1. Harrison 2012 Baghbanian M. MD
Gall bladder disease
Harrison 2012
Baghbanian M. MD

2. Bile Secretion and Composition
Hepatic bile :
isotonic fluid with an electrolyte composition resembling blood plasma.
Gallbladder:
water reabsorption → concentration of bile increases

3. components of bile bile acids (80%), lecithin and phospholipids (16%)
cholesterol (4.0%).
In the lithogenic state, the cholesterol value can be as high as 8–10%.

4. components of bile conjugated bilirubin
proteins (all immunoglobulins, albumin, metabolites of hormones)
Electrolytes
Mucus
drugs and their metabolites.

5. daily basal secretion 500–600 mL.
Many substances taken up or synthesized by the hepatocyte are secreted into the bile

6. primary bile acids cholic acid chenodeoxycholic acid
are synthesized from cholesterol in the liver,
conjugated with glycine or taurine
secreted into the bile.

7. Secondary bile acids deoxycholate lithocholate
ursodeoxycholic acid (UDCA).
formed in colon as bacterial metabolites of the primary bile acids.

8. Bile acids are detergent-like molecules
Cholesterol solubility in bile depends on:
lipid concentration
percentages of bile acids and lecithin.
Normal ratios of these →formation of solubilizing mixed micelles
abnormal ratios → cholesterol crystals

9. Bile acids major physiologic force for hepatic bile flow
aid in water and electrolyte transport in the small bowel and colon.

10. Enterohepatic Circulation
normal bile acid pool: 2–4 g.
During digestion of a meal, one or more enterohepatic cycles
Normally: 5–10 times daily.
95% efficient; fecal loss of bile acids is in the range of 0.2–0.4 g/d.

11. Enterohepatic Circulation
fecal loss =daily synthesis of bile acids
bile acid pool is maintained.
the maximum rate of synthesis is 5 g/d

12. Gallbladder and Sphincteric Functions
capacity of gallbladder is 30 mL
In the fasting state, the sphincter of Oddi →resistance to bile flow
prevent reflux of duodenal contents into the pancreatic and bile ducts
filling of the gallbladder.

13. cholecystokinin(CCK)
major factor for : GB evacuation
released from : duodenal mucosa
In response to: fats and amino acids.
CCK produces
(1) powerful contraction of the gallbladder,
(2) decreased resistance of the sphincter of Oddi,
(3) enhanced flow of bile into duodenum.

14. Phrygian cap
partial or complete septum (or fold) separates the fundus from the body.

15. Anomalies of position or suspension
are not uncommon :
left-sided
intrahepatic
retrodisplacement
"floating" gallbladder
predisposes to acute torsion, volvulus, or herniation

16. Gallstones Epidemiology and Pathogenesis
prevalent in most western countries.
USA : 7.9% in men and 16.6% in women.
high in Mexican Americans
low in African Americans

17. gallstones two major types: cholesterol stones : > 80%
pigment stone < 20%.

18. gallstones
Cholesterol gallstones : >50% cholesterol + calcium salts, bile pigments, and proteins.
Pigment stones : calcium bilirubinate; <20% cholesterol :
"black"
"brown" (chronic biliary infection.)

19. Cholesterol Stones and Biliary Sludge
Cholesterol : water insoluble
excess of cholesterol in relation to phospholipids and bile acids→ unstable, cholesterol-rich vesicles → aggregate into large vesicles → cholesterol crystals

20. mechanisms in the formation of lithogenic bile
The most important : increased biliary secretion of cholesterol.
This occur in :
obesity
metabolic syndrome
high-caloric and cholesterol-rich diets
drugs (e.g., clofibrate)
increased hepatic uptake of cholesterol from blood. (e.g., estrogen)

21. genetic
In patients with gallstones, dietary cholesterol increases biliary cholesterol secretion.
This does not occur in non-gallstone patients on high-cholesterol diets.
In addition to environmental factors such as high-caloric and cholesterol-rich diets, genetic factors play an important role in gallstone disease.

22. pronucleating factors
Mucin
non-mucin glycoproteins
immunoglobulins

23. antinucleating factors
apolipoproteins A-I and A-II
other glycoproteins.

