Gallstone disease

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Gallstone disease

Bile

   Volume = 500-1500 ml/day Hepatocytes and canalicular cells Bile salts + bilirubine + cholesterol + phospholipids   Bile flow depends on:   Its hepatic secretion; Contraction of the gall bladder  Activity of the Oddi sphincter Colecistokinine (CCK) postprandial contraction of the gallbladder and relaxation of the Oddi sphincter (vagal nerve facilitates this action)

Bile salts

 Cholesterol-derived steroids synthesized in the hepatocyte  Function:  Induce bile flow;    Lipid transport; Binds calcium ions in the bile; In the jejunum – bile salts take part in the digestion and absorbtion of lipids. In the last 200 cm of the ileum bile salts are reabsordeb by active transport – 95 %, and the rest end up in the colon – secondary bile salts

Bilirubine

      Results from the destruction of RBC (75%) and from the hepatic turnover of the heme molecule and of the haemoproteines (25%); Haem is released from the haemoglobin and the iron and the globine are processed to be reused; Biliverdine, the first pigment resulted from the heme and it is reduced to unconjugated bilirubine (it must be linked to albumin because it is not soluble in water) Unconjugated bilirubine is extracted from the blood by the hepatocytes and conjugated using glicuronic acid – direct bilirubine (water soluble) – conjugation is catalyzed by glicuroniltransferase; In the intestine bilirubine is reduced by the bacterial population in mesobilirubinogen, stercobilirubinogen and urobilinogen which are oxidized to urobiline; Part of the urobilinogen is reabsorbed from the intestine and reaches the blood flow to be excreted in urine.

Gallstone disease

   2 types of gallstones   Cholesterol – based: 70-80% Pigmentary – black or brown 20-30%

Cholesterol

3 necessary conditions  Oversaturation of cholesterol in the bile   Cholesterol is insoluble in water – micelae of bile salts phospholipidic vesicles (lecitine) when cholesterol concentration in the bile increases above the transport capacity cholesterol crystals precipitate out of the phospholipid vesicles. Obesity, oral contraceptives, more than one pregnancy, dislipidemia   Nucleation  Pronucleation factors (immunoglobins, glicoproteins, fibronectines, orosomucoid) have a more important effect than antinucleation factors (glicoproteins, apolipoproteins, citokeratine). Gallstone increase  Nucleae and cholesterol accumulation in the gallbladder leads to stasis and further gall stone development.

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Pigmentary

      Made from mixtures of calcium bilirubinate, bilirubine polymers, bile acids. 50% - radioopaques Electron microscopy – mixture of bacteria along with bile pigments Risk factors: Cirrhosis, bile stasis, chronic haemolysis, bacterial infection Bacterial β glicuronidase – deconjugation of the bilirubin diglucuronid which is soluble to unconjugated bilirubine which forms a conglomerate with the glicocalix and becomes a gallstone.

Gallstone disease

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Incidence increases with age Drugs

 ceftriaxone, clofibrate, oral contraceptives, estrogen suppliments, progesterone, octreotide

Sex Ethnicity

  Pima indians - Arizona (70%), Canada, hispanics Masai Africa – 0%

Obesity

 BMI>30kg/m2 - 2X risk increase  Cholesterol hipersecretion

Weight loss

 Mobilizes cholesterol from fat deposits and it eliminates it through bile

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Gallstone disease CLINICAL

subjective

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Asymptomatic Cholicative pain

   Spasm due to temporary obstruction of the cystic duct Sudden onset – epigastrium, right hypochondria Progrssive increase in intensity   15 min to a few hours Iradiates în the right lumbar area and the righ interscapulo-vertebral area  Reoccurs in days-months-years

Symptoms related to a complication

  Acute cholecystitis Jaundice  Acute pancreatitis

Objective

   Normal Tenderness - epigastrium, right hypochondria Complication   Murphy sign – Acute cholecystitis Jaundice

