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Factors Contribute Inflammation

Mechanical inflammation: by increased intraluminal

pressure and distention with resulting ischemia of the

gall bladder mucosa and wall

Chemical inflammation: by release of lysolecithinand other local tissue factor

Bacterial inflammation: play a role in 50 to 85% of

patients E Choli, Klebsiella, Streptococcus,

Clostridium


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Persistent cystic duct obstruction

Pain lasts > 4 hours Usually fatty food ingestion 1 hr before pain

Biliary Colic


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Acute Cholecystitis

Early stages Edema and hyperemia

Later stages Adhesions, fibrosis, and necrosis

Courtesy of Netter


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Lanjutan komplikasi.

Limey (milk of calcium) bile and porcelain

gallbladder : calcium salts may be secreted into the

lumen of gallbladder in sufficient concentration and

diffuse, hazy opacification of bile or a layering ofplain abdominal roentgenography


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Mirrizzis syndrome: rare complication in

which a gallstone becomes impacted in the

cystic duct or neck of the gallbladder causing

compression of the CBD, resulting in CBD

obstruction and jaundice. Ultrasound shows

gallstone lying outside the hepatic duct


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Algorithm for the diagnosis of Acute cholecystitis


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Complications of Cholecystitis

Empyema and Hydrop Gangrene and Perforation

Fistula formation and Gall stones ileus


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Acute Cholecystitis2

Thickened gallbladder wall or edema

Pericholecystic Fluid Sonographic Murphys Sign


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Acute Cholecystitis


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Acute cholecystitis


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Contracted gb w/ wall thickening


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Management of Acute Cholecystitis

Supportive care with IVFs, bowel rest, & Abx

Almost half of patients have positive bile cultures

E. Coli is most common organism

Antibiotic choice: Ampicillin + Aminoglycoside

or 3rd generation cephalosporin


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Management cont.

No evidence exists showing a definite benefit

with use of antibiotics

NSAIDs may improve course of acute

cholecystitis6

SURGERY is the only definitive treatment


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Management cont.

1st open cholecystectomy: 1886 by Justus

Ohage

1st half of 20th Century: Supportive care

delayed open cholecystectomy

In 1970s mid-1980s: Open

cholecystectomy early in the treatment course

Golden 72 hours Rule


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Studies in early 1980s early surgery was

better than delayed surgery (using standard

open approach)14

Laparoscopic surgery developed in late 1980s

Complications from LC dependent on

laparoscopic skill of surgeon (major bleeding,

wound infection, bile leak, and biliary injury)

Was the benefit of early surgery by the open

approach true laparoscopically??


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Timing of Surgery

Early surgery = Within 72 hours of admission

or onset of symptoms

Delayed surgery = Supportive care only

followed by discharge and readmission in 6-12

weeks for surgery


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Chronic Cholecystitis

Chronic inflammation of the gallbladder wall which

is always associated with the presence of gallstones

and is thought to result from repeated bouts of

subacute or acute cholecystitis or from persistentmechanical irritation of the gallbladder wall by

gallstones

The presence of bacteria in the bile occurs in more

than one-quarter of patients with chronic cholecystitis


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Whos at Risk?

Immunosuppressed

Critically ill (trauma, burns, sepsis, vent)

CAD Diabetes

Cholesterol emboli

TPN Obstetric patients

Recent surgery


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Pathogens

Usual: Klebsiella, ecoli, enterococcus,

pseudomonas, bacteroides

Unusual: typhoid, campylobacter,leptospirosis, clostriudium, vibrio, Q fever,

dengue fever

Immunosuppressed: CMV, microsporidium,cryptosporidium, salmonella, candida


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Presentation

May be subtlevague RUQ pain (25%),

leukocytosis, fever

May rapidly progress to septic shock May also be similar to classic cholecystitis w/

positive Murphys sign

May become jaundiced

Mortality 10-50%


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To the lab

LFT abnormalities: +/- elevated TBili,

AlkPhos and aminotransferases

Blood cultures prior to antibiotics


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To the basement

Ultrasound (1st test of choice)

Absence of stones

Thickened GB wall >5mm

US Murphys sign

champagne bubble sign

Perforation +/- abcess formation (oops)

30-92% sensitive, >90% specific

HIDA scan: failure to opacify the gallbladder =positive

79% sensitive, 87% specific


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Normal HIDA scan


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Treatment

Blood cultures

Antibiotics

If untreated: Zosyn, Unasyn or Imipenam

If already on broad spectrum:

3rd generation ceph PLUS

Metronidazole OR Imipenam PLUS/MINUS Fluconazole

If known MRSA hx consider Vanc


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Cholelithiasis

Prevalence: 6-10 % men, 12-20 % women

Three types of stone:Mixed cholesterol 80 %

Pure cholesterol 10 %

Pigment 10 %

18-50% become symptomatic over 10-15 yr.


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Statistics

About 3 million adults in the U.S. have

gallstones

Elderly, diabetics, obese patients, debilitated

patients increased incidence of gallstones

90% of acute cholecystitis cases due to

gallstones


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Incidence of Biliary Tract

Disease Cholelithiasis affects > 15 million in U.S.

