1.gall bladder

Anatomy
17/01/2012 G.CMx of cholelithiasis and complications2

Mx of cholelithiasis and complications
Anatomy
 In the inferior surface of the liver
 Pear shaped
 7-10cm long
 30-50ml capacity
 Has four parts; Fundus, Body,
Infundibulum and neck
 Calot’s triangle bounded medially
by CHD, superiorly the liver
surface
17/01/2012 G.C3

 Both GB neck and the cystic duct contain spirally oriented mucosal folds, known as valves of Heister, preventing passage
of gallstones and excessive distention or collapse of cystic duct.
 Small veins and lymphatics course between the GB fossa and GB wall connecting the lymphatic and veinous
drainage of the liver and GB  Causes carcinomatous and inflammatory spread from the GB into the liver
 CBD is about 7 to 11 cm in length and 5 to 10 mm in diameter.
Vascular supply
 The arterial supply to the bile ducts is derived from the gastroduodenal and the right hepatic arteries, with
major trunks running along the medial and lateral walls of the common duct (sometimes referred to as 3
o'clock and 9 o'clock).
 cystic artery – may arise from Rt or Lt. hepatic, common hepatic, gastroduodenal, Lt.gastric or superior
mesenteric artery
 Cystic artery passes through calot’s triangle in 90% of cases
 venous drainage – small veins into liver or large cystic vein to portal vein
Anatomy…

 CBD is about 7 to 11 cm in length and 5 to 10 mm in
diameter.

Physiology
Bile Ducts
 Liver produces 500-1000ml of bile per day and excretes into the bile canaliculi.
 The secretion of bile is responsive to neurogenic, hormonal and chemical stimuli:
 Vagal stimulation- ⁭ secretion
 CCK, gastrin, etc. - ⁭ bile secretion
 Secretin - ⁭ bile flow
 Bile composed of water, electrolytes, bile salts, proteins, lipids, and bile pigments.
 ~ 95% of bile acid pool → liver by enterohepatic circulation
 Sodium, potassium, calcium, and chlorine have the same concentration in bile as in
plasma or extracellular fluid

• The pH of hepatic bile is usually neutral or slightly alkaline, but varies with diet; an
increase in protein shifts the bile to a more acidic pH.
• The primary bile salts, cholate and chenodeoxycholate, are synthesized in the liver from
cholesterol. They are conjugated there with taurine and glycine, and act within the bile as
anions (bile acids) that are balanced by sodium.
• Bile salts are excreted into the bile by the hepatocyte and aid in the digestion and
absorption of fats in the intestines.6

• In the intestines, about 80% of the conjugated bile acids are absorbed in the terminal
ileum. The remainder is dehydroxylated (deconjugated) by gut bacteria, forming secondary
bile acids deoxycholate and lithocholate. These are absorbed in the colon, transported to
the liver, conjugated, and secreted into the bile.
• Eventually, about 95% of the bile acid pool is reabsorbed and returned via the portal
venous system to the liver, the so-called enterohepatic circulation.
• Five percent is excreted in the stool, leaving the relatively small amount of bile acids to
have maximum effect.

• Cholesterol and phospholipids synthesized in the liver are the principal lipids found in
bile. The synthesis of phospholipids and cholesterol by the liver is, in part, regulated by
bile acids.
• The color of the bile is due to the presence of the pigment bilirubin diglucuronide, which
is the metabolic product from the breakdown of hemoglobin, and is present in bile in
concentrations 100 times greater than in plasma.
• Once in the intestine, bacteria convert it into urobilinogen, a small fraction of which is
absorbed and secreted into the bile.

• Vagal stimulation increases secretion of bile, whereas splanchnic nerve stimulation results
in decreased bile flow.
• Hydrochloric acid, partly digested proteins, and fatty acids in the duodenum stimulate the
release of secretin from the duodenum that, in turn, increases bile production and bile
flow.
• Bile flows from the liver through to the hepatic ducts, into the common hepatic duct,
through the common bile duct, and finally into the duodenum. With an intact sphincter of
Oddi, bile flow is directed into the gallbladder.

Physiology…
Gallbladder
 Concentrates and stores hepatic bile
 The concentration of bile affects the solubility
of calcium and cholesterol.
Sphincter of Oddi
 Regulates flow of bile and pancreatic juice
into the duodenum
 Divert bile into the GB
 Prevents regurgitation of duodenal contents
into the biliary tract.

Absorption and Secretion
• In the fasting state ( risk), approximately 80% of the bile secreted by the liver is stored in the
gallbladder. This storage is made possible because of the remarkable absorptive capacity of the
gallbladder, as the gallbladder mucosa has the greatest absorptive power per unit area of any
structure in the body.
• It rapidly absorbs sodium, chloride, and water against significant concentration gradients,
concentrating the bile as much as 10-fold and leading to a marked change in bile composition

• The epithelial cells of the gallbladder secrete at least two important products into the
gallbladder lumen: glycoproteins and hydrogen ions.
• The mucosal glands in the infundibulum and the neck of the gallbladder secrete mucus
glycoproteins that are believed to protect the mucosa from the lytic action of bile and to
facilitate the passage of bile through the cystic duct.
• This mucus makes up the colorless "white bile" seen in hydrops of the gallbladder resulting
from cystic duct obstruction.
• The transport of hydrogen ions by the gallbladder epithelium leads to a decrease in the
gallbladder bile pH. The acidification promotes calcium solubility, thereby preventing its
precipitation as calcium salts

The effect of cholecystokinin on the gallbladder and the sphincter of Oddi. A. During fasting, with the sphincter of Oddi
contracted and the gallbladder filling. B. In response to a meal, the sphincter of Oddi relaxed and the gallbladder
emptying

