Calculous biliary

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CALCULOUS BILIARY DISEASE Fabian Ovidiu

Biliary physiologyCystic duct

The bile ducts, gallbladder and sphincter of Oddi act in concert to modify, store, and regulate the flow of bile

Common hepatic duct

Common bile duct

Choledocus

Gallbladder Sphincter of Oddi

Biliary physiologyThe functions of the gallbladder: -to concentrate -to store the bile Bile is concentrated 5-fold to 10-fold by the absorption of water and electrolytes a marked change in bile composition The concentration of bile may affect the solubilities of two important components: - cholesterol and - calcium the gallbladder bile becomes concentrated -several changes occur in the capacity of bile to solubilize cholesterol.

Biliary physiologyThe major organic solutes in bile are: - bilirubin

- bile salts- phospholipids - cholesterol Cholesterol = highly nonpolar

= insoluble in water

Biliary physiologyCholesterol is maintained in solution in some complex biochemical structures:The hidrophobic molecules of cholesterol are surounded by hidrophilic molecules

micelles

vesicles

Cholesterol solubility depends on the relative concentration of cholesterol, bile salts, and phospholipid

Gallstones formationSupersaturated bile: - the capability of these micelles and vesicles to solubilise the cholesterol is exceded the precipitation (cristalisation) of the cholesterol occur Pronucleating factors -mucin glycoproteins -immunoglobulins

-transferrinaccelerate the precipitation of cholesterol in bile

Gallstones formation

Sludge = a mixture of cholesterol crystals, calcium bilirubinate granules, and a mucin gel matrix

The cristals of cholesterol growth, include glicroproteins from mucin gel and calcium bilirubinate

gallstones

Gallstones formation

Gallstone typesgallstones cholesterol gallstones The pathogenesis of cholesterol gallstones involves four factors: -cholesterol supersaturation in bile -crystal nucleation pigment gallstones Black pigment stones = associated with -hemolytic conditions or -cirrhosis unconjugated bilirubin increased Brown pigment stones -earthy in texture -some bacteria produces enzymatic hydrolysis of soluble conjugated bilirubin free bilirubin it precipitates with calcium

-gallbladder dysmotility-gallbladder absorption

Gallstone types

cholesterol gallstones

Gallstone types

black gallstones

Gallstone types

brown gallstones

Gallstone types

cholesterol and pigment gallstones

Natural history of gallstonesasimptomatic gallstones-discovered at the time of laparotomy or during abdominal imaging for nonbiliary disease -the vast majority of patients with gallstones are asymptomatic

gallstones

during years

biliary colic acute cholecystitis

simptomatic gallstones complications

choledocholithiasis gallstone pancreatitis gallstone ileus gallbladder carcinoma

Natural history of gallstones

Simptomatic gallstones1.Pain -tipical pain: biliary colic -atipical pain

2.Other simptoms: -nausea -vomitingobstruction of the cystic duct results in a progressive increase in tension in the gallbladder wall, leading to constant pain in the majority of patients

-bloating-belching

Biliary colicThe pain: -in the right upper quadrant and/or epigastrium -frequently radiates to the back and right scapula -the intensity of the pain = severe -occurs following fatty meals (50% of patients) -the duration of pain: 1 to 5 hours (tipically) rarely persist for more than 24 hours if > 24 hours suggests an acute cholecystitis) rarely shorter than 1 hour

-the episodes of biliary colic = less frequent than one per week.

Atipical painAtypical pain is common -some patients do not relate their pain to meals or time of day -not all attacks are necessarily severe -the pain is continuous rather than episodic -the pain located predominantly in the back or the left upper or right lower quadrant -the less typical the pain search for another cause,renal colic, peptic ulcer, hiatal hernia, abdominal wall hernia, liver disease, disease of the small bowell, disease of the large bowell

even in the presence of stonesTreatment of atypical biliary colic is appropriate when other causes of pain have been eliminated.

