2. • Cholecystitis (Greek, -cholecyst, "gallbladder",
combined with the suffix -itis, "inflammation") is
inflammation of the gallbladder, which
occurs most commonly due to
obstruction of the cystic duct with
gallstones (cholelithiasis).
Gall bladder- Cholecyst, Biliary Vesicle, Bile Bladder
3. Classification of Cholecystitis
I. Acute Cholecystitis: calculous & acalculous
II. Chronic Cholecystitis
III. Acute superimposed on chronic
4.
5. Acute Calculous Cholecystitis (90%)
• Acute Calculous cholecystitis is an acute
inflammation of the gallbladder, precipitated 90%
of the time by obstruction of the neck or cystic
duct (by gallstones).
It is the primary complication of gallstones and
the most common reason for emergency
cholecystectomy.
Obstruction→Distension→Inflammation
(due to chemical irritation & Infection)
Hartmann's pouch is an out-pouching of the wall of the gallbladder at the junction
of the neck of the gallbladder and the cystic duct.
The commonest location of impaction of a gallstone is Hartmann’s pouch.
6. Acalculous cholecystitis (10%)
• Cholecystitis without gallstones,
called acalculous cholecystitis may occur in
severely ill patients and accounts for about 10% of
patients with cholecystitis.
7. Pathogenesis- Calculous cholecystitis
• Acute CALCULOUS cholecystitis results from
chemical irritation and inflammation of the
obstructed gallbladder.
• The action of mucosal phospholipases hydrolyzes
luminal lecithins (Phospholipids) to toxic
LYSOLECITHINS.
• The normally protective glycoprotein mucus layer
is disrupted, exposing the mucosal epithelium to
the direct DETERGENT action of bile salts.
8. • Prostaglandins released within the wall of the
distended gallbladder contribute to mucosal and
mural inflammation.
• Gallbladder dysmotility develops; distention and
increased intraluminal pressure compromise blood
flow to the mucosa.
• Acute calculous cholecystitis frequently develops
in diabeticpatients who have symptomatic
gallstones.
10. Pathogenesis- Acalculous cholecystitis
• Acute ACALCULOUS cholecystitis is thought to
result from ISCHEMIA.
The cystic artery is an end artery with essentially
no collateral circulation.
11. ***Risk factors for acute Acalculous
cholecystitis include:
(1) Sepsis with hypotension and multisystem
organ failure;
(2) Immunosuppression;
(3) Major trauma and burns;
(4) Diabetes mellitus; &
(5) Infections.
(Salmanellosis & Cholera), Parasitic infestation
Major nonbiliary surgery
Dehydration, gallbladder stasis
and sludging, vascular
compromise, and, ultimately,
bacterial contamination.
Sepsis: The presence of pus-forming bacteria or their toxins in blood or tissues.
Recent childbirth, Torsion of GB
Cause
Ischemia
12. Morphology
GROSS:
Size: The gallbladder is usually enlarged and tense,
Color: bright red or blotchy, violaceous to green-
black discoloration, imparted by subserosal
hemorrhages.
Serosa : The serosal covering is frequently layered by
fibrin and, in severe cases, by a definite
suppurative, coagulated exudate.
Except for the presence or absence of calculi, the two forms of acute cholecystitis are
morphologically similar.
13.
14.
15.
16. Morphology
• Neck & Cystic duct: an obstructing stone is usually
present
• LUMEN: Stones + Bile (cloudy or turbid bile that may contain large
amounts of fibrin, pus, & hemorrhage).
• WALL: Thickened, edematous, and hyperemic.
17. • In more severe cases GB is transformed into a
green-black necrotic organ, termed Gangrenous
cholecystitis, with small-to-large perforations.
• The invasion of GAS-FORMING ORGANISMS,
notably clostridia and coliforms, may cause an
acute “Emphysematous” cholecystitis.
• Mucosa: Bright Red, swollen.
• When obstruction of the cystic duct is complete,
the lumen is filled with purulent exudate and the
condition is known as EMPYEMA of the
gallbladder.
