Gall bladder disease

Harrison 2012Baghbanian M. MD

Bile Secretion and Composition

• Hepatic bile : – isotonic fluid with an electrolyte composition

resembling blood plasma.

• Gallbladder:– water reabsorption → concentration of bile

increases

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%.

components of bile

• conjugated bilirubin• proteins (all immunoglobulins, albumin,

metabolites of hormones)• Electrolytes• Mucus• drugs and their metabolites.

daily basal secretion

• 500–600 mL. • Many substances taken up or synthesized by

the hepatocyte are secreted into the bile

primary bile acids

1. cholic acid 2. chenodeoxycholic acid

are synthesized from cholesterol in the liver,

conjugated with glycine or taurine

secreted into the bile.

Secondary bile acids

1. deoxycholate 2. lithocholate3. ursodeoxycholic acid (UDCA).

formed in colon as bacterial metabolites of the primary bile acids.

Bile acids are detergent-like molecules

• Cholesterol solubility in bile depends on: 1. lipid concentration 2. percentages of bile acids and lecithin.

Normal ratios of these →formation of solubilizing mixed micelles

abnormal ratios → cholesterol crystals

Bile acids • major physiologic force for hepatic bile flow

• aid in water and electrolyte transport in the small bowel and colon.

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.

Enterohepatic Circulation

• fecal loss =daily synthesis of bile acids

• bile acid pool is maintained.

the maximum rate of synthesis is 5 g/d

Gallbladder and Sphincteric Functions

• capacity of gallbladder is 30 mL

• In the fasting state, the sphincter of Oddi →resistance to bile flow(1) prevent reflux of duodenal contents into the

pancreatic and bile ducts (2) filling of the gallbladder.

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.

Phrygian cap

• partial or complete septum (or fold) separates the fundus from the body.

Anomalies of position or suspension

• are not uncommon : left-sidedintrahepatic retrodisplacement

"floating" gallbladderpredisposes to acute torsion, volvulus, or

herniation

GallstonesEpidemiology 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

gallstones

• two major types:

cholesterol stones : > 80%

pigment stone < 20%.

gallstones

• Cholesterol gallstones : >50% cholesterol + calcium salts, bile pigments, and proteins.

• Pigment stones : calcium bilirubinate; <20% cholesterol :"black" "brown" (chronic biliary infection.)

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

mechanisms in the formation of lithogenic bile

• The most important : increased biliary secretion of cholesterol.

• This occur in : obesity metabolic syndromehigh-caloric and cholesterol-rich diets drugs (e.g., clofibrate) increased hepatic uptake of cholesterol from blood.

(e.g., estrogen)

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.

pronucleating factors

• Mucin • non-mucin glycoproteins• immunoglobulins

antinucleating factors

• apolipoproteins A-I and A-II • other glycoproteins.

• Vesicle fusion leads to liquid crystals→ nucleate into solid cholesterol crystals.

• direct nucleation of cholesterol from supersaturated biliary vesicles → growth of the crystals

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.

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

biliary sludge

• precursor for gallstone• 14%, gallstones developed

• gallbladder hypomotility and gallstone formation ; – surgery, burns, total parenteral nutrition,

pregnancy, and oral contraceptives

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.

gallbladder sludge in pregnancy

20–30% of women

asymptomatic

often resolves after delivery.

gallstones in pregnancy

5–12%.

less common than sludge

frequently associated with biliary colic

may disappear after delivery

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

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.

Increasing age→ cholesterol gallstone

• → Increased biliary secretion of cholesterol

• → decreased size of bile acid pool

• → decreased secretion of bile salts

Obesity → cholesterol gallstone

• Normal bile acid pool and secretion • increased biliary secretion of cholesterol

Weight loss → cholesterol gallstone

• Mobilization of tissue cholesterol leads to increased biliary cholesterol secretion

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

Gallbladder hypomotility → cholesterol gallstone

• Prolonged parenteral nutrition • Pregnancy • Fasting • octreotide

Clofibrate therapy → cholesterol gallstone

→ Increased biliary secretion of cholesterol

Decreased bile acid secretion → cholesterol gallstone

• Primary biliary cirrhosis

• High-calorie, high-fat diet → cholesterol gallstone

• Spinal cord injury → cholesterol gallstone

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

Pigment Stones

• Black : pure calcium bilirubinate with calcium and mucin glycoproteins.