Diagnostic imagingAbdominal X-ray -only 15% of gallstones contain sufficient calcium to appear on X-ray Ultrasound -noninvasive, inexpensive, and widely available -identifies gallstones and bile duct dilation -gallstones create echoes and are free-floating -the ultrasound waves cannot penetrate the stones shadowing gallstones shadowing sludge

Diagnostic imagingCholescintigraphy -Tc99m labeled iminodiacetic acid - injected intravenously -the radionuclide is excreted into the bile

-delayed filling of the gallbladder and CBD

or absent filling of the duodenum suggests an obstruction at CBD

Diagnostic imagingComputerized Tomography

multiple distinct large stones

ayering of small stones and sludge

In fact the role of CT scanning is limited to the diagnosis of complications of gallstone disease such as acute cholecystitis (gallbladder wall thickening, pericholecystic fluid), choledocholithiasis (intrahepatic and extrahepatic bile duct dilation), pancreatitis (pancreatic edema and inflammation) and gallbladder cancer

TreatmentNonoperative Therapy The nonsurgical options for the treatment of gallstone disease include: -oral dissolution therapy with the bile acids (ursodeoxycholic acid and chenodeoxycholic acid)

-contact dissolution therapy with organic solvents (methyl tertbutyl ether)-extracorporeal shock wave biliary lithotripsy. These treatments are rarely used today.

TreatmentNonoperative Therapy The nonsurgical options for the treatment of gallstone disease include: -oral dissolution therapy with the bile acids (ursodeoxycholic acid and chenodeoxycholic acid) cholesterol gallstones

-contact dissolution therapy with organic solvents (methyl tert-butyl ether) cannulation of the gallbladder with direct infusion of the agent -only cholesterol gallstones-extracorporeal shock wave biliary lithotripsy -0.5 to 2 cm diameter gallstone -risk of choledocholitiasis These treatments are rarely used today.

Treatment operative therapyLaparoscopic cholecistectomy -pneumoperitoneum -trocar placement

Treatment operative therapyLaparoscopic cholecistectomy the Calot triangle (on its area pass the cystic artery)

The peritoneum overlying the cystic duct gallbladder junction is opened

Treatment operative therapyLaparoscopic cholecistectomy

The cystic duct is isolated

The cystic duct is clipped proximal and distal and divided with the hook scissors

Treatment operative therapyLaparoscopic cholecistectomy

The cystic artery is dissected, clipped and divided

The gallbladder is dissected from the liver by scoring the serosa with electrocautery

Treatment operative therapyOpen cholecistectomy-upper midline or right subcostal incision -identification and division of the cystic duct and artery -removal of cholecist from the gallbladder bed

If the anatomy cannot be clearly identified, the gallbladder should be dissected from the fundus downward towards the gallbladder neck, making the ductal and vascular anatomy easier to identify.

Chronic calculous cholecystitisPathogenesis -gallstones lead to recurrent episodes of cystic duct obstruction recurrent inflammatory proces -over time scarring and a nonfunctioning gallbladder -histopathologically: subepithelial and subserosal fibrosis and a mononuclear cell infiltrate Clinical Presentation: -pain (biliary colic or atypical pain), nausea and vomiting -physical examination: is usually completely normal during biliary colic, mild right upper quadrant tenderness may be present -laboratory values bilirubin transaminases alkaline phosphatase are also usually normal

Chronic calculous cholecystitisDiagnosis -requires two findings abdominal pain consistent the presence of gallstones -usualy documented by ultrasonography.

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Management -the treatment of choice: elective laparoscopic cholecystectomy -conversion to an open cholecystectomy is necessary in less than 5%

Acute calculous cholecystitisPathophysiology -the most common complication of gallstones (20% to 30% of patients with symptomatic disease) -results from a stone impaction at the gallbladder-cystic duct junction -as in biliary colic -primarily: inflammation (without bacteria) -secondary: bacterial infection Escherichia coli = the most common organism

Acute calculous cholecystitisPathophysiologyGallstones Cystic duct obstruction Pain (biliary colic) Inflammation

acute calculous cholecystitis

Obstruction is relieved (90%)

Obstruction not relieved (10%) Inflammation and edema Vascular compromise

Minimal histological changes (scarring and fibrosis) Cronic cholecystitis

Ischemia, necrosis, perforation

Acute calculous cholecystitisClinical Presentation -right upper quadrant pain similar to that of biliary colic -the pain is usually unremitting may last several days -often associated with nausea, emesis, anorexia, and fever On physical examination: -low-grade fever -localized right upper quadrant tenderness and guarding which distinguishes the episode from simple biliary colic -Murphy's sign inspiratory arrest during deep palpation of the right upper quadrant =the classic physical finding of acute cholecystitis -a palpable right upper quadrant mass is appreciated in one third of patients omentum that has migrated to the area around the gallbladder -mild jaundice may be

Acute calculou