24. Vesicle fusion leads to liquid crystals→ nucleate into solid cholesterol crystals.
direct nucleation of cholesterol from supersaturated biliary vesicles → growth of the crystals

25. gallbladder hypomotility
If the gallbladder emptied all supersaturated or crystal-containing bile completely, stones would not be able to grow.
patients with gallstones :
↓gallbladder emptying.
↑gallbladder volume in fasting and after meal
Gallbladder fractional emptying is decreased.

26. Biliary sludge Thick mucous material and
cholesterol monohydrate crystals
calcium bilirubinate, and mucin gels.
crescent-like in the most dependent portion of the gallbladder
recognized by ultrasonography

27. biliary sludge precursor for gallstone 14%, gallstones developed
gallbladder hypomotility and gallstone formation ;
surgery, burns, total parenteral nutrition, pregnancy, and oral contraceptives

28. pregnancy →cholesterol-stone or sludge
pregnancy ="cholelithogenic state":
(1) ↑cholesterol saturation of bile in 3th trimester
(2) ↓gallbladder contraction
reversal of these abnormalities quite rapidly after delivery.

29. gallbladder sludge in pregnancy
20–30% of women
asymptomatic
often resolves after delivery.

30. gallstones in pregnancy
5–12%.
less common than sludge
frequently associated with biliary colic
may disappear after delivery

31. rapid weight reduction
10–20% of persons with rapid weight reduction develop gallstones.
UDCA in a dosage of 600 mg/d effective in preventing gallstone formation

32. cholesterol gallstone disease occurs because of several defects:
(1) bile supersaturation with cholesterol (2) nucleation of cholesterol with crystal retention and stone growth (3) abnormal gallbladder motor function with delayed emptying and stasis.

33. Increasing age → cholesterol gallstone
→ Increased biliary secretion of cholesterol
→ decreased size of bile acid pool
→ decreased secretion of bile salts

34. Obesity → cholesterol gallstone
Normal bile acid pool and secretion
increased biliary secretion of cholesterol

35. Weight loss → cholesterol gallstone
Mobilization of tissue cholesterol leads to increased biliary cholesterol secretion

36. Female sex hormones → cholesterol gallstone
 Estrogens → increase hepatic uptake of dietary cholesterol → increase biliary cholesterol secretion  
Natural estrogens, other estrogens, and OCP→ decreased bile salt secretion

37. Gallbladder hypomotility → cholesterol gallstone
Prolonged parenteral nutrition
Pregnancy   
Fasting   
octreotide

38. Clofibrate therapy → cholesterol gallstone
→ Increased biliary secretion of cholesterol

39. Decreased bile acid secretion → cholesterol gallstone
Primary biliary cirrhosis

40. High-calorie, high-fat diet → cholesterol gallstone   
Spinal cord injury → cholesterol gallstone

41. Pigment Stones ethiology
 Asia, rural setting
Chronic hemolysis
Alcoholic cirrhosis
Pernicious anemia
Cystic fibrosis
Chronic biliary tract infection, parasite
Increasing age
Ileal disease, ileal resection or bypass

42. Pigment Stones
Black : pure calcium bilirubinate with calcium and mucin glycoproteins.
more common in :
chronic hemolytic states
liver cirrhosis,
Gilbert's syndrome
cystic fibrosis.

43. ileal diseases→black stones
ileal resection,
ileal bypass.
Enterohepatic recycling of bilirubin in ileal disease states

44. Brown pigment stones
calcium salts of unconjugated bilirubin with cholesterol and protein.
in Asians and is often associated with infections in the gallbladder and biliary tree

45. Diagnosis _Ultrasonography
Gallstone
emptying function of the gallbladder
Biliary sludge

46. Diagnosis _Ultrasonography
very accurate in cholelithiasis
Stones as small as 1.5 mm may be identified
false-negative and false-positive rates for ultrasound in gallstone patients are 2–4%.