Contributes to 6-10,000 deaths annually

>500,000 cholecystectomies per year Annual cost of surgery > $3 billion

Majority of gallstones clinically silent

18-50 % become symptomatic over 10-15yr


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Cholesterol Stones

Compromised primary of cholesterol (generally

>60%) and mucin, calcium salts of bilirubin,

phosphate, carbonate and palmitate, and small

amounts of various other substances

Some stones contain less than 60% cholesterol buthave the morphologic and microstructural features of

typical cholesterol stones mixed stones

Risk factors: aging, female gender, obesity,

pregnancy, rapid weight loss, native american

ethnicity


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Pigment stones

Compromised mostly of pigment and calcium salts

Two types of pigment stones: black, brown

Black pigment stones: black colored, compromised

primarily of calcium bilirubinate and other pigment,

mucin, calcium salts of phosphate and carbonate, andsmall amounts of various other substances

exclusively in gall bladder

The major known associated conditions are: old age,

cirrhosis, hemolysis, possibly total parenteralnutrition

Brown pigment stones: brown colored, compromised

primarily of calcium bilirubinate, cholesterol, calcium


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. palmitate, and small amounts of various

other substances mostly in bile ducts

Predisposing condition: stasis and/or infection


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Processes of Gallstone Formation

Cholesterol Gall Stones: supersaturation on bile

with cholesterol, increase in gallbladder mucin, and

gall bladder stasis are the factors that play a role

Black pigment: precipitation of calcium salts and

pigment is the major patophysiologic event. Failureto maintain calcium ions in solution is considered

important, resulting in the precipitation of calsium

bilirubinate, phosphate, and carbonate

Brown pigment: precipitation of calcium bilirubinateand calcium salts of fatty acids are the major

pathophisiologic events. Biliary stasis and bacteria

in bile are important for stone formation


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Pathology

Obstruction Intraluminal

Extraluminal

Intramural

Infection Host

Sufficient inoculum

Stasis

Symptoms Pain, Jaundice, fever

Constitutional; nausea, vomiting, weight loss, anorexia


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Abdominal pain

Biliary colic Misnomer, constant RUQ

Visceral

Precipitated by any food or spontaneous

Pain due to obstruction (neck, duct)

Resolve spontaneously

Acute Cholecystitis RUQ

visceral Positive Murphys

Fever, WCC


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Risk Factors

Age Time dependent, typical 40, decrease in conversion of cholesterol

to bile salts

Gender F:M, 3:!, oestrogen decrease cholesterol uptake by liver

Race High: Hispanics, whites. Low: Black Africans

Genetics Family history

Obesity Increased activity of HMG reductase lead to increased cholesterol

synthesis

Crohns Decreased ileal resorption of bile salts

TPN GB stasis,

WT loss Low calorie, high protein diet, bypass surgery


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Scanning Considerations: Cholelithiasis

Ultrasonography: accuracy 90-95 %

Liver as acoustic window

Location: inferior hepatic surface, medial and

anterior to kidney, lateral and anterior to vena

cava 15 % of gall stones are radiopaque on plain

abdominal X-rays

CT scanning: provide more extensiveinformation than ultrasonography, but its

sensitivity is lower

ERCP: endoscopic retrograde cholangio

pancreatography: detects stones in bile ducts


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Natural History

Asymptomatic gallstones: the majority of

patients are asymptomatic and remainasymptomatic after decades of follow up

Billiary pain: arise from transient obstruction of

the cystic duct by stones or sludge Location is in the right upper quadrant or epigastrium

May range from mild to severe

Duration 15-30 minutes up to 3-4 hours

The interval between episodes varies from daily toonce every months or even longer


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Large stone with shadowing


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Many small stones


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Cholelitiasis multiple


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Layer of gravel with shadowing

Therapy: elective treatment


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Therapy: elective treatment

Bile salts (ursodeoxycholic acid or chenodeoxy cholic

acid) In patients who are at high risk for surgical

The cystic duct must be patent and the stones radiolucent

The complete dissolution rate for all patients is only 20-

30%. The highest success rates (60-70%) are in patientswith stones < 5 mm

Ursodeoxyc: agent of choice, chenodeoxy is rarely used

because of side effects

ESWL (extracorporeal shock wave litotripsy): forsingle stones < 20 mm in diameter


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Choledocholithiasis

Predictive tests

Pre operative

Bilirubin and Alk. phosphatase

Jaundice, pancreatitis Cholangitis

CBD stones on US

Operative

Dilated CBD Palpable stone


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Cholangitis

Stone in distal CBD

Bacteria in bile in 50% - 70%

Charcot Triad

Fever, jaundice, pain

Progress to septic shock

Treatment

Supportive, antibiotics Endoscopic decompression of biliary system

Surgery


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Medical treatment

Oral Dissolution Early 1970

Chenodeoxycholic acid

Treatment needed for 12 months

Cholesterol stones less than 10mm

Contact Dissolution

Methyl tertbutyl ether (organic solvent)

Pump directly into gallbladder

Cholesterol stones dissolve within hours

Technically feasible


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Medical treatment

Extracorporeal shock wave lithotripsy Mid 1980

Advantages Noninvasive

Reduced morbidity and mortality Which stones

Non calcified, less than 30mm

Complications Biliary colic, pancreatitis, haemobilia

Success rate 90% early

Recurrence 15%


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Post-cholecystectomy syndrome

40% of patients

Presentation Biliary colic

Gas bloating 40%

Abdominal pain

Dyspepsia

Causes

Misdiagnosis

Reflux, ulcer, diverticulosis, hepatitis, IBS

Management Further evaluation


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Choledocholithiasis

CBD stones

Primary

Migrated from GB

Retained Other diseases

Benign biliary stricture, scleorsing cholangitis

Incidence Not known, up to 15% have stones during

surgery


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Choledocholithiasis

Predictive tests

Pre operative

Bilirubin and Alk. phosphatase

Jaundice, pancreatitis Cholangitis

CBD stones on US

Operative

Dilated CBD Palpable stone


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CBD

CBD internal

diameter is < 4 mm

in 98% of normal

individuals

Cystic duct 1.8 mm

diameter and 1-2 cmlong

CBD

Portal vein


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