Diagnostic Studies of gallbladder disease
Blood Tests
• When patients with suspected diseases of the gallbladder or the extrahepatic biliary tree are evaluated,
CBC and LFT are routinely requested.
• An elevated WBC count may indicate cholecystitis.
• If associated with an elevation of bilirubin, alkaline phosphatase, and aminotransferase, cholangitis
should be suspected.
• Cholestasis, an obstruction to bile flow, is characterized by an elevation of bilirubin (i.e., the conjugated
form), and a rise in alkaline phosphatase.
• Serum aminotransferases may be normal or mildly elevated. In patients with biliary colic or chronic
cholecystitis, blood tests will typically be normal

Ultrasonography
• An ultrasound is the initial investigation of any patient suspected of disease of the biliary
tree.
• It is noninvasive, painless, NO radiation, and can be performed on critically ill patients.
• It is dependent upon the skills and the experience of the operator, and it is dynamic (i.e.,
static images do not give the same information as those obtained during the ultrasound
investigation itself).
• Adjacent organs can frequently be examined at the same time. Obese patients, patients with
ascites, and patients with distended bowel may be difficult to examine satisfactorily with an
ultrasound

• Ultrasound will show stones in the gallbladder with sensitivity and specificity of >90%. Stones
are acoustically dense and reflect the ultrasound waves back to the ultrasonic transducer.
• Because stones block the passage of sound waves to the region behind them, they also produce
an acoustic shadow (Fig. 32-6).
• Stones move with changes in position. Polyps may be calcified and reflect shadows, but do not
move with change in posture.
• Some stones form a layer in the gallbladder; others a sediment or sludge.
• A thickened gallbladder wall and local tenderness indicate cholecystitis

 The patient has acute cholecystitis if a layer of edema is seen within the wall of the
gallbladder or between the gallbladder and the liver in association with localized
tenderness.
 When a stone obstructs the neck of the gallbladder, the gallbladder may become
very large, but thin walled.
 A contracted, thick-walled gallbladder is indicative of chronic cholecystitis.

An ultrasonography of the gallbladder. Arrows indicate the acoustic shadows
from stones in the gallbladder

Oral Cholecystography
• Once considered the diagnostic procedure of choice for gallstones, oral cholecystography
has largely been replaced by ultrasonography.
• It involves oral administration of a radiopaque compound that is absorbed, excreted by the
liver, and passed into the gallbladder. Stones are noted on a film as filling defects in a
visualized, opacified gallbladder.
• Oral cholecystography is of no value in patients with intestinal malabsorption, vomiting,
obstructive jaundice, and hepatic failure

Biliary Radionuclide Scanning (Hida Scan)
• Biliary scintigraphy provides a noninvasive evaluation of the liver, gallbladder, bile
ducts, and duodenum with both anatomic and functional information. 99mTechnetium-
labeled derivatives of dimethyl iminodiacetic acid (HIDA) are injected intravenously,
cleared by the Kupffer cells in the liver, and excreted in the bile.
• Uptake by the liver is detected within 10 minutes, and the gallbladder, the bile ducts, and
the duodenum are visualized within 60 minutes in fasting subjects

Computed Tomography
• Abdominal CT scans are inferior to ultrasonography in diagnosing gallstones. The major
application of CT scans is to define the course and status of the extrahepatic biliary tree
and adjacent structures.
• It is the test of choice in evaluating the patient with suspected malignancy of the
gallbladder, the extrahepatic biliary system, or nearby organs, in particular, the head of the
pancreas.
• Use of CT scan is an integral part of the differential diagnosis of obstructive jaundice.
• Spiral CT scanning provides additional staging information, including vascular
involvement in patients with periampullary tumors

GALBLADDER Disease
1 Gallstones/cholelithiasis and its cxn below
2 Acute cholecystitis(ACC, AAC,and AEC)
3 Chronic cholecystitits
4 Choledocholithiasis(CBD)
5 CHolangitis (BD)- charcot and renold pentad ,DDx of Obstructive Jaundice
6 Gallbladder cancer

• Gallstone disease is one of the most common problems affecting the digestive tract.
Autopsy reports have shown a prevalence of gallstones from 11 to 36%.
Natural History
• Most patients will remain asymptomatic from their gallstones throughout life. For
unknown reasons, some patients progress to a symptomatic stage, with biliary colic
caused by a stone obstructing the cystic duct. Symptomatic gallstone disease may
progress to complications related to the gallstones
• These include acute cholecystitis, choledocholithiasis with or without cholangitis,
gallstone pancreatitis, cholecystocholedochal fistula, cholecystoduodenal or
cholecystoenteric fistula leading to gallstone ileus, and gallbladder carcinoma.

Gallstone Formation
• Gallstones form as a result of solids settling out of solution.
• The major organic solutes in bile are
- bilirubin
- bile salts ( cholate and chenodeoxycholate)
- Lipids (phospholipids and cholesterol).
• Gallstones are classified by their cholesterol content as either cholesterol stones or pigment
stones.
• Pigment stones can be further classified as either black or brown. In Western countries, about
80% of gallstones are cholesterol stones and about 15 to 20% are black pigment stones.
• Brown pigment stones account for only a small percentage. Both types of pigment stones are
more common in Asia

 Cholesterol, which is insoluble in water, is secreted from the canalicular membrane in
phospholipid vesicles. Whether cholesterol remains in solution depends on the concentration of
phospholipids and bile acids in bile and the type of phospholipid and bile acid.
 Micelles formed by the phospholipid hold cholesterol in a stable thermodynamic state. When
bile is supersaturated with cholesterol or bile acid concentrations are low, unstable unilamellar
phospholipid vesicles form, from which cholesterol crystals may nucleate, and stones may form.

Risk factors/etiology for stone
Major risk factors for pigmented stones
• Infection
• Sickle cell anemia
• Hemolysis
• Stasis
• Parasitic infestation
5f:
Fat
Fertile
Flatulent
female – 3x
Above fourty

Sex
 More common in women.
 estrogen causing increased cholesterol secretion
 progesterone causing bile stasis.
 Pregnant women more likely to have symptoms.
 Women with multiple pregnancies at higher risk
 Oral contraceptives, estrogen replacement therapy.