47. Biliary sludge Ultrasonography
low echogenic
a layer in the most dependent position of the gallbladder
distinguish sludges from gallstones:
This layer shifts with postural changes
no acoustic shadowing;

48. Gallbladder Ultrasound
Rapid
Accurate in gallstones (>95%)
Simultaneous scanning of GB, liver, bile ducts, pancreas
assessment of GB volume, contractility
Not limited by pregnancy
May detect very small stones(1.5 mm)
Procedure of choice for detection of stones

49. Ultrasound Limitations
Bowel gas
Massive obesity
Ascites

50. Plain Abdominal x-ray Low cost low yield
Pathognomonic in: calcified gallstones
Readily available
Contraindicated in pregnancy
porcelain GB
Emphysematous cholecystitis
 Gallstone ileus

51. Radioisotope Scans (HIDA)
Accurate in cystic duct obstruction
confirmation of acute cholecystitis;
less sensitive in chronic cholecystitis;
useful in diagnosis of acalculous cholecystopathy, especially if given with CCK to assess gallbladder emptying
Simultaneous assessment of bile ducts

52. Radioisotope Scans Diagnostic Limitations
Serum bilirubin >6–12 mg/dL
Cholecystogram of low resolution
Contraindicated in pregnancy 

53. Oral cholecystography (OCG)
historically useful procedure for the diagnosis of gallstones
but replaced by ultrasound
may be used to assess the patency of the cystic duct and gallbladder emptying function.
delineate the size and number of gallstones
determine whether are calcified.

54. HIDA
Radiopharmaceuticals such as 99mTc-labeled N-substituted iminodiacetic acids
rapidly extracted from the blood
excreted into the biliary tree in high concentration

55. HIDA
Failure to image the gallbladder in the presence of biliary ductal visualization may indicate;
cystic duct obstruction
acute or chronic cholecystitis
surgical absence of the organ

56. Symptoms of Gallstone Disease
Gallstones usually produce symptoms by:
causing inflammation or obstruction following their migration into the cystic duct or CBD.

57. biliary colic constant long-lasting pain
Obstruction of the cystic duct or CBD by a stone →increased intraluminal pressure and distention
visceral pain is severe, in the epigastrium or (RUQ) with radiation to the interscapular area, shoulder.

58. Biliary colic
begins suddenly and may persist with severe intensity for 15 min to 5 h, subsiding gradually or rapidly.
biliary pain persisting beyond 5h should raise the suspicion of acute cholecystitis

59. Biliary colic Nausea and vomiting
elevated bilirubin and/or alkaline phosphatase suggests a common duct stone.
Fever or chills (rigors) usually imply a complication, i.e., cholecystitis, pancreatitis, or cholangitis.

60. should not be confused with biliary pain
Complaints of vague epigastric fullness, dyspepsia, or flatulence
are not specific for biliary calculi.

61. Biliary colic may be precipitated by eating
fatty meal
large meal following a period of prolonged fasting
normal meal
frequently nocturnal, occurring within a few hours of retiring.

62. Natural History Gallstone in asymptomatic patient :
symptoms/complications is low.
10% at 5 years
15% at 10 years
18% at 15 years.
Asymptomatic Patients for 15 years→unlikely develop symptoms

63. diabetic patients with silent gallstones
more susceptible to septic complications
(1) cumulative risk of death due to gallstone is small
(2) prophylactic cholecystectomy is not warranted.

64. ↑symptoms(biliary pain)
↑Complications
↑ cholecystectomy

65. Gallstones in young age
more likely to develop symptoms from cholelithiasis than patients >60 years

66. Treatment: Gallstones
Surgical Therapy
Medical Therapy
Gallstone Dissolution

67. Surgical Therapy In asymptomatic gallstone patients:
risk of developing symptoms or complications requiring surgery is small (in the range of 1–2% per year).

68. cholecystectomy in a patient with gallstones
1) symptoms
2) prior complication of gallstone disease, (acute cholecystitis, pancreatitis, gallstone fistula)
3) underlying condition with risk of gallstone complications (calcified or porcelain gallbladder , previous attack of acute cholecystitis).

69. laparoscopic cholecystectomy
gold standard for treating symptomatic cholelithiasis
Biliary duct damage are more frequent than with open cholecystectomy.

70. prophylactic cholecystectomy
very large gallstones (>3 cm in diameter)
gallstones in a congenitally anomalous gallbladder might be considered .