• more common in :chronic hemolytic statesliver cirrhosis, Gilbert's syndrome cystic fibrosis.

ileal diseases→black stones

• ileal diseases ,• ileal resection, • ileal bypass.

Enterohepatic recycling of bilirubin in ileal disease states

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

Diagnosis _Ultrasonography

• Gallstone• emptying function of the gallbladder • Biliary sludge

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%.

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;

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

Ultrasound Limitations

• Bowel gas• Massive obesity• Ascites

Plain Abdominal x-ray

• Low cost• low yield• Pathognomonic in: calcified gallstones• Readily available• Contraindicated in pregnancy• porcelain GB• Emphysematous cholecystitis• Gallstone ileus

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

Radioisotope Scans Diagnostic Limitations

• Serum bilirubin >6–12 mg/dL• Cholecystogram of low resolution• Contraindicated in pregnancy

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.

HIDA

• Radiopharmaceuticals such as 99mTc-labeled N-substituted iminodiacetic acids

• rapidly extracted from the blood • • excreted into the biliary tree in high

concentration

HIDA

• Failure to image the gallbladder in the presence of biliary ductal visualization may indicate;

cystic duct obstruction acute or chronic cholecystitissurgical absence of the organ

Symptoms of Gallstone Disease

• Gallstones usually produce symptoms by: causing inflammation or obstruction following

their migration into the cystic duct or CBD.

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.

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

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.

should not be confused with biliary pain

• Complaints of vague epigastric fullness, dyspepsia, or flatulence

• are not specific for biliary calculi.

Biliary colic

• may be precipitated by eating fatty meallarge meal following a period of prolonged fastingnormal meal

frequently nocturnal, occurring within a few hours of retiring.

Natural History

• Gallstone in asymptomatic patient : symptoms/complications is low.

10% at 5 years 15% at 10 years18% at 15 years.

• Asymptomatic Patients for 15 years→unlikely develop symptoms

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.

↑symptoms(biliary pain)

• ↑Complications• ↑ cholecystectomy

Gallstones in young age

• more likely to develop symptoms from cholelithiasis than patients >60 years

Treatment: Gallstones

• Surgical Therapy• Medical Therapy

Gallstone Dissolution

Surgical Therapy

• In asymptomatic gallstone patients:

– risk of developing symptoms or complications requiring surgery is small (in the range of 1–2% per year).

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).

laparoscopic cholecystectomy

• gold standard for treating symptomatic cholelithiasis

• Biliary duct damage are more frequent than with open cholecystectomy.

prophylactic cholecystectomy

• very large gallstones (>3 cm in diameter) • gallstones in a congenitally anomalous

gallbladder might be considered .

young age

• is worrisome factor in asymptomatic gallstone

• few authorities recommend routine cholecystectomy in all young patients with silent stones.

Laparoscopic cholecystectomy

• removal of the gallbladder together with its stones.

procedure of choice

Medical Therapy—Gallstone Dissolution

• Ursodeoxycholic acid (UDCA) decreases cholesterol saturation of bile

• UDCA may also retard cholesterol crystal nucleation.

Medical Therapy—Gallstone Dissolution

• Selection: 1. functioning gallbladder 2. 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.

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

Stones not responsive to UDCA

1. larger than 15 mm2. Pigment stones

Acute Cholecystitis

• obstruction of the cystic duct by a stone→ Acute inflammation of the gallbladder wall

Inflammation: 1) mechanical inflammation 2) chemical inflammation 3) bacterial inflammation,

mechanical inflammation

• Obstruction by stone → increased intraluminal pressure and

distention → ischemia of the gallbladder mucosa and wall

bacterial inflammation

• 50–85% of patients with acute cholecystitis.

• The organisms most frequently isolated by culture of gallbladder bile: Escherichia coliKlebsiella Streptococcus and Clostridium

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.

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.

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.

fever in Acute cholecystitis

• A low-grade fever

but shaking chills or rigors are not uncommon.

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.

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

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).

Ultrasound in Acute cholecystitis :

calculi in 90–95%

gallbladder inflammation including: thickening of the wall pericholecystic fluiddilation of the bile duct.

HIDA in Acute cholecystitis

• may be confirmatory if – bile duct imaging is seen without visualization of

the gallbladder.

• 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.

• acute cholecystitis who undergo remission of symptoms, 25% will recurrent cholecystitis within 1 year60% will recurrent within 6 years.