Risk factors…
 Cirrhosis
 Hemolytic anemias
 Hypertriglyceridemia
 Medications
 Estrogen and oral contraceptives – stasis?
 Clofibrate
 Ceftriaxone
 Octreotide- dec. splan. circulation
 Terminal ileal resection – decrease bile absorbtion

Risk factors…
 Gallbladder stasis 2ry to
 Diabetes mellitus
 Total parenteral nutrition-passive portal circuln
 Postvagotomy
 Octreotide or somatostatinoma
 Spinal cord injury
 Reduced physical activity

Pathogenesis of gallstones
A Cholesterol Stones _70-80%
- Pure cholesterol stones are uncommon and account for <10% of all stones.
- They usually occur as single large stones with smooth surfaces.
- Most other cholesterol stones contain variable amounts of bile pigments and calcium,
but are always >70% cholesterol by weight= mixed
- usually multiple, of variable size

3 stages of cholesterol stone formation
1. Cholesterol supersaturation
Key to maintain cholesterol in solution is the formation of
Micelles, a bile-phospholipid-cholesterol complex, and
Cholesterol-phospholipid vesicles.
Secretion of hepatic bile with either high cholesterol or low bile acids or lecithin:
⋙⋙ Cholesterol precipitation
2. Crystals nucleation
 Nucleating agents
 Bile proteins and pigments, bacteria, cellular debris, gallbladder mucus, and
calcium salts
 Stasis of bile in the GB
3. Stone Growth

Risk factors & mechanisms for
cholesterol gallstone:
 ↑Cholesterol secretion
 Old age
 Female sex
 Obesity
 Rapid weight loss - lipolysis
 Pregnancy
 ↓ Bile salt secretion
 Pregnancy
 Impaired gallbladder emptying
 Diabetes mellitus
 Total parenteral nutrition
 Postvagotomy
 Octreotide/somatostatinoma
 Spinal cord injury

• Impaired GB
function
• Emptying
• Absorption
• Excretion
• Supersaturated bile
• Age
• Sex
• Genetics
• Obesity
• Diet
Absorption/EHC
•Deoxycholate
•SBS
•Fecal flora
•Ileal resection
Nucleating agents
•Mucus
•Glycoprotein
•Infection

Pathogenesis of gallstones…
B Pigment Stones _ 20-30%
• Due to altered solubilization of unconjugated bilirubin with precipitation
of Ca bilirubinate & insoluble salts.
• Pigment stones contain <20% cholesterol and are dark because of
the presence of calcium bilirubinate
2 types
1. Black pigment stones
2. Brown pigment stones

• Black pigment stones are usually small, brittle, black, and sometimes spiculated.
• They are formed by supersaturation of calcium bilirubinate, carbonate, and phosphate,
most often secondary to hemolytic disorders such as hereditary spherocytosis and sickle
cell disease, and in those with cirrhosis.
• Like cholesterol stones, they almost always form in the gallbladder
• Brown stones are typically found in the biliary tree of Asian populations and are
associated with stasis secondary to parasite infection.
• In Western populations, brown stones occur as primary bile duct stones in patients with
biliary strictures or other common bile duct stones that cause stasis and bacterial
contamination

• Brown stones are usually <1 cm in diameter, brownish-yellow, soft, and often mushy.
• They may form either in the gallbladder or in the bile ducts, usually secondary to bacterial
infection caused by bile stasis. Precipitated calcium bilirubinate and bacterial cell bodies
compose the major part of the stone.
• Bacteria such as Escherichia coli secrete -glucuronidase that enzymatically cleaves
bilirubin glucuronide to produce the insoluble unconjugated bilirubin.
• It precipitates with calcium, and along with dead bacterial cell bodies, forms soft brown stones
in the biliary tree.

Pigment Stones…
Black pigment stones
 Common in Asia such as
Japan
 Almost exclusively in GB
 Risk factors:
 Haemolytic dd.
 Cirrhosis
 Terminal ileal
resection
Brown pigment stones
 Common in Southeast Asia
 Typically in bile ducts
 Risk factors:
 Disorders of biliary
motility/ stasis
 Infected bile
→Release of β-glucuronidase.

Types of stones

Investigation of the Biliary Tract
 CBC
 LFT
 Serum Amylase ….. Acute pancreatitis
 Bile culture

Investigation…
Plain radiography
 Only ~ 10% of GS are radio opaque-
unlike kidneys
 Not routinely indicated
 In acutely ill pts to R/O perforated viscus
 Gas in the GB or BD
 Porcelain gallbladder – Ca2+

Plain FilmsX-rays= for calcification
 10-15% stones are
radiopaque,
 porcelain GB may be seen.
 Air in biliary tree,
 emphysematous GB wall.

Investigation…
Porcelain gallbladder – calcified GB or
cholecystopathia chronica calcarea
 Curvilinear or rim-like calcifications in the
gallbladder wall
 GB carcinoma - 11 to 33 %,
 Cholecystectomy even in asymptomatic patients.

Investigation…
Ultrasound
 Should be part of routine evaluation of
patients suspected of having GS
 Specificity of >98%, sensitivity of >95%

Ultrasound examination. Single large gallstone
casting an ‘acoustic shadow
pericholecystic fluid (thin arrow), gall bladder
wall (thick arrow) and biliary sludge (broken
arrow).

Ultrasound findings in gallstone
 Wall thickening (2-4mm)
 Distension
 Pericholecystic fluid, sonographic Murphy’s.
 Dilated CBD (7-8mm). .
 Single large gallstone casting an ‘acoustic shadow

Investigation…
CT & MRI
 The sensitivity CT for
gallstones is poor,
 More accurate at identifying
site and cause of
extrahepatic biliary
obstruction.

Investigation…
ERCP — Becoming a therapeutic rather than a
diagnostic technique.
Basket extraction of a
large CBD stone
(arrow) via ERCP
Pt ĉ obstructive jaundice ĉ
multiple stones (arrows) in a
dilated CBD.