18. Microscopy
The inflammatory reactions are not distinctive and
consist of the usual patterns of acute
inflammation:
Edema,
Leukocytic infiltration,
Vascular congestion,
Frank abscess formation, or
Gangrenous necrosis.
19. Clinical Features
•PAIN, fever, anorexia, tachycardia,
sweating, nausea, vomiting & mild jaundice.
• The pain may be referred pain that is felt in the
right scapula rather than the right upper quadrant
or epigastric region (Boas' sign). Phrenic Nerve
Boas's sign is hyperaesthesia (increased or altered sensitivity) below the right
scapula .
The patients of acute cholecystitis of either type have similar clinical features.
with features of peritoneal irritation such as guarding and hyperaesthesia.
The gallbladder is tender and may be palpable.
Leucocytosis with
neutrophilia
20. • PAIN may also correlate with eating greasy, fatty,
or fried foods. CCK
• The Murphy sign is specific, but not sensitive for
cholecystitis.
• Elderly patients and those with diabetes may have
vague symptoms that may not include fever or
localized tenderness.
Classically Murphy's sign is tested for during an abdominal examination; it is performed by
asking the patient to breathe out and then gently placing the hand below the costal margin
on the right side at the mid-clavicular line (the approximate location of the gallbladder). The
patient is then instructed to inspire (breathe in). Normally, during inspiration, the abdominal
contents are pushed downward as the diaphragm moves down (and lungs expand). If the
patient stops breathing in (as the gallbladder is tender and, in moving downward, comes in
contact with the examiner's fingers) and winces with a 'catch' in breath, the test is
considered positive. In order for the test to be considered positive, the same maneuver must
not elicit pain when performed on the left side. Ultrasound imaging can be used to ensure
the hand is properly positioned over the gallbladder
21. Clinical features
• More severe symptoms such as high fever, shock
and jaundice indicate the development of
complications such as
•Abscess formation,
•Perforation or
•Ascending cholangitis.
22. • Another complication, gallstone ileus,
occurs if the gallbladder perforates and forms a
fistula with the nearby small bowel, leading to
symptoms of intestinal obstruction.
Ileus is a disruption of the normal
propulsive ability of the gastrointestinal tract
. It is caused by failure of peristalsis i.e.
non-mechanical obstruction.
23. • Clinical symptoms of acute acalculous cholecystitis
tend to be more insidious, since symptoms are
obscured by the underlying conditions
precipitating the attacks.
• As a result of either delay in diagnosis or the
disease itself, the incidence of gangrene and
perforation is much higher in acalculous
than in calculous cholecystitis.
Early cholecystectomy within the first three days has a mortality of less than
0.5% and risk of complications such as perforation, biliary fistula, recurrent
attacks and adhesions is avoided. However, medical treatment brings about
resolution in a fairly large proportion of cases though chances of recurrence of
attack persist.
24.
25. Chronic cholecystitis is the commonest type of clinical gallbladder disease. There
is almost constant association of chronic cholecystitis with cholelithiasis.
26. Chronic Cholecystitis
• Chronic cholecystitis may be a sequel to repeated
bouts of mild to severe acute cholecystitis,
• but in many instances it develops in the apparent
absence of antecedent attacks.
• Since it is associated with cholelithiasis in more
than 90% of cases, the patient
populations are the same as those for gallstones.
27. • Supersaturation of bile predisposes to
both chronic inflammation and, in most
instances, stone formation.
• Unlike acute calculous cholecystitis, obstruction of
gallbladder outflow is NOT a requisite.
• The symptoms of calculous chronic cholecystitis
are biliary colic to indolent right upper quadrant
pain & epigastric distress.
29. Morphology
• The morphologic changes in chronic cholecystitis
are extremely variable & sometimes minimal.
The serosa is usually smooth and glistening
but may be dulled by subserosal fibrosis.
• Dense fibrous adhesions
• On sectioning, the WALL is variably thickened,
and has an opaque gray-white APPEARANCE.
30. • In the uncomplicated case
• The LUMEN contains fairly clear, green-
yellow, mucoid BILEand usually STONES.
