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Cholecystitis :

Definition:

Inflammation of the gallbladder may be acute, chronic, or acute superimposed on chronic. It almost always occurs in association with gallstones

Epidemiology:

United States cholecystitis is one of the most common indications for abdominal surgery.

distribution closely parallels that of gallstones.

Types:

Acute cholesystitis:o Acute inflammation of the gallbladder, precipitated

90% of the time by obstruction of the neck or cystic duct.

o It is the primary complication of gallstones and the most common reason for emergency cholecystectomy.

o Cholecystitis without gallstones called acalculous cholecystitis may occur in severely ill patients and accounts for about 10% of patients with cholecystitis.

Pathogenesis:

Impaction of gallstones in the cystic duct (>90% cases)

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Obstruction and dilatation of gallbladder

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Vascular congestion and oedema

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Necrosis of wall, bacterial proliferation

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Complications eg. gangrene, perforation, liver abscess, cholangitis, bacteraemia etc.

Acute calculous cholecystitis:o Results from chemical and inflammation of

obstructed gall bladder.o Normal protective glycoprotein layer is disrupt

exposed epithelium to direct action detergent of bile salts.

o Prostaglandin released from distended gall bladder inflammation.

o Gallbladder dysmotility; distension & increased intraluminal pressure compromise blood flow to mucosa

o Occur in absences of bacterial infections.

Acute acalculous cholecystitis

o Results from inflammationo Due to inflammation & edema of wall that

compromise blood flow gallbladder statisaccumulation of microcrystal of

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cholesterol viscious bile gall bladder mucus cystic duct obstruction

o Risk factors: Sepsis with hypotension & multisystem failure Immuno-suppression Major trauma & burns infections

Morphology:o Tense & Enlarged gall bladdero Bright red or blotchy, violaceous to green black

discolouration subserosal haemorrhageo Serosal layered by fibrin, if severe

suppurative& coagulated exudateso Acalculous absences of macroscopic stoneso Calculous stone usually in neck of gallbladdero Empyema of gallbladder exudates virtually with

puso Thickened gallbladder wall o Edematous & hyperemico Gangrenous cholecystistis

Clinical features;o Progressive RUQ/ epigastric paino Associated : Mild fever, anorexia, tachycardia,

sweating, nausea, vomitingo Jaundice if obstruct CBD o Acute calculous sudden pain or acute emergency

needed, wout intervention subsides in 7- 10 days.o Acute acalculous insidious in onset, , higher

incidence of gangrene and perforation.

Chronic cholecystitis;o Sequel to repeated bout of acute cholecystitiso Associated with cholelithiasis in >90% of cases.

Pathogenesis: Not clear Supersaturation predisposed to both chronic inflammation

& stone formation. E.coli & Enterococci found in 1/3rd cases. Obstruction of outflow is not main for chronic cholecystitis

Morphology:

Serosa smooth & glistening / dulled by serosal fibrous. Dense fibrous adhesion as sequel of preexisting reapted

acute cholecystitis. Wall thickened, opaque-grey white appearance. Lumen fairly clear, green-yellow, mucoid bile & usually

stones. Histology :

o Mild lymphocytes, plasma cells, macrophages, in mucosa & subserosal fibrous.

o Severe fibrous,mononuclear cell infiltration, buried crypts ( reactive proliferation mucosa + mucosal folds) , Rokitansky Aschoff sinuses (outpouch of epithelium through wall),

o Rare porcelain gall bladder ( dystrophic calcification), xanthogranulomatous cholecystitis ( massive thickened gall bladder + shrunken nodular + chronic inflamed with foci necrosis), Atrophic ( hydrops of gall bladder)

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Clinical features:o Recurrent attack of colicky paino RUQ pain

o Nausea & vomiting frequent associated symptomso Intolerance for fatty foods.

Complications:

Bacterial superinfections with cholangitis / sepsis Gallbladder perforation & local abcess formation. Biliary enteric fistula W draining of bile into adjacent organ Aggravating of preexisting medical illness with cardiac,

pulmonary renal or liver decompensation.

Investigation:

FBC TWBC : leukocytosis elevated mild to moderate Serum bilirubin : slightly elevated USG ; calculi in 90- 95% of cases Cholesyntigraphy : abnormal CCK gall bladder ejection

fraction <40%

Treatment:

Usually surgical as main choices.

Medical therapyo Pre cholecystectomy:

Oral intake is eliminated nasogastric suction may be indicated

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extracellular volume depletion and electrolyte abnormalities are repaired.