Investigation…
PTC- percutaneous trans hepatic cholangiography
 Intrahepatic bile ducts are accessed
percutaneously with a small needle under
fluoroscopic guidance
 Close to 100% sensitivity and specificity for
identifying the cause and site of biliary tract
obstruction.
 Technically limited and associated with a higher
incidence of complications.

Through the catheter, a cholangiogram can be performed and
therapeutic interventions done, such as biliary drain insertions and
stent placement

Investigation…
 Catheter placed in cystic duct and
contrast injected into biliary tree to
exclude stones.
 Indications:
 Obstructive jaundice ,
 Recent Hx of cholangitis ,
 Dilated CBD on U/S ,
 Abnormal LFT,
 Pancreatitis.
Perioperative cholangiography

Investigation…
Cholescintigraphy — to Dx acute cholecystitis
 Indicated if the diagnosis remains
uncertain following U/S,
 99mTc labeled hepatic iminodiacetic acid
(HIDA) injected IV,
 Patent cystic duct,visualization gallbladder.
Sensitivity – 84%, specificity – 99%

Clinical features
 Biliary colic - ’misnomer’
 Chronic Cholecystitis (Biliary Colic) About two thirds of patients with gallstone disease present with
chronic cholecystitis characterized by recurrent attacks of pain, often inaccurately labeled biliary colic
 The classic attack - intense dull pressure-like discomfort in the RUQ or mid abdomen or in the
chest that may radiate to the back and the right shoulder blade.
 Classically follows ingestion of a fatty meal (about one to two hours after).
 Associated Sx - diaphoresis, nausea and vomiting.

Symptomatic cholelithiasis
Definition
On and off postprandial epigastric/RUQ pain due to transient cystic duct obstruction by
stone, no fever/WBC, normal LFT
 The pain occurs due to a stone obstructing the cystic duct, causing wall tension; pain resolves
when stone passes
 Pain usually lasts 1-5 hrs, rarely > 24hrs
 Small stones more symptomatic.

History
 3 clinical stages of gallstne:
 Asymptomatic - Most (~80%)
 Symptomatic, and
 With complications (cholecystitis, cholangitis, CBD stones).
 A history of epigastric pain with radiation to shoulder may suggest
it.
 A detailed history of pattern and characteristics of symptoms as
well as Ultrasound make the diagnosis.

History
 Most patients develop symptoms before complications.
 Once symptoms occur, severe symptoms develop in
3-9%, with complications in 1-3% per year.
 Indigestion, bloating, fatty food intolerance occur in similar
frequencies in patients without gallstones, and are not
commonly cured with cholecystectomy.

Spectrum of Gallstone Disease
Cholelithiasis
Asymptomatic
cholelithiasis
Symptomatic
cholelithiasis
Chronic
calculous
cholecystitis
Acute
calculous
cholecystitis
 Symptomatic cholelithiasis
can be a herald to:
 an attack of acute
cholecystitis
 ongoing chronic
cholecystitis
 May also resolve
17/01/2012 G.C Mx of cholelithiasis and complications60

• The pain develops when a stone obstructs the cystic duct, resulting in a progressive
increase of tension in the gallbladder wall.
• The pathologic changes, which often do not correlate well with symptoms, vary from an
apparently normal gallbladder with minor chronic inflammation in the mucosa, to a
shrunken, nonfunctioning gallbladder with gross transmural fibrosis and adhesions to
nearby structures.
• The mucosa is initially normal or hypertrophied, but later becomes atrophied, with the
epithelium protruding into the muscle coat, leading to the formation of the so-called
Aschoff-Rokitansky sinuses.

Clinical presentation of a patient with biliary ds
• Pain
 typical
 (RUQ,epigastric)
 Biliary colic
 Tightness/dullness
 Radiation
 Nausea/vomiting
 Atypical
 Indigestion,flatulence
 Dyspepsia,retrosternal pain
• Jaundice
– Associated symptoms
– Fever,chills & rigor
– Urine/stool discoloration
– pruritus
• Constitutional symptoms
– Wt loss,anorexia,back pain

Complications of GS
IN THE GALLBLADDER
 Biliary colic
 Acute cholecystitis
 Chronic cholecystitis
 Empyema of the gall bladder
 Mucocele= white bile
 Perforation
IN THE BILE DUCTES
 Obstructive jaundice
 Cholangitis - CBD
 Acute pancreatitis
IN THE INTESTINE
 Acute intestinal obstruction (GS ileus)
17/01/2012 G.C Mx of cholelithiasis and complications 64

• Physical Examination
– No remarkable
– May mild tenderness in
RUQ/epigastric area
• Laboratory
– CBC
– LFT
• Ultrasound
– Most important modality
– First line of investigation
– Sensitive/specific()
– Superior to CT scan
• Characteristic finding
– Echogenic
– Acoustic shadow
– Move when pt change position – ie
stone
• May
– Polp/stone in the cystic duct
– Stone<5mm ,sluge
– Obese,ascitic,bowel gas

• When the pain lasts >24 hours, an impacted stone in the cystic duct or acute cholecystitis
should be suspected.
• An impacted stone without cholecystis will result in what is called hydrops of the gallbladder.
• The bile gets absorbed, but the gallbladder epithelium continues to secrete mucus, and the
gallbladder becomes distended with mucinous material.
• The gallbladder may be palpable but usually is not tender. Hydrops of the gallbladder may
result in edema of the gallbladder wall, inflammation, infection, and perforation

Approach to patients GSD
4 Clinical groups: Based on ultrasound finding & symptoms
1. category 1- Gallstones seen w/o symptoms
2. category 2- gallstones seen with typical symptoms
3. category 3- gallstones seen with atypical symptoms
4. category 4- No gallstones but typical symptoms.

