SGD ON GALLSTONES , ACUTE CHOLECYSTITIS

AND CHRONIC CHOLECYSTITIS

GALLSTONES
TYPES
There are two main types of gallstones:
cholesterol stones, containing crystalline cholesterol monohydrate (80% of stones in
Western countries), and pigment stones, made of bilirubin calcium salts
Pathogenesis
• Bile formation is the only significant pathway for elimination of excess cholesterol
from the body, either as free cholesterol or as bile salts. Cholesterol is rendered
water-soluble by aggregation with bile salts and lecithins. When cholesterol
concentrations exceed the solubilizing capacity of bile (supersaturation), cholesterol
can no longer remain dispersed and crystallizes out of solution.
• Cholesterol gallstone formation is enhanced by hypomobility of the gallbladder
(stasis), which promotes nucleation, and by mucus hypersecretion, with consequent
trapping of the crystals, thereby enhancing their aggregation into stones.
• Pigment stones form when the bile contains a high concentration of unconjugated
bilirubin in the biliary tree, as may occur in patients with chronic extravascular red
cell hemolysis or with certain infections of the biliary tract, such as liver flukes. The
precipitates are primarily insoluble calcium bilirubinate salts.
 Risk Factors
• • Age and gender. The prevalence of gallstones increases throughout life.
The prevalence in women of all ages is about twice as high as in men.
• Ethnic and geographic. Cholesterol gallstone prevalence approaches 50%
to 75% in certain Native American populations . The high prevalence in
these populations to be related to biliary cholesterol hypersecretion.
• Heredity. a positive family history imparts increased risk.
• Environment. Estrogens increase hepatic cholesterol uptake and
synthesis, leading to excess biliary secretion of cholesterol. i-e increased
risk for gallstone disease with oral contraceptive use and with pregnancy.
Obesity, rapid weight loss, and treatment with the hypocholesterolemia
agent clofibrate also are strongly associated with increased biliary
cholesterol secretion and risk for gallstone disease.
• Acquired disorders. Any condition in which gallbladder motility is reduced
predisposes to gallstones, such as pregnancy, rapid weight loss, and spinal
cord injury. In most cases, however, gallbladder hypo motility is present
without obvious cause
• MORPHOLOGY
• Cholesterol stones consist of 50% to 100% cholesterol. Pure cholesterol stones are pale yellow;
increasing proportions of calcium carbonate, phosphates, and bilirubin impart gray-white to
black discoloration . They are ovoid and firm; they can occur singly, but most often there are
several, with faceted surfaces Most cholesterol stones are radiolucent, although as many as 20%
may contain sufficient calcium carbonate to be radiopaque.
• Pigment stones classified into black and brown stones. black pigment stones are found in sterile
gallbladder bile, while brown stones are found in infected intrahepatic or extrahepatic ducts. The
stones contain calcium salts of unconjugated bilirubin and lesser amounts of other calcium salts,
mucin glycoproteins, and cholesterol. Black stones are usually small, numerous, and fragile to
the touch . Brown stones tend to be single or few in number and to have a soft, greasy, soap like
consistency owing to the presence of fatty acid salts released from biliary lecithin's by bacterial
phospholipases. Because of calcium carbonates and phosphates, 50% to 75% of black stones are
radiopaque. Brown stones, which contain calcium soaps, are radiolucent.
• Clinical Feature
• 70% to 80% of individuals with gallstones remain asymptomatic throughout life. There is usually
right upper-quadrant or epigastric pain, often excruciating, which may be constant or, less
commonly, spasmodic. Such “biliary” pain is caused by gallbladder or biliary tree obstruction or
by inflammation of the gallbladder itself.
COMPLICATION S
• include empyema, perforation, fistulas, inflammation of the biliary tree, obstructive cholestasis
and pancreatitis. Occasionally large stone may erode directly into an adjacent loop of small
bowel, generating intestinal obstruction (gallstone ileus)
• CHOLECYSTITIS
• Inflammation of the gallbladder may be acute, chronic, or acute superimposed on chronic.