71. young age is worrisome factor in asymptomatic gallstone
few authorities recommend routine cholecystectomy in all young patients with silent stones.

72. Laparoscopic cholecystectomy
removal of the gallbladder together with its stones.
procedure of choice

73. Medical Therapy—Gallstone Dissolution
Ursodeoxycholic acid (UDCA) decreases cholesterol saturation of bile
UDCA may also retard cholesterol crystal nucleation.

74. Medical Therapy—Gallstone Dissolution
Selection:
functioning gallbladder
radiolucent stones <10 mm in diameter,
complete dissolution = 50% of patients within 6 months to 2 years.
For good results, this therapy should be limited to radiolucent stones smaller than 5 mm
dose of UDCA = 10–15 mg/kg per day.

75. Dissolution
The highest success rate (>70%) occurs in small (<5 mm) floating radiolucent gallstones.
problem of recurrent stones → expensive drug for up to 2 years

76. Stones not responsive to UDCA
larger than 15 mm
Pigment stones

77. Acute Cholecystitis
obstruction of the cystic duct by a stone→ Acute inflammation of the gallbladder wall
Inflammation:
mechanical inflammation
chemical inflammation
3) bacterial inflammation,

78. mechanical inflammation
Obstruction by stone
→ increased intraluminal pressure and distention → ischemia of the gallbladder mucosa and wall

79. bacterial inflammation
50–85% of patients with acute cholecystitis.
The organisms most frequently isolated by culture of gallbladder bile:
Escherichia coli
Klebsiella
Streptococcus
and Clostridium

80. pain in Acute cholecystitis
progressively worsens.
the pain of acute cholecystitis becomes more generalized in the right upper abdomen.
may radiate to the interscapular area, right scapula, shoulder.

81. Acute cholecystitis
Peritoneal signs such as increased pain on deep respiration
The patient is anorectic and often nauseated.
Vomiting is common and may volume depletion.

82. Jaundice in Acute cholecystitis
Jaundice is unusual early in the course of acute cholecystitis
may occur:
edematous inflammatory changes involve the bile ducts and surrounding lymph nodes.

83. fever in Acute cholecystitis
A low-grade fever
but shaking chills or rigors are not uncommon.

84. P/E in Acute cholecystitis
RUQ tender
enlarged, tense gallbladder is palpable in 25–50%
Deep inspiration or cough during subcostal palpation of the RUQ usually produces increased pain and inspiratory arrest (Murphy's sign).
generalized peritoneal signs and abdominal rigidity are usually lacking, in the absence of perforation.

85. diagnosis of acute cholecystitis
characteristic history and examination.
The triad of sudden onset of RUQ tenderness, fever, and leukocytosis is highly suggestive.
Typically, leukocytosis in the range of 10,000–15,000 with a left shift

86. LFT in Acute cholecystitis
half of patients : bilirubin is mildly elevated (5 mg/dL)
one-fourth have modest elevations in serum aminotransferases (usually less than a fivefold elevation).

87. Ultrasound in Acute cholecystitis :
calculi in 90–95%
gallbladder inflammation including:
thickening of the wall
pericholecystic fluid
dilation of the bile duct.

88. HIDA in Acute cholecystitis
may be confirmatory if
bile duct imaging is seen without visualization of the gallbladder.

89. 75% of patients treated medically → remission of acute symptoms within 2–7 days
25%, a complication of acute cholecystitis will occur despite conservative treatment →surgical intervention is required.

90. acute cholecystitis who undergo remission of symptoms,
25% will recurrent cholecystitis within 1 year
60% will recurrent within 6 years.
In view of the natural history of the disease, acute cholecystitis is best treated by early surgery whenever possible.

91. Mirizzi's syndrome
gallstone impacted in the cystic duct or neck of the gallbladder causing compression of the CBD, →CBD obstruction and jaundice.
Ultrasound shows gallstone(s) lying outside the hepatic duct.
ERCP or PTC or MRCP demonstrate the extrinsic compression of the CBD.

92. Mirizzi's syndrome
Surgery consists of removing the cystic duct, gallbladder, and the impacted stone.
The preoperative diagnosis of Mirizzi's syndrome is important to avoid CBD injury.