Management
 Surgery is almost the only option (cholecystectomy)
 Based on ultrasound finding & symptoms four categories
 Category I = stone+ asymptomatic
 Category II = stone+ typical symptoms
 Category III = stone+ atypical symptoms
 Category IV =no stone + typical symptoms

Approach to patients …
category 1 - should be left alone.
Exceptions are pts at ↑risk for GB carcinoma or gallstone complications:
Calcification of the GB wall (porcelain gallbladder)
Very large stone (>3cm ∅)
Congenital anomalous gallbladder
Prophylactic or incidental cholecystectomy can be considered.

Category I
 Indication for surgery
 GB polp > 1cm
 No immediate access to health care
facility
 Incidental(intra operative)
 Non functional GB
 Porcelain
 Large stone(> 2.5cm)
 Chronic immunosuppresion
 Sickle cell anemia
 Bariatic surgery
 Small multiple stone
 Child
 ?DM

category 2
–cholecystectomy is must
–Good outcome (all relieved from their symptom
 Have biliary type symptoms or complications (such as cholangitis, pancreatitis, cholecystitis,
choledocholithiasis, gallstone ileus(fistula) and Mirizzi syndrome)
- Mirizz synd- stone lodged in either cystic duct or hartmann pouch, externally compress the
CHD- s/s of obst. Jaundiec
- These stones can produce common hepatic duct obstruction (the Mirizzi syndrome) by two
mechanisms: mechanical obstruction of the hepatic duct because of the proximity of the cystic
duct and the common hepatic duct, and secondary inflammation with frequent episodes of
cholangitis

CLASSIFICATION -
 The original classification by McSherry described two types of Mirizzi
syndrome
 Type I – Compression of the common hepatic duct or common bile duct
by a stone impacted in the cystic duct or Hartmann's pouch.
 Type II – Erosion of the calculus from the cystic duct into the common
hepatic duct or common bile duct, producing a cholecystocholedochal
fistula.

 DIAGNOSIS — The Mirizzi syndrome is part of the differential diagnosis of obstructive
jaundice.
 Most patients present with the clinical triad of jaundice, fever, and RUQ pain.
 The major laboratory findings are elevations in the serum concentrations of alkaline
phosphatase and bilirubin in over 90 percent of patients

Patients with gallstones but atypical symptoms (category 3)
• Only sub groug of patient relieved from their symptoms after cholecystectomy
• Such patients should undergo a search for non-gallstone-related causes of symptoms. Consider the ff
 Liver diseases
 Diverticular disease
 Pleuritic pain
 Myocardial pain
 PUD
 GERD
 Abdominal wall hernias
 Irritable bowl disease
 Renal calculi
DDx

Patients with typical biliary symptoms but without gallstones
(category 4)
DDx
 Small stones (microlithiasis),
 Sludge that were missed on conventional imaging studies,
 Sphincter of Oddi dysfunction.

• Patients with symptomatic gallstones should be advised to have elective laparoscopic
cholecystectomy (offers excellent long-term results)
• While waiting for surgery, or if surgery has to be postponed, the patient should be advised to
avoid dietary fats and large meals.
• Diabetic patients with symptomatic gallstones should have a cholecystectomy promptly, as
they are more prone to develop acute cholecystitis that is often severe
• Pregnant women with symptomatic gallstones who cannot be managed expectantly with diet
modifications can safely undergo laparoscopic cholecystectomy during the second trimester

2 Acute cholecystitis/ ACC, AAC, AEC
 Secondary to gallstones in 90 to 95% of cases
 Acute acalculous cholecystitis- other acute systemic diseases
 In <1% of acute cholecystitis, the cause is a tumor obstructing the cystic duct
 About 80% of patients with acute cholecystitis give a history compatible with chronic
cholecystitis.
 Acute cholecystitis begins as an attack of biliary colic, but in contrast to biliary colic, the
pain does not subside; it is unremitting and may persist for several days.

Complications of acute cholecystitis
Empyema of
gallbladder
Pus-filled GB due to bacterial proliferation in obstructed
GB. Usually more toxic, high fever
Emphysematous
cholecystitis
More commonly in men and diabetics. Severe RUQ pain,
generalized sepsis. Imaging shows air in GB wall or
lumen
Perforated
gallbladder
Occurs in 10% of acute cholecystitis, usually becomes a
contained abscess in RUQ
Less commonly, perforates into adjacent viscus =
cholecystoenteric fistula & the stone can cause SBO
(gallstone ileus) with ~20% mortality rate

Prognosis
 Uncomplicated cholecystitis has low mortality.
 Emphysematous GB mortality is 15%
 Perforation of GB occurs in 3-15% with up to 60% mortality.
 Gangrenous GB 25% mortality.

Pathophysiology
 Impaction of stone at the cystic
duct/ hartman’s pouch
 Chemical inflammation
 Secondary bacterial infection

Bacteriologic profiles
 Secondary bacterial contamination is documented in 15
to 30%

1/ Acute calculous cholecystitis
Defnition
 Acute GB inflammation due to cystic duct obstruction. Persistent
RUQ pain +/- fever, ↑WBC, ↑LFT, +Murphy’s = inspiratory arrest
 Persistent cystic duct obstruction leads to GB distension, wall
inflammation & edema
 Can lead to: empyema, gangrene, rupture
 Pain usu. persists >24hrs & N/V/Fever
 Palpable/tender or even visible RUQ mass 17/01/2012 G.CMx of cholelithiasis and complications83

Clinical presentation
 Abdominal pain
 Similar to biliary colic but longer duration/severity (greater than four to six
hours)
 Fever
 Nausea/vomiting
 Physical exam
 GA: ill appearing, and lie still on the examining table
 Vital signs: febrile, and tachycardic
 RUQ tenderness/ Murphy sign

c

Magt of ACC
A Conservative followed by interval /delayed cholecystectomy
 Intravenous hydration and correction of any associated electrolyte disorders
 NPO/NGT/ maintaince fluid
 ANALGESIC
 Antibiotic
 Choice/duration/route of administration
 Monitor response
 Early cholecystectomy

A. Conservative treatment followed by cholecystectomy
• Experience shows that, in more than 90% of cases, the symptoms of acute
cholecystitis subside with conservative measures.
• Nonoperative treatment is based on four principles:
1 Nil per mouth (NPO) and intravenous fluid administration.
2 Administration of analgesics.
3 Administration of antibiotics. As the cystic duct is blocked in most instances, the
concentration of antibiotic in the serum is more important than its concentration in bile.
A broadspectrum antibiotic effective against Gram-negative aerobes is most appropriate
(e.g. cefazolin, cefuroxime or gentamicin).
4 Subsequent management. When the temperature, pulse and other physical signs show
that the inflammation is subsiding, oral fluids are reinstated followed by regular diet.