• The MUCOSAitself is generally preserved?.
31. Microscopy- Chronic cholecystitis
• In the mildest cases, only scattered
LYMPHOCYTES, PLASMA CELLS, & MACROPHAGES
are found in the mucosa and in the subserosal
fibrous tissue.
• In more advanced cases there is marked
subepithelial and subserosal FIBROSIS,
accompanied by MONONUCLEAR CELL
INFILTRATION.
CHRONIC INFLAMMATION
32. • Outpouchings of the mucosal epithelium through
the wall
(Rokitansky-Aschoff sinuses) may
be quite prominent.
Rokitansky–Aschoff sinuses, also
entrapped epithelial crypts, are
pseudodiverticula or pockets in the wall of
the gallbladder.Histologically they are outpouchings of gallbladder mucosa into the gallbladder
muscle layer and subserosal tissue.
They are not of themselves considered abnormal,
but they can be associated with cholecystitis.
They form as a result of increased pressure in the gallbladder and recurrent
damage to the wall of the gallbladder. They are associated with gallstones
(cholelithiasis).
Carl Freiherr von Rokitansky and Ludwig Aschoff
Germans.
33. Outpouchings of gallbladder mucosa into the gallbladder muscle layer and
subserosal tissue
Rokitansky-Aschoff
sinuses
Entrapped epithelial
crypts
Ppseudodiverticula
Pockets in the wall of the gallbladder
34. Chronic cholecystitis, microscopic appearance. There is penetration of epithelium-lined
spaces into the gallbladder wall (Rokitansky- Aschoff sinus) in an area. There is
subepithelial and subserosal fibrosis and hypertrophy of muscularis. Mononuclear
inflammatory cell infiltrate is present in subepithelial and perimuscular layers.
37. Microscopy- HM
• 1. Thickened and congested mucosa but
occasionally mucosa may be totally destroyed.
• 2. Penetration of the mucosa deep into the wall of
the gallbladder up to muscularis layer to form
Rokitansky- Aschoff’sinuses.
• 3. Variable degree of chronic inflammatory
reaction, consisting of lymphocytes, plasma cells
and macrophages, present in the lamina propria
and subserosal layer.
• 4. Variable degree of fibrosis in the subserosal and
subepithelial layers.
38. A few morphologic variants of chronic cholecystitis are considered below:
Cholecystitis glandularis, Porcelain gallbladder, Acute
on chronic cholecystitis.
• Cholecystitis glandularis:
when the mucosal folds fuse together due to
inflammation and result in formation of crypts of
epithelium buried in the gallbladder wall.
39. Acute superimposed on
chronic cholecystitis
Superimposition of acute
inflammatory changes implies acute
exacerbation of an already chronically
injured gallbladder.
40. Porcelain gallbladder
• In rare instances extensive dystrophic
calcification
within the gallbladder wall may yield a porcelain
gallbladder, notable for a markedly increased
incidence of associated CANCER.
Chinaware, Pottery, ceramic
Porcelain GB: When the gallbladder wall is calcified and cracks like an egg-shell.
41.
42. Clinical Features
Chronic cholecystitis has ill-defined and vague
symptoms. Generally, the patient presents with
abdominal distension or epigastric discomfort,
especially after a fatty meal. There is a constant
dullache in the right hypochondrium and
epigastrium and tenderness over the right upper
abdomen. Nausea and flatulence are common.
Biliary colic may occasionally occur due to passage
of stone into the bile ducts.
43. Xanthogranulomatous cholecystitis
• is also a rare condition in which the gallbladder
has a massively thickened wall, is
shrunken, nodular, and chronically inflamed with
foci of necrosis and hemorrhage.
Strawberrygallbladder, more formally cholesterolosis of the
gallbladder, is a change in the gallbladder wall due to excess cholesterol
44. Hydrops of the gallbladder
• Finally, an atrophic, chronically
obstructed gallbladder may
contain only clear secretions, a condition
known as
.Hydrops is the excessive accumulation of
serous fluid in tissues or cavities of the body.