93. Acalculous Cholecystitis
In 5–10% of patients with acute cholecystitis
In >50% of such cases, an underlying explanation not found.
serious trauma or burns
prolonged labor
orthopedic and other nonbiliary major surgical operations
prolonged parenteral hyperalimentation.
Vasculitis
obstructing adenocarcinoma of the gallbladder
diabetes mellitus
torsion of the gallbladder
"unusual" bacterial infections of gallbladder (Leptospira, Streptococcus, Salmonella, or Vibrio cholerae)
parasitic infestation of the gallbladder
Sarcoidosis
cardiovascular disease
tuberculosis, syphilis, actinomycosis

94. Acalculous Cholecystitis
clinically acalculous cholecystitis are indistinguishable from calculous cholecystitis,
complicating severe underlying illness

95. Acalculous Cholecystitis
Ultrasound, CT, or radionuclide examinations demonstrating a large, tense, static gallbladder without stones and with evidence of poor emptying over a prolonged period

96. Acalculous Cholecystitis
The complication rate for acalculous cholecystitis exceeds that for calculous cholecystitis.
Successful management of acute acalculous cholecystitis appears to depend primarily on early diagnosis and surgical intervention, with meticulous attention to postoperative care.

97. Acalculous Cholecystopathy
Disordered motility of the gallbladder can produce recurrent biliary pain in patients without gallstones.
Infusion of CCK can be used to measure the gallbladder ejection fraction during cholescintigraphy. .

98. Acalculous Cholecystopathy surgical findings
chronic cholecystitis
gallbladder muscle hypertrophy,
narrowed cystic duct.

99. acalculous cholecystopathy criteria
(1) recurrent episodes of typical RUQ biliary pain
(2) abnormal CCK cholescintigraphy
gallbladder ejection fraction of <40%
(3) infusion of CCK reproduces pain.

100. acalculous cholecystopathy
An additional clue: large gallbladder on ultrasound examination.
sphincter of Oddi dysfunction can also give rise to recurrent RUQ pain and CCK-scintigraphic abnormalities.

101. Emphysematous Cholecystitis
acute cholecystitis (calculous or acalculous) followed by ischemia or gangrene of the gallbladder wall and infection by gas-producing organisms.
Anaerobes Bacteria, such as aerobes, such as E. coli.

102. Emphysematous Cholecystitis
most frequently in elderly men and in patients with diabetes mellitus.
The clinical manifestations are essentially indistinguishable from those of nongaseous cholecystitis.

103. Emphysematous Cholecystitis diagnosis
plain abdominal film :
gas within the gallbladder lumen
dissecting within the gallbladder wall to form a gaseous ring
gas in pericholecystic tissues.

104. Emphysematous Cholecystitis treatment
The morbidity and mortality rates with emphysematous cholecystitis are considerable.
Prompt surgical intervention coupled with appropriate antibiotics is mandatory.

105. Chronic Cholecystitis
Chronic inflammation of the gallbladder wall is almost always associated gallstones and is result from
repeated bouts of subacute or acute cholecystitis
persistent mechanical irritation of the gallbladder wall by gallstones.

106. Chronic Cholecystitis
The presence of bacteria in the bile occurs in >25% of patients with chronic cholecystitis.

107. Chronic Cholecystitis
Chronic cholecystitis may be:
asymptomatic for years
progress to symptomatic gallbladder disease
acute cholecystitis
present with complications (see below).

108. Complications of Cholecystitis
Empyema and Hydrops
Gangrene and Perforation
Fistula Formation and Gallstone Ileus
Limey (Milk of Calcium) Bile and Porcelain Gallbladder

109. Empyema of the gallbladder
progression of acute cholecystitis with persistent cystic duct obstruction to superinfection
The clinical picture = cholangitis with high fever; severe RUQ pain; marked leukocytosis
risk of gram-negative sepsis and/or perforation.
Emergency surgical intervention with proper antibiotic as soon as the diagnosis is suspected.

110. Hydrops or mucocele of the gallbladder
may also result from prolonged obstruction of the cystic duct, by a large solitary calculus.
by mucus (mucocele)
by a clear transudate (hydrops) produced by mucosal epithelial cells.