B. Definitive Rx
 Removal of GB & stones after 6-8wks
 Open cholecystectomy
 Laparoscopic cholecysectomy
*Emergency cholecystectomy
 Pts not settling within 48 hrs
*Early operation (with in 2-3days of Sx) does not carry a higher risk of
mortality and morbidity compared to delayed operation.

 Complications of acute cholecystitis
 Gangrene = up to 20% of cases
 Perforation = 2% of cases
 Emphysematous cholecystitis = 1% of cases
 Others:
 Hydrops of the GB
 Cholecystoenteric fistula – GS - ileus

Acute acalculous cholecystitis
 GB inflammation due to biliary stasis(5% of time) and not stones
(95%).
 In 5-10% of cases of acute cholecystitis
 Seen in critically ill pts or prolonged TPN
 More likely to progress to gangrene, empyema, perforation due to
ischemia

• It accounts for ~5-10 % of acute cholecystitis
• Strongly associated with a variety of clinical conditions:
 Sepsis/hypotension
 Immunosuppression
 Major trauma
 Burns, etc.
• Clinical F: as that of acute calculous cholecystitis.
• Rx: IV broad spectrum antibiotics + Emergency cholecystectomy who are fit
for anesthesia

 Caused by gallbladder stasis from lack of enteral stimulation
by cholecystokinin
 Tx: Emergent cholecystectomy usually open
 If patient is too sick, percutaneouse cholecystostomy tube and
interval cholecystectomy later on

Investigation- acute cholecystitis
 CBC
 Mild leukocytosis
 (15x103)
 WBC > 18x103
 Empyema
 perforationm
 Mild elevation of LFT
 bil , alk phospha
 Ultrasound
 Sensitivity/specificity(80)
 US Evidences of ACC!!!!!
 stone
 Wall Thickening
 Double wall sign- edema
 Pericholecystic fluid
 Sonographic murphy sign
 HIDA (97 and 90%)
 highly sensitive and specific for acute
cholecystitis, if US not sure

 Commonly men in their 5th -7th decade
 ~ 1/3 -1/2 are diabetic
 CFs: as AC but pts are more toxic
 DX: air in the GB or wall on plain abd.
Film
 Rx: Cholecystectomy and antibiotic
therapy.
3/ Emphysematous cholecystitis
 Secondary infection of the gallbladder wall with gas-forming organisms (such as Clostridium
welchii).

Cholesterosis (‘strawberry gall bladder’)
 In the fresh state, the interior of the gall bladder looks something like a strawberry; the
yellow specks (submucous aggregations of cholesterol crystals and cholesterol esters)
correspond to the seeds.
 It may be associated with cholesterol stones.

17/01/2012 G.CMx of cholelithiasis and complications
Post cholecystectomy syndrome.
 Persistent or recurrent signs and symptoms after
cholecystectomy excluding early post op. complications
 10% of patients
 common in middle aged
DDx of Post cholecystectomy syndrome con’t
 Retained or recurrent stones in the bile duct.
 Stump cholelithiasis and bile duct stricture
 Pancreatic or liver disease.
 PUD or Bile gastritis.
 Diverticular disease and irritable bowel syndrome.
 Psychiatric problems (anxiety or depression)
96

3. Choledocholithiasis
• Common bile duct stones may be small or large, single or multiple, and are found in 6 to
12% of patients with stones in the gallbladder
• Stones in the CBD should be removed, even if patients are asymptomatic.
= CHOLEDOCHOTOMY
• The vast majority of ductal stones in Western countries are formed within the gallbladder
and migrate down the cystic duct to the common bile duct

Choledocholithiasis…
 Classification:
 1o stones -- originate in the CBD
 2o stones -- originate in the gallbladder
Most CBD stones are 2o stones.
 Other definitions of CBD stones:
 Retained -- discovered within 2yrs of cholecystectomy
 Recurrent -- detected >2yrs of cholecystectomy

Choledocholithiasis
 Gallstone in the common bile duct (primary means originated
there, secondary = from GB)
 Can present similarly to cholelithiasis, except with the addition
of jaundice
 Tx: Endoscopic retrograde cholangiopancreatography (ERCP)-
current modality of therapy
 Stone extraction and sphincterotomy
 Interval cholecystectomy after recovery from ERCP or at the
same time

 The secondary stones are usually cholesterol stones, whereas the primary stones are
usually of the brown pigment type.
 The primary stones are associated with biliary stasis and infection and are more
commonly seen in Asian populations.
 The causes of biliary stasis that lead to the development of primary stones include
biliary stricture, papillary stenosis, tumors, or other (secondary) stones

 Choledochal stones may be silent and often are discovered
incidentally. They may cause obstruction, complete or
incomplete, or they may manifest with cholangitis or
gallstone pancreatitis

 As stones in the bile ducts tend to move down to the distal
part of the common duct, bowel gas can preclude their
demonstration on ultrasonography. A dilated common bile
duct (>8 mm in diameter) on ultrasonography in a patient
with gallstones, jaundice, and biliary pain is highly
suggestive of common bile duct stones

Choledocholithiasis …
 The traditional indications for choledochotomy where the modern
diagnostic armamentarium is not available:
1. Palpable CBD stones
2. If there is jaundice or
Hx of jaundice or
cholangitis
3. Dilated CBD
4. Abnormal LFT, in particular, the alkaline phosphatase is raised