Gallstone disease

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DIAGNOSTIC

Ultrasound Abdominal X-ray

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CT

Gallstone disease

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ERCP

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echoendoscopia

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Cholangio-MRI Scintigraphy

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Gallstone disease Differential

Gastric disease

 Peptic ulcer, GERD, Hiatal hernia

Liver disease

 Hydatic cyst, cirrhosis, hepatocarcinoma, cholangiocarcinoma

Pancreatic disease

 Chronic pancreatitis, pancreatic tumors

Bowel disease

 Irritable bowel syndrome, appendicitis

Kidney disease

 Kidney stone, pielonefritis

Lung disease

 Pneumonia, pleural effusion

Heart disease

 Myocradial infarction

Gallstone disease

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Complications

          Chronic colecystitis Acute colecystitis Lytiasis of the main bile duct Acute pancreatitis Cholangitis Fistulae Ileus Gallbladder cancer Mirrizi syndrome Porcelain gallbladder

Gallstone disease

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Treatment

Wait and see Medical

 Ursodezoxicolic acid     Small gallstones 15% of the cases 6-12 Months Recurrence - 50% at 5 ani

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Surgical

Gallstone disease

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Extracorporeal sound wave lithotripsy

       High surgical risk patients Cholesterol gallstones Small stones 4-30 mm Permeable cystic duct < 4 stones 15% of patients Side effects  Petechiae, ecchymosis    Pain Hematuria Nausea

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Percutaneous therapy

Gallstone disease

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ERCP

Gallstone disease

     90-95% due to lytiasis

Acute cholecystitis

80% - obstruction of cystic duct Gallbaldder – inflamed, distended - pain. Most cases – spontaneous remission, but sometimes - peritonitis.

Histology  Subserosal oedema, haemmorhage, necrosis of the mucosa    Later – polymorphonucleary infiltrate Fibrosis Sometimes – gangrene and perforation 3 days-2 weeks from first symptoms

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Acute cholecystitis

Obstruction theory

    Sudden accumulation of bile in the gallbladder – parietal ischemia Bile stasis – increase in bile concentration – chemical irritation – aseptic inflammation Progressive parietal ischemia – necrosis Cystic duct obstruction

Pancreatic enzymes theory

 Activation of pancreatic enzymes that backflowed to the gallbladder – chemical irritation.

Septic theory

 Hematogeneous pathway (portal or systemic);  Septic backflow;

Acute cholecystitis

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Alytiasic acute cholecystitis

    5-10% of cases Patients with:     Severe trauma Burns Long-term parenteral nutrition Major surgery outside the biliary tree Etiology  Bile stasis and ischemia More severe than lytiasic acute cholecystitis  Gangrene, empyema, perforation

Acute cholecystitis

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Diagnosis

     Pain in right hypochondria Murphy sign Fevre Leucocitosis >12-13000/mm3 US  Gallstone   Oedematous gallbladder walls >5 mm Enlarged gallbladder Also possible     Nausea, vomiting Chills Gallbladder palpable US   Liquid aroung the gallbladder Abscess

Acute cholecystitis

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Differential

Perforated peptic ulcer Acute pancreatitis Acute apendicitis Digestive tract perforations Peritonitis Acute kidney disease Acute lung disease Gonococic perihepatitis Hepatomegaly with sudden distension of the capsula of Glisson

Acute cholecystitis

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Complication

Gangrenous acute cholecystitis Emphysematous acute cholecystitis Clostridium perfringens, E. coli, streptococus

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Acute cholecystitis

Perforation  Localized peritonitis  Abscess located under the liver    Generalized peritonitis Choleperitonitis Fistulae    Duodenum, colon, stomach

Ileus

In the main bile duct

Acute cholecystitis

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Treatment

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Medical

 Pain  Hidroelectrolitic balance  Stop oral food intake  ± NG tube  Antibiotherapy  Cefalosporines  Type A penicilinestip A+aminoglicozides ± metronidazole  Carbapenemes