111. Hydrops or mucocele of the gallbladder
A visible, palpable, nontender mass from the RUQ into the right iliac fossa
hydrops frequently remains asymptomatic, although chronic RUQ pain may occur.
Cholecystectomy is indicated, because empyema, perforation, or gangrene may complicate

112. Gangrene and Perforation
results from ischemia or tissue necrosis.
Underlying conditions :
marked distention of the gallbladder,
Vasculitis
diabetes mellitus
empyema
torsion resulting in arterial occlusion.

113. Gangrene and Perforation
Gangrene usually predisposes to perforation , but perforation may occur in chronic cholecystitis without warning symptoms.
Localized perforations are usually contained by the omentum or by adhesions produced by recurrent inflammation of the gallbladder.

114. Gangrene and Perforation
Bacterial superinfection of the walled-off gallbladder contents results in abscess formation.
Most patients are best treated with cholecystectomy, but some seriously ill patients may be managed with cholecystostomy and drainage of the abscess.

115. Free perforation
is less common but is associated with a mortality rate of 30%.
sudden transient relief of RUQ pain followed by signs of generalized peritonitis.
(distended gallbladder decompresses)

116. Fistula Formation and Gallstone Ileus
Fistulas into the
duodenum are most common
hepatic flexure of the colon
stomach or jejunum
abdominal wall
renal pelvis

117. Fistula Formation and Gallstone Ileus
Clinically "silent" biliary-enteric fistulas is a complication of acute cholecystitis found in 5% of cholecystectomy.
Asymptomatic cholecystoenteric fistulas may be diagnosed by gas in the biliary tree on plain abdominal.

118. Fistula Formation and Gallstone Ileus
Barium contrast or endoscopy of the upper gastrointestinal tract or colon may demonstrate the fistula.
Treatment in the symptomatic cholecystectomy
+ CBD exploration
+ closure of the fistulous tract.

119. Fistula Formation and Gallstone Ileus
a large gallstone →mechanical intestinal obstruction (duodenum)
The site of obstruction by the impacted gallstone ileocecal valve →proximal small bowel is of normal caliber.
The majority of patients do not have prior biliary tract symptoms or complaints suggestive of acute cholecystitis or fistulization.

120. Fistula Formation and Gallstone Ileus
stones, >2.5 cm →fistula formation by gradual erosion through the gallbladder fundus.
Diagnostic confirmation
plain abdominal film
small-intestinal obstruction
gas in the biliary tree
calcified, ectopic gallstone)
upper gastrointestinal series
cholecystoduodenal fistula
small-bowel obstruction at ileocecal valve).

121. Fistula Formation and Gallstone Ileus
Laparotomy with stone extraction (or propulsion into the colon) = procedure of choice to relieve obstruction.
Evacuation of large stones within the gallbladder should also be performed.
In general, the gallbladder and its attachment to the intestines should be left alone.

122. Limey (Milk of Calcium) Bile
Calcium salts diffuse calcium precipitation , hazy opacification of bile or a layering effect on plain abdominal.
clinically innocuous
but cholecystectomy is recommended, especially when it occurs in a hydropic gallbladder.

123. Porcelain Gallbladder
calcium salt deposition within the wall of a chronically inflamed gallbladder
may be detected on the plain abdominal film.
carcinoma of the gallbladder.
Cholecystectomy

124. Treatment: Acute Cholecystitis
Medical Therapy:
NPO NG
volume electrolyte are repaired.
Meperidine or NSAIDs for analgesia less spasm of the sphincter of Oddi than drugs such as morphine.
Intravenous antibiotic even though bacterial superinfection of bile not have occurred in the early
Surgical Therapy

125. Intravenous antibiotic
piperacillin or mezlocillin
ampicillin sulbactam
ciprofloxacin, moxifloxacin
third-generation cephalosporins
Anaerobic coverage metronidazole should be added if gangrenous or emphysematous .
Postoperative complications of wound infection, abscess formation, or sepsis are reduced in antibiotic-treated patients.