Choledocholithiasis…
 Complications of CBD stone
 Obstructive Jaundice
 Cholangitis – BD inflamation.
Fever, RUQ pain, jaundice => Charcot’s triad
Charcot’s triad + Altered mental status + Shock
=> Reynolds’s pentad
 Other Complications
 Suppurative cholangitis=>liver abscess
 Impaired LF =>Biliary cirrhosis

Mx of Choledocholithiasis
I. Non surgical
 Endoscopic sphincterotomy or balloon dilation + Extraction of CBD stones.
II. Surgical
 Laparoscopic CBD exploration
 Open surgical exploration
 Alternatives – if all above are not successful:
- Choledochoduodenostomy
- Roux-en-Y Choledochojejunostomy

4 Cholangitis
 Infection within bile ducts usually due to obstruction of CBD
2ndary to stones, strictures.
Charcot triad: can lead to septic shock
RUQ pain,
jaundice,
fever (seen in 70% of pts),
 Raynaud’s pentad = Charcot’s triad + altered mentation and
hypotension
 May lead to life-threatening sepsis and septic shock

 Tx: NPO, aggressive IV Fluids, broad spectrum IV Antibiotics
 Emergent decompression via ERCP or percutaneous
transhepatic cholangiogram (PTC)
 Used to require emergency laparotomy

5 Gallstone pancreatitis
 35% of acute pancreatitis 2ndary to stones
 Pathophysiology
 Reflux of bile into pancreatic duct and/or obstruction of
ampulla by stone
 ALT > 150 (3-fold elevation) has 95% PPV for diagnosing
gallstone pancreatitis

 Tx: ABC, resuscitate, NPO/IVF, pain meds
 Once pancreatitis resolving, ERCP with stone
extraction/sphincterotomy
 Cholecystectomy before hospital discharge

DDx of Obstructive Jaundice
Benign Biliary Stricture
1. Postoperative (80%)
 Cholecystectomy
 Choledochotomy
 Gastrectomy
2. Inflammatory (20%)
 Stones
 Cholangitis
 Parasitic
 Pancreatitis
 Sclerosing cholangitis
 Radiotherapy
Malignant Biliary
Stricture/obstruction
1. Intraluminal
 Bile duct cancer
 Ampullary carcinoma
2. Extrinsic compression
 Pancreatic cancer
 Gallbladder cancer
 Hepatocellular cancer
Congenital
Idiopathic

sclerosing cholangitis
 Primary sclerosing cholangitis is an idiopathic fibrosing inflammatory condition of
the biliary tree that affects both intrahepatic and extrahepatic ducts.
 It is of unknown origin, but association with hypergammaglobulinaemia and
elevated markers such as smooth muscle antibodies and anti-nuclear factor
suggests an immunological basis.

 The round worm, Ascaris lumbricoides, commonly infests the intestine of
inhabitants of Asia, Africa and Central America. It may enter the biliary tree
through the ampulla of Vater and cause biliary pain.
 Complications include strictures, suppurative cholangitis, liver abscesses and
empyema of the gall bladder
 In the uncomplicated case, anti-spasmodics can be given to relax the
sphincter of Oddi, and the worm will return to the small intestine to be dealt
with by antihelminthic drugs. Operation may be necessary to remove the
worm or deal with complications.
 worms can be extracted via the ampulla of Vater by ERCP.
Mx of cholelithiasis and complications115

Clonorchiasis (Asiatic cholangiohepatis
 The disease is endemic in the Far East. The fluke, up to 25 mm long and 5 mm
wide, inhabits the bile ducts, including the intrahepatic ducts.
 Fibrous thickening of the duct walls occurs.
 Many cases are asymptomatic. Complications include biliary pain, stones,
cholangitis, cirrhosis and bile duct carcinoma.
 Choledochotomy and T-tube drainage and, in some cases,
choledochoduodenostomy are required.

Hydatid disease
 A large hydatid cyst may obstruct the hepatic ducts. Sometimes, a cyst will rupture
into the biliary tree and its contents cause obstructive jaundice or cholangitis,
requiring appropriate surgery

Obstructive jaundice
 Due to obstruction to the excretion of bilirubin
 Confirmation that is obstructive is essential
 Most frequent causes varies depending on
age,geography,sex,..
 Choledocholethiasis is most common(benign lesion) in
many countries
 Pancreatic head tumor commonest malignant

Classification of causes
I. Excessive production (hemolytic jaundice):-
A. Inherited hemolytic anemia's
B. Acquired hemolytic anemia's
II. Impaired transport to liver:-
-Gilbert’s syndrome
III. Impaired hepatic conjugation:-
A. Inborn errors
B. Immaturity of enzymes
IV Impaired excretion(hepatocellular jaundice)
A. Acquired liver diseases
B.Intrahepatic cholestasis

V. Bile duct obstruction(obstructive jaundi)
A. Extra hepatic:-
1.Stone
2.Neoplasms
3.Stricture
4.Atresia,ect
B. Intrahepatic

 Pain similar to biliary colic
 Associated symptoms: fever/chills , pruritus , darken urine , pale/
clay colored stool
 Physical exam
 No remarkable finding
 Jaundice,
 Vital signs
 Scratch marks
 Tenderness
 Corvesouires law
 Stigma for malignancy/liver disease

Imaging
 Abdominal ultrasound
 Important first line
 Sensitivity varies(55-91%)
 CBD Dilation > site> causes
 Combination of clinical ,biochemical & U/S
 Jaundice + biliary + gall stone + increased LFTS + Dilated
CBD
 As the No of criteria increases probability of stone in the CBD
increases

Other imaging (not routinely used)
 MRCP
 ERCP
 PTC
 EUS
 Helical CT scan
 HIDA- liver sccan
 Highly sensitive & specific

Management
 Endoscopic removal/drainage(ERCP
 Open/lap
 Choledochotomy
 Spincterotomy/ plasty
 Drainage
 Choledochduedunostomy
 choledochjejunostomy

Candidates for drainage
 Irremovable, impacted, distal CBD stones
 Markedly dilated CBD, >1.5cm
 Distal duct obstruction from tumor or
stricture
 Recurrence after previous duct exploration

Introduction
 An uncommon but highly fatal malignancy
 5th decade, 2-6X more common in ♀ than in ♂ of any age.
 Majority are found incidentally
 Poor prognosis:
 Advanced stage at diagnosis, which is due both to the anatomic position of the
gallbladder, and
 The vagueness and none specificity of symptoms.