• Acute Calculous Cholecystitis
• Acute inflammation of a gallbladder that contains stones is termed acute calculous
cholecystitis and is precipitated in 90% of cases by obstruction of the gallbladder neck or
cystic duct
• Acute calculous cholecystitis initially results from chemical irritation and inflammation of the
gallbladder wall due to obstruction of bile outflow.
• Gallbladder injury in the setting of bile obstruction stems from several sources, including:
phospholipases derived from the mucosa hydrolyze biliary lecithin to lysolecithin, which is
toxic to the mucosa; the normally protective glycoprotein mucous layer is disrupted, exposing
the mucosal epithelium to the detergent action of bile salts.; prostaglandins released within
the wall of the distended gallbladder enhance mucosal and mural inflammation; and
distention and increased intraluminal pressure may compromise blood flow to the mucosa.
All of these effects occur in the absence of bacterial infection, which may be superimposed
later.
• Acute Acalculous Cholecystitis
• Between 5% and 12% of gallbladders removed for acute cholecystitis contain no gallstones.
Most cases occur in seriously ill patients. Some of the most common predisposing insults are
as follows:
• • Major surgery • Severe trauma (e.g., from motor vehicle crashes) • Severe burns •
Sepsis .Other contributing factors include dehydration, gallbladder stasis and sludging,
vascular compromise, and bacterial contamination .
• Chronic Cholecystitis
• Chronic cholecystitis may be the sequel to
repeated bouts of acute cholecystitis, but in most
instances it develops without any antecedent
history of acute attacks. Like acute cholecystitis, it
is almost always associated with gallstones
• MORPHOLOGY
• In acute cholecystitis, the gallbladder usually is enlarged and tense, and has a bright red
or blotchy, violaceous color, the latter imparted by subserosal hemorrhages. The serosa
frequently is covered by a fibrinous or, in severe cases, a fibrinopurulent exudate.
• The gallbladder lumen is filled with cloudy or turbid bile that may contain fibrin, blood,
and pus. When the contained exudate is mostly pus, the condition is referred to as
empyema of the gallbladder. In mild cases, the gallbladder wall is thickened,
edematous, and hyperemic. In more severe cases, the gallbladder wall is green-black
and necrotic—a condition termed gangrenous cholecystitis.
• On histologic examination, the inflammatory reactions are not distinctive and consist of
some combination of the usual patterns of acute inflammation (i.e., edema, leukocytic
infiltration, vascular congestion, abscess formation, gangrenous necrosis).
• The morphologic changes in chronic cholecystitis are extremely variable and sometimes
subtle. The mere presence of stones within the gallbladder, even in the absence of
acute inflammation, often is taken as sufficient justification for a diagnosis. The
gallbladder may be contracted, of normal size, or enlarged.
• Mucosal ulcerations are infrequent; the submucosa and subserosa often are thickened
from fibrosis. In the absence of superimposed acute cholecystitis, collections of
lymphocytes in the wall are the only sign of inflammation . Outpouchings of mucosal
epithelium through the wall of the gallbladder (Rokitansky- Aschoff sinuses) may be
quite prominent.
• Clinical Features
• Acute calculous cholecystitis
• presents with biliary pain that lasts for more than 6 hours. The pain is severe, usually steady,
upper abdominal in location, and often radiates to the right shoulder. Fever, nausea, and
jaundice The right subcostal region is markedly tender and rigid as a result of spasm of the
abdominal muscles; occasionally a tender, distended gallbladder can be palpated. Mild
attacks usually subside spontaneously over 1 to 10 days
• COMPLICATIONS
• Bacterial superinfection leading to cholangitis or sepsis
• Gallbladder perforation and local abscess formation
• Gallbladder rupture leading to diffuse peritonitis
• Biliary enteric (cholecystenteric) fistula, with drainage of bile into adjacent organs, entry of air
and bacteria into the biliary tree, and potentially gallstone-induced intestinal obstruction (ileus)
• Aggravation of preexisting medical illness, with cardiac, pulmonary, renal, or liver
decompensation .Symptoms arising from acute acalculous cholecystitis usually are obscured by
another serious medical or surgical condition.
• Chronic cholecystitis
• usually characterized by recurrent attacks of steady
epigastric or right upper quadrant pain. Nausea,
vomiting, and intolerance for fatty foods are
frequent accompaniments.