mechnical), and bile
salts have bacteriastatic properties.
Although the exact mechanism is unclear, it is
believed that bacteria gain access to the biliary
tree by retrograde ascent from the duodenum or
from portal venous blood.
Statis contributes to bacterial growth, increased
pressures leads to backflow of infection into
other parts of the system. Can lead to
bacteremia and severe sepsis via portal system

Charcots Triad

Jaundice, fever, and RUQ pain &

Reynolds Pentad

Addition of altered mental status, and

hypotension

Investigation :

transabdominal ultrasound

Endoscopic ultrasound

CT

Magnetic resonance
cholangiopancreatography(MRCP)

MH

Endoscopic retrograde
cholangiopancreatography (ERCP)

Lab tests

80% have IBD usually UC

~44% asymptomatic at diagnosis
Median survival ~ 12 years

abnormal LFTs, elevated CRP, WBC

Etiology:

Treatment :

Broad spectrum antibiotics

Biliary drainage

ERCP

Percutaneous transhepatic
cholangiography (PTC)

EUS guided drainage

Open surgical drainage

Primary sclerosing cholangitis

Definition:
A chronic inflammatory cholestatic disease
Progressive destruction of bile ducts
May progress to cirrhosis
Epidemiology:
Prevalence 6-8/100000
Usually diagnosed in 20s and 30s
Male predominance ~3:1

Aetiology unknown
Familial incidence
HLA associations-B8,DR3,DRw52a,DR2,DR4
Polymorphism of TNF gene
Immunology factors:
o Increased frequency of autoimmune
disorder
o Increased T cell in blood and liver
o Increased circulating immune complexes.

Pathogenesis :
Association between PSC and Ulcerative Colitis
suggests a pathogenic interaction
Bacteria or toxic substances absorbed via
inflammed mucosa
Bile duct injury suggest ischaemic injury
immune complex mediated
Clinical features:
44% asymptomatic but most develop symptoms
over time
Pruritis , jaundice, pain and fatigue are common
symptoms
Later on develop symptoms of cirrhosis and
portal hypertension

MH

Investigation :
Cholangiography :
o ERCP (endoscopic retrograde
cholangiopancreatogram) or MRCP
(Magnetic resonance
cholangiopancreatography)

Management:
Many strategies tried but only transplantation
shown to improve survival
Medical therapy;
o Ursodeoxycholic acid (UDCA)
MOA: reduces cholesterol
absorption
Used to dissolve (cholesterol)
gallstones in patients who want an
alternative to surgery.
Expensive
Usually <10 mmd 8-10 mg/kg / day
Combination Rx with UDCA and steroids
showed clinical and biochemical improvement in
a small trial

MH

 Endoscopic Treatment Balloon dilation or

stenting can improve clinical,biochemical and
cholangiographic appearances

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