• In view of the natural history of the disease, acute cholecystitis is best treated by early surgery whenever possible.

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.

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.

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

Acalculous Cholecystitis

• clinically acalculous cholecystitis are indistinguishable from calculous cholecystitis,

• complicating severe underlying illness

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

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.

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.

• .

Acalculous Cholecystopathy surgical findings

chronic cholecystitis gallbladder muscle hypertrophy,narrowed cystic duct.

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.

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.

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.

Emphysematous Cholecystitis

• most frequently in elderly men and in patients with diabetes mellitus.

• The clinical manifestations are essentially indistinguishable from those of nongaseous cholecystitis.

Emphysematous Cholecystitis diagnosis

• plain abdominal film :

gas within the gallbladder lumendissecting within the gallbladder wall to form a

gaseous ringgas in pericholecystic tissues.

Emphysematous Cholecystitis treatment

• The morbidity and mortality rates with emphysematous cholecystitis are considerable.

• Prompt surgical intervention coupled with appropriate antibiotics is mandatory.

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.

Chronic Cholecystitis

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

Chronic Cholecystitis

• Chronic cholecystitis may be: asymptomatic for yearsprogress to symptomatic gallbladder disease acute cholecystitispresent with complications (see below).

Complications of Cholecystitis

• Empyema and Hydrops• Gangrene and Perforation• Fistula Formation and Gallstone Ileus• Limey (Milk of Calcium) Bile and Porcelain

Gallbladder

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.

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.

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

Gangrene and Perforation

• results from ischemia or tissue necrosis.

• Underlying conditions :marked distention of the gallbladder, Vasculitisdiabetes mellitus empyematorsion resulting in arterial occlusion.

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.

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.

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)

Fistula Formation and Gallstone Ileus

• Fistulas into the– duodenum are most common– hepatic flexure of the colon– stomach or jejunum– abdominal wall– renal pelvis

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.

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.

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.

Fistula Formation and Gallstone Ileus

• stones, >2.5 cm →fistula formation by gradual erosion through the gallbladder fundus.

• Diagnostic confirmation 1. plain abdominal film

small-intestinal obstructiongas in the biliary tree calcified, ectopic gallstone)

2. upper gastrointestinal series cholecystoduodenal fistula small-bowel obstruction at ileocecal valve).

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.

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.

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

Treatment: Acute Cholecystitis

• Medical Therapy:1. NPO2. NG 3. volume electrolyte are repaired.4. Meperidine or NSAIDs for analgesia less spasm of

the sphincter of Oddi than drugs such as morphine.5. Intravenous antibiotic even though bacterial

superinfection of bile not have occurred in the early • Surgical Therapy

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.

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

acute cholecystitis Surgical Therapy

optimal timing :depends on stabilization of the patient.

• trend is toward earlier surgeryUrgent (emergency) cholecystectomy or

cholecystostomy :Empyema emphysematous cholecystitis perforation

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.

acute cholecystitis Surgical Therapy

• uncomplicated acute cholecystitis → early elective laparoscopic cholecystectomy, within 72 hours after diagnosis.

• Delayed surgical intervention reserved for :(1) overall medical condition imposes risk for

early surgery (2) diagnosis of acute cholecystitis is in doubt.

Postcholecystectomy Complications

Early complications :atelectasis and other pulmonary disordersabscess formation (often subphrenic)external or internal hemorrhagebiliary-enteric fistulabile leaks.

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.

persistent postcholecystectomy symptoms

• The most common : nonbiliary disorders

• small percentage :disorder of the extrahepatic bile ducts

persistent postcholecystectomy symptoms- nonbiliary disorders

reflux esophagitis peptic ulceration pancreatitismost often—irritable bowel syndrome.

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

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

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

biliary colic without stone

• papillary stenosis• papillary dysfunction• spasm of the sphincter of Oddi• biliary dyskinesia

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

papillary stenosis Treatment

endoscopic or surgical sphincteroplasty

ensure wide patency distal portions of both the bile ducts. and pancreatic duct

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

sphincter of Oddi dyskinesia

• Endoscopic or surgical biliary sphincterotomy may be indicated in patients who :

1. fail to respond to a 2- to 3-month trial of medical therapy

2. especially if basal sphincter of Oddi pressures are elevated.

Bile Salt–Induced Gastritis

• Postcholecystectomy patients may develop symptoms of dyspepsia, which have been attributed to duodenogastric reflux of bile.

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.

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.