Meperidine / NSAIDS used due to produced less spasm to the sphincter of Oddi than morphine.

I.V antibiotics given: piperacillin or mezlocillin, ampicillin sulbactam, and third-generation cephalosporins. Anaerobic coverage by a drug such as metronidazole should be added if gangrenous or emphysematous cholecystitis is suspected.

Surgical therapy:o Optimal timing depend on pt. stabilizations.o Urgent (emergency) cholecystectomy or

cholecystostomy is probably appropriate in most patients in whom a complication of acute cholecystitis such as empyema, emphysematous cholecystitis, or perforation is suspected or confirmed

o Delayed if: patients in whom the overall medical

condition imposes an unacceptable risk for early surgery .

pt in whom the diagnosis of acute cholecystitis is in doubt

Extrahepatics bile ducts:

Ascending Cholangitis:

Definition:

Term used for bacterial infection of the bile ducts

Causes : Due to any obstruction to bile flow E.g.: choledocolithiasis

Types :

Ascending cholangitis Primary sclerosing cholangitis Recurrent pyogenic cholangitis AIDS-related cholangitis

Etiology :

Obstruction of the common bile duct due to gallstones Benign strictures Malignant strictures Sclerosing cholangitis Parasites

Pathophysiology :

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Bile is normally sterile. Biliary tree normally protected because there is normal flow of bile to flush, the sphincter of oddi prevents backflow from the small intestine (mechnical), and bile salts have bacteriastatic properties.

Although the exact mechanism is unclear, it is believed that bacteria gain access to the biliary tree by retrograde ascent from the duodenum or from portal venous blood.

Statis contributes to bacterial growth, increased pressures leads to backflow of infection into other parts of the system. Can lead to bacteremia and severe sepsis via portal system

Risk factors:

• Age > 50 years

• Cholelithiasis (formation of gallstones)

• Benign strictures

• Malignant strictures

• Postprocedure injury of bile ducts

• History of sclerosing cholangitis

Sign & Symptoms :

• Charcot’s Triad

▫ Jaundice, fever, and RUQ pain &

• Reynold’s Pentad

▫ Addition of altered mental status, and hypotension

Investigation :

• transabdominal ultrasound

• Endoscopic ultrasound

• CT

• Magnetic resonance cholangiopancreatography(MRCP)

• Endoscopic retrograde cholangiopancreatography (ERCP)

• Lab tests

▫ abnormal LFTs, elevated CRP, WBC

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Treatment :

• Broad spectrum antibiotics

• Biliary drainage

▫ ERCP

▫ Percutaneous transhepatic cholangiography (PTC)

▫ EUS guided drainage

▫ Open surgical drainage

Primary sclerosing cholangitis

Definition:

A chronic inflammatory cholestatic disease Progressive destruction of bile ducts May progress to cirrhosis

Epidemiology:

Prevalence 6-8/100000 Usually diagnosed in 20s and 30s Male predominance ~3:1 80% have IBD –usually UC ~44% asymptomatic at diagnosis Median survival ~ 12 years

Etiology:

Aetiology unknown Familial incidence HLA associations-B8,DR3,DRw52a,DR2,DR4 Polymorphism of TNF gene Immunology factors:

o Increased frequency of autoimmune disordero Increased T cell in blood and livero Increased circulating immune complexes.

Pathogenesis :

Association between PSC and Ulcerative Colitis suggests a pathogenic interaction

Bacteria or toxic substances absorbed via inflammed mucosa

Bile duct injury suggest ischaemic injury immune complex mediated

Clinical features:

44% asymptomatic but most develop symptoms over time Pruritis , jaundice, pain and fatigue are common symptoms Later on develop symptoms of cirrhosis and portal

hypertension

Investigation :

Cholangiography : o ERCP (endoscopic retrograde

cholangiopancreatogram) or MRCP (Magnetic resonance cholangiopancreatography)

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Management:

Many strategies tried but only transplantation shown to improve survival

Medical therapy;o Ursodeoxycholic acid (UDCA)

MOA: reduces cholesterol absorption Used to dissolve (cholesterol) gallstones in

patients who want an alternative to surgery.

Expensive Usually <10 mmd 8-10 mg/kg / day

Combination Rx with UDCA and steroids showed clinical and biochemical improvement in a small trial

Endoscopic Treatment Balloon dilation or stenting can improve clinical,biochemical and cholangiographic appearances

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