Cholesistitis, cholelitiasis

Sigit Widyatmoko Fakultas Kedokteran Universitas Muhammadiyah Surakarta

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 lysolecithin and other local tissue factor Bacterial inflammation: play a role in 50 to 85% of patients E Choli, Klebsiella, Streptococcus, Clostridium

 Persistent cystic duct obstruction Pain lasts > 4 hours Usually fatty food ingestion 1 hr before pain Biliary Colic

Acute Cholecystitis
Early stages Edema and hyperemia

Later stages Adhesions, fibrosis, and necrosis

Courtesy of Netter

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 of plain abdominal roentgenography

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

Algorithm for the diagnosis of Acute cholecystitis

Complications of Cholecystitis

Empyema and Hydrop Gangrene and Perforation Fistula formation and Gall stones ileus

Acute Cholecystitis2

Thickened gallbladder wall or edema

Pericholecystic Fluid
Sonographic Murphys Sign

Acute Cholecystitis

Acute cholecystitis

Thickened gb wall with stone

Contracted gb w/ wall thickening

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

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

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

 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??

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

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 persistent mechanical 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

Acalculous Cholecystitis
Definition

Acute necroinflammatory disease of the gallbladder Absence of stones (bet you figured that out) 10% of cholecystitis cases Males>females

Whos at Risk?

Immunosuppressed Critically ill (trauma, burns, sepsis, vent) CAD Diabetes Cholesterol emboli TPN Obstetric patients Recent surgery

Pathophysiology

Gallbladder stasis and/or ischemia Inflammatory response in GB wall Bile salts concentrate in GB tissue Progresses to tissue necrosis Inflammation of cystic duct can progress to CBD, leading to biliary obstruction

Pathogens

Usual: Klebsiella, ecoli, enterococcus, pseudomonas, bacteroides Unusual: typhoid, campylobacter, leptospirosis, clostriudium, vibrio, Q fever, dengue fever Immunosuppressed: CMV, microsporidium, cryptosporidium, salmonella, candida

Presentation

May be subtle vague 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%

To the lab

LFT abnormalities: +/- elevated TBili, AlkPhos and aminotransferases Blood cultures prior to antibiotics

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

Normal HIDA scan

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

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.

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

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 10-15 yr

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 but have the morphologic and microstructural features of typical cholesterol stones mixed stones Risk factors: aging, female gender, obesity, pregnancy, rapid weight loss, native american ethnicity

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, and small amounts of various other substances exclusively in gall bladder The major known associated conditions are: old age, cirrhosis, hemolysis, possibly total parenteral nutrition Brown pigment stones: brown colored, compromised primarily of calcium bilirubinate, cholesterol, calcium

. palmitate, and small amounts of various other substances mostly in bile ducts Predisposing condition: stasis and/or infection

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. Failure to maintain calcium ions in solution is considered important, resulting in the precipitation of calsium bilirubinate, phosphate, and carbonate Brown pigment: precipitation of calcium bilirubinate and calcium salts of fatty acids are the major pathophisiologic events. Biliary stasis and bacteria in bile are important for stone formation

Pathology

Obstruction

Intraluminal Extraluminal Intramural Host Sufficient inoculum Stasis Pain, Jaundice, fever Constitutional; nausea, vomiting, weight loss, anorexia

Infection

Symptoms

Abdominal pain

Biliary colic

Misnomer, constant RUQ Visceral Precipitated by any food or spontaneous Pain due to obstruction (neck, duct) Resolve spontaneously
RUQ visceral Positive Murphys Fever, WCC

Acute Cholecystitis

Risk Factors
Age Time dependent, typical 40, decrease in conversion of cholesterol to bile salts

Gender
Race Genetics Obesity Crohns

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

High: Hispanics, whites. Low: Black Africans Family history Increased activity of HMG reductase lead to increased cholesterol synthesis Decreased ileal resorption of bile salts

TPN
WT loss

GB stasis,
Low calorie, high protein diet, bypass surgery

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 extensive information than ultrasonography, but its sensitivity is lower ERCP: endoscopic retrograde cholangio pancreatography: detects stones in bile ducts

Natural History

Asymptomatic gallstones: the majority of patients are asymptomatic and remain asymptomatic 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 to once every months or even longer

Large stone with shadowing

Many small stones

Cholelitiasis multiple

Layer of gravel with shadowing

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 2030%. The highest success rates (60-70%) are in patients with stones < 5 mm Ursodeoxyc: agent of choice, chenodeoxy is rarely used because of side effects

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

Choledocholithiasis

Predictive tests

Pre operative

Bilirubin and Alk. phosphatase Jaundice, pancreatitis Cholangitis CBD stones on US Dilated CBD Palpable stone

Operative

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

Medical treatment

Oral Dissolution

Early 1970 Chenodeoxycholic acid Treatment needed for 12 months Cholesterol stones less than 10mm
Methyl tertbutyl ether (organic solvent) Pump directly into gallbladder Cholesterol stones dissolve within hours Technically feasible

Contact Dissolution

Medical treatment

Extracorporeal shock wave lithotripsy

Mid 1980 Advantages

Noninvasive Reduced morbidity and mortality Non calcified, less than 30mm Biliary colic, pancreatitis, haemobilia 90% early Recurrence 15%

Which stones

Complications

Success rate

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

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

Choledocholithiasis

Predictive tests

Pre operative

Bilirubin and Alk. phosphatase Jaundice, pancreatitis Cholangitis CBD stones on US Dilated CBD Palpable stone

Operative

CBD

CBD

CBD internal diameter is < 4 mm in 98% of normal individuals

Cystic duct 1.8 mm diameter and 1-2 cm long

Portal vein

Alhamdulillahi robbil alamien