126. Imipenem/meropenem
cover the whole spectrum of bacteria causing ascending cholangitis.
They should be reserved for:
most severe life-threatening infections when other regimens have failed

127. acute cholecystitis Surgical Therapy
optimal timing :depends on stabilization of the patient.
trend is toward earlier surgery
Urgent (emergency) cholecystectomy or cholecystostomy :
Empyema
emphysematous cholecystitis
perforation

128. acute cholecystitis Surgical Therapy
Early cholecystectomy (within 72 hours) is the treatment of choice for most patients with acute cholecystitis.
Seriously ill or debilitated patients may be managed with cholecystostomy and tube drainage of the gallbladder.
Elective cholecystectomy may then be done at a later date.

129. acute cholecystitis Surgical Therapy
uncomplicated acute cholecystitis → early elective laparoscopic cholecystectomy, within 72 hours after diagnosis.
Delayed surgical intervention reserved for :
overall medical condition imposes risk for early surgery
(2) diagnosis of acute cholecystitis is in doubt.

130. Postcholecystectomy Complications
Early complications :
atelectasis and other pulmonary disorders
abscess formation (often subphrenic)
external or internal hemorrhage
biliary-enteric fistula
bile leaks.

131. Postcholecystectomy Jaundice
may indicate:
absorption of bile from an intra-abdominal collection following a biliary leak
mechanical obstruction of the CBD by retained calculi
intraductal blood clots
extrinsic compression.

132. persistent postcholecystectomy symptoms
The most common : nonbiliary disorders
small percentage :disorder of the extrahepatic bile ducts

133. persistent postcholecystectomy symptoms- nonbiliary disorders
reflux esophagitis
peptic ulceration
pancreatitis
most often—irritable bowel syndrome.

134. persistent postcholecystectomy symptoms- disorder of extrahepatic bile ducts
biliary strictures
retained biliary calculi
cystic duct stump syndrome
stenosis or dyskinesia sphincter of Oddi
bile salt–induced diarrhea
bile salt–induced gastritis

135. Cystic Duct Stump Syndrome
long (>1 cm) cystic duct remnant
In the absence of cholangiographically demonstrable retained stones
symptoms resembling biliary pain or cholecystitis in postcholecystectomy

136. Cystic Duct Stump Syndrome
in almost all patients in whom the symptom was thought to result from the existence of a long cystic duct stump
postcholecystectomy complaints are due to other causes

137. biliary colic without stone
papillary stenosis
papillary dysfunction
spasm of the sphincter of Oddi
biliary dyskinesia

138. Papillary stenosis
acute or chronic inflammation of the papilla of Vater
glandular hyperplasia of the papillary segment.
Five criteria :
(1) upper abdominal pain, usually RUQ or epigastric;
(2) abnormal liver tests
(3) dilatation of the CBD in ERCP
(4) delayed (>45 min) drainage of contrast from the duct
(5) increased basal pressure of the sphincter of Oddi

139. papillary stenosis Treatment
endoscopic or surgical sphincteroplasty ensure wide patency distal portions of both the bile ducts. and pancreatic duct

140. dyskinesia of the sphincter of Oddi
spasm and hypertonicity of the sphincter
When
evaluation has failed to demonstrate another cause for the pain
cholangiographic and manometric criteria suggest a diagnosis of biliary dyskinesia,
medical treatment with nitrites or anticholinergics relaxation of the sphincter

141. sphincter of Oddi dyskinesia
Endoscopic or surgical biliary sphincterotomy may be indicated in patients who :
fail to respond to a 2- to 3-month trial of medical therapy
especially if basal sphincter of Oddi pressures are elevated.

142. Bile Salt–Induced Gastritis
Postcholecystectomy patients may develop symptoms of dyspepsia, which have been attributed to duodenogastric reflux of bile.

143. Bile Salt–Induced Diarrhea
Cholecystectomy shortens gut transit time by accelerating passage of the fecal bolus
marked acceleration in the right colon
increase in colonic bile acid output and a shift in bile acid composition toward the more diarrheagenic secondary bile acids.

144. Bile Salt–Induced Diarrhea
5–10% of patients undergoing elective cholecystectomy.
Treatment with bile acid–sequestering agents such as cholestyramine or colestipol is often effective in ameliorating diarrhea.