Acute cholecystitis

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Surgical

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Cholecystectomy

 Laparoscopic  Open  Timing of the procedure  60% spontaneous remission  Early – first 72-96 hours  Secondary – after 4-6 weeks

Cholecystectomy

 Severely altered state of patients

Main bile duct litiasis

  7-15% of patients with galbladder litiasis also present main bile duct litiasis types   Secondary Primitive  Associated with stasis and infection  Stasis can be due to  Strictures   Stenosis of the papila Oddi sphincter disfunction

Main bile duct litiasis

 Severe complications   

Jaundice Cholangitis Acute pancreatitis

Main bile duct litiasis

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Jaundice

Possibly no pain Frequent episodes of jaundice  Obstacle+spasm+oedema Stasis – increased pressure in the bile canaliculy

Main bile duct litiasis

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colicative pain+(fever)+jaundice

  Hypochromic stools Hyperchromic urine   Pruritus

Laboratory

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Serum

 Bilirubine      Alkalyne phosphatasis Cholesterol is increased Increased bile salts  ALAT,ASAT almost normal

Urine

 Urobilinogen - absent   Bile salts – increased Conjugated bilirubine

Stool

 Stercobilinogen, urobiline

Main bile duct litiasis

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Paraclinical

    NG tube – no bile US   Gallstones in main bile duct Biliary ducts - dilated ERCP CT

Main bile duct litiasis

  Echoendoscopy Cholangio - MRI

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Main bile duct litiasis

Differential Prehepatic jaundice

 Serum   Unconjugated bilirubine Normal hepatic tests  Urine   Urobilinogen – increased Absence of bilirubine   Stool – increased stercobiline US – normal bile ducts

Hepatic jaundice

   Hepatitis, cirrhosis Conjugation defficit and elimination defficit Serum   Unconjugated and conjugated bilirubine increased Bile salts increased    Increased cytolisis Urine  Conj bilirubine, bile salts, urobilinogen US – bilre duct not dilated

Main bile duct litiasis

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Endoscopic

  Baloon probe Sphincterotomy

 Percutaneous

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Surgical

Laparoscopic or open  Cholecystectomy   Cholangiography Extraction of the gallstones   Transcystic Transcoledocian     Choledocoscopy Cholangiography Kehr drain Bilo-digestive anastomosis Transduodenal sphicterotomy

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CHOLANGITIS

Bacterial infection of bile ducts – no obstruction, no clinical symptoms Not every obstruction leads to cholangitis Obstruction – increased bile duct pressure – bacterial proliferation – systemic disease

Charcot triade: colicative pain, jaundicem, fever.

Most common: E. Coli, Klebsiella, Pseudomonas, Enterococi, Proteus. Bacteroides fragilis, Clostridium perfingens Supurative cholangitis is used for severe disease associated with sepsis:      Abdominal pain Jaundice Fever Confusion shock   90% - i.v. antibiotics Severe cholangitis or lack of response to antibiotics – decompression of the main bile duct:   Endoscopically Percutaneously  Surgicaly

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Biliary fistulae

Biliodigestive Biliobiliary

Old litiasis patient with frequent inflammatory episodes Inflammed gallbladder adheres to an organ which is in the vicinity – necrosis – perforation First an acute episode and then a decrease in symptoms after fistula occured Gallstones can pass through the fistula and cause  Vomiting and nausea     Ileus Bouvert piloro-duodenal obstruction Cholangitis Main bile duct litiasis

    Abdominal X-ray  Air in the main bile duct   Air-fluid levels Radioopaque gallstone Barium meal  Contrast passes into the main bile duct US   Gallbladder stones Radioopaque stones abnormally located Endoscopy, echoendoscopy, CT

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Mirrizi syndrome

ERCP US Cholecystectomy

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Porcelain gallbladder

Calcification of the walls of the gallbladder Complication  Gallbladder cancer Profilactic cholecystectomy