Risk Factors for GB Cancer
• Cholelithiasis, especially single large stones
- up to 95% of patients with carcinoma of the gallbladder have gallstones
• Calcified gallbladder wall (Porcelain gallbladder)
• Adenomatous gallbladder polyps
• Choledochal cysts
• Anomalous pancreatobiliary duct junction
• Chemical carcinogens (nitrosamine, azotoluene)
• Chronic Salmonella typhi infection
• Obesity
• Estrogen

Pathology
• Adenocarcinoma – 90%
• Others:
– Squamous,
– Oat cell,
– Undeferrentiated,
– Adenosquamous,
– Carcinoid tumors.

 are adenocarcinomas with biliary differentiation arising from cholangiocytes in
ducts within and outside of the liver, bifurcation of L and R HD
 Extrahepatic cholangiocarcinomas, constituting approximately 2/3 of these tumors,
may develop at the hilum (known as Klatskin tumors) or more distally in the
biliary tree.
- cholangiosarcoma that involves the CHD and R and
L HDs

 causing painless jaundice
 pruritus (66 %)- bilirubin effect in the skin
 abdominal pain (30 to 50 %),
 weight loss (30 to 50%)
 fever (up to 20%)
 constant dull ache in the RUQ
 clay-colored stools and dark urine

 Physical signs include jaundice (90%), hepatomegaly (25 to 40%), or a right upper
quadrant mass (10%)
 A palpable gallbladder, caused by obstruction distal to the take off of the cystic
duct (Courvoisier's sign).

Courvoisier’s law
If the CBD is obst. due to calculus , the GB
is usually not distended owing to previous
inflammatory fibrosis.
In obstr. of the CBD due to growth, the GB
becomes distended in order to reduce the
press. in the biliary system.
8/29/2019138

STAGING
 At diagnosis:
 25% are localized to GB
 35% are metastases to regional LNs or extension to adjacent
organs
 40% - distant metastases
 TNM staging system

TNM staging
Primary tumor (T)
TX ------ Primary tumor cannot be assessed
T0 -------No evidence of primary tumor
Tis ------ Carcinoma in situ
T1----Tumor invades lamina propria or muscle layer
T1a---Tumor invades lamina propria
T1b---Tumor invades muscle layer
T2 ----Tumor invades perimuscular connective tissue; no extension beyond
serosa or into liver
T3 ----Tumor perforates the serosa (visceral peritoneum) and/or directly
invades the liver and/or one other adjacent organ or structure, such as
the stomach, duodenum, colon, or pancreas, omentum or extrahepatic
bile ducts
T4 -----Tumor invades main portal vein or hepatic artery, or invades multiple
extrahepatic organs or structures.

TNM staging …
Regional lymph nodes (N)
NX = Regional lymph nodes cannot be assessed
N0 = No regional lymph node metastasis
N1 = Regional lymph node metastasis
Distant metastasis (M)
MX = Distant metastasis cannot be assessed
M0 = No distant metastasis
M1 = Distant metastasis

TNM staging …
Stage 0 = Tis N0 M0
Stage IA = T1 N0 M0
Stage IB = T2 N0
M0
Stage IIA = T3 N0
M0
Stage IIB = T1 N1 M0
T2 N1 M0
T3 N1 M0
Stage III = T4 Any N M0
Stage IV = Any T Any N M1
Stage grouping

Clinical Presentation
 Asymptomatic,
 RUQ pain, followed by anorexia, N, or V,
 Fatigue, weight loss, or jaundice
 A firm fixed mass in the RUQ or symptoms of obstruction of the duodenum
>>>> Advanced unresectable disease.
 Because of the similarity with symptomatic cholelithiasis, patients with
gallbladder cancer are often misdiagnosed with benign gallbladder disease.

Diagnostic Evaluation
 Laboratory _ generally unrevealing:
 Nonspecific liver function abnormalities
 Anemia
 Ultrasound
 A mass larger than 1 cm, a calcified GB
wall, a discontinuous wall layer, or a loss
of the interface between the GB wall and
the liver.
 A fixed mass filling the gallbladder lumen
is the classic finding.
 CT, MRI, MRCP
Transabdominal ultrasound of the
GB demonstrating a large
hyperechoic mass within the lumen
of the GB .

Management
 Only 10 - 30% of patients are eligible for potentially curative
resection.
 Five-year survival rates are 5 to 12 percent in many large series.
 Better outcomes have been noted in the last decade, and attributed
to more aggressive surgery.

Management …
Surgical options include:
• Simple cholecystectomy
• Radical or extended cholecystectomy, removal of:
 Gallbladder plus at least 2 cm of the gallbladder bed,
 Regional LNs from the hepatoduodenal ligament behind the second portion of the
duodenum, head of the pancreas and the celiac axis
• Radical cholecystectomy with resection of liver (segmental or lobar), or bile duct/
pancreaticoduodenectomy.

Management…
 Stages I
 Stage IA => cholecystectomy alone
 stage IB =>radical cholecystectomy
 Stage II
 Radical cholecystectomy
 Locally advanced (T3/4) resectable disease
 Locally advanced, unresectable disease

Management…
• Radiation and chemoradiotherapy
No survival benefit

Prognosis…
 Fewer than 15% of all patients with GB cancer are alive at 5
years.
 Stage IV = median servival is only 1-3 months.

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