Leslie Kobayashi, MD January 31, 2012 Liver Bile ducts Pancreas Duodenum Transverse colon Fundus Body Infundibulum/Neck Cystic duct Spiral Valves of Heister Triangle of calot Borders: CHD, cystic duct, liver edge Contents: Cystic artery, node of Calot Right and Left Hepatic ducts Common Hepatic duct Cystic duct Common bile duct Vascular Normally (>90%) cystic a. arises from RHA Replaced right hepatic a. Replaced left hepatic a. 500-1500mL produced daily Composition: water, electrolytes, bile salts, proteins, lipids Ductal epithelium products ▪ Alkaline phosphatase ▪ HCO3 Hepatocyte products ▪ Bile in conjugated soluble form synthesized from cholesterol ▪ Primarily cholate and chenodeoxycholate 95% of bile re-absorbed into the liver via portal vein (enterohepatic circulation) 85-90% in terminal ileum via active transport 10-15% deconjugated in colon, absorbed passively 5% excreted in stool Cycles 6-10x daily 80% of bile stored in GB in fasting state Function store and concentrate bile Absorption: NaCL, H2O occurs rapidly Secretion: mucus, H+ GB average capacity 30-50mL Can increase to 300mL with obstruction Normal ejection 50-70% in 30-40min Do gallbladder problems create a significant healthcare burden? Health burden 6.2 Billion$ in US 1.8 million ambulatory care visits Increased 20% since 1980’s Cholecystectomy most common elective abdominal procedure in the US ▪ 750,000 annually Stones Cholesterol stones (75%) Female fat fertile Black stones (20%) Hemolytic diseases (Sickle cell disease) Cirrhosis *primarily form in the Brown stones (5%) ducts Infection PSC Low calcium, radiolucent Created when fractional cholesterol content of bile increased, and with incomplete emptying of GB Associated with obesity, rapid weight loss, Native American/Hispanic heritage, ↑TG’s, ↓HDL, Spinal cord injury Hormonal influence Estrogen increases lithogenicity of bile ▪ Increased risk for females ▪ Increased risk in obesity Progesterone increases SM relaxation and bile stasis, decrease bile salt secretion ▪ Increased risk in pregnancy Increase risk of stone formation TPN Octreotide Ceftriaxone Decrease risk of stone formation Statins ?ursodiol Often radiopaque due to calcium bilirubinate, calcium fatty acid soaps and inorganic calcium salts Two types Black Brown Black Form in GB Bile sterile Associated with age, hemolytic DO’s, alcoholism, cirrhosis, Gilbert’s syndrome, Cystic fibrosis, pancreatitis and TPN Cholecystectomy curative Brown Form in ducts as well as GB Always infected 1O with enteric organisms, often associated with cholangitis Associated with parasitic infection (liver fluke) Associated with IBD, duodenal diverticulae Will often recur after LC/OC And what do they do? Stones Asymptomatic Symptomatic Biliary Uncomplicated colic Complicated No obstruction + Obstruction + Cholecystitis Infection/inflammation GSP CBD Choledocho - Infection Ampulla Cholangitis +infection Incidence: 10-30% of the population Asymptomatic (80%) Symptomatic (1-3% per year) No inflammation: Biliary colic +inflammation: acute cholecystitis +obstruction : choledocholithiasis, GSP +obstruction+inflammation: cholangitis History Transient abdominal pain Occurs after fatty meals Exam Benign Labs Normal Ultrasound GS Hyperechoic masses, dependent in location Acoustic shadowing History Labs Prolonged pain Leukocytosis Fevers Mild ↑ LFT’s Nausea/emesis Exam Imaging Fever, tachycardia Ultrasound RUQ TTP, Murphy’s HIDA sign Gallstones Obstruction of gallbladder Obstruction causes inflammation Inflamed wall is thickened Edema or emphysema of GBW Inflammation may or may not be associated with infection 50-70% of bile cultures are positive E. coli, Klebsiella, Streptococcus, Enterobacter 95% sensitivity/specificity Signs of cholecystitis Gallstones GBW >3mm Pericholecystic fluid GBW striations or air within GBW Sonographic Murphy’s sign GS with GBW thickening Normal GBW <3mm Pericholecystic fluid Cholescintigraphy: Injection of Tc99 labeled hydroxyl iminodiacetic acid HIDA→hepatocytes→secreted into bile Normal visualization of GB, CBD and SB within 30-60 min +scan if no visualization of GB within 1hr and +uptake in CBD or SB Normal HIDA Positive HIDA Rim sign *Sphincter, ↙CBD False positives common in fasting patients Up to 40-60% in critically ill Can decrease false+ rate with morphine ↑sphincter of Oddi pressure causing preferential filling of the GB ↑Tension in GBW =↓perfusion →Necrosis of GBW Gangrenous/emphysematous cholecystitis ▪ 1% of cases, 3:1 M>F ▪ Conversion rate 30-50% GB Perforation ▪ Assoc with ↑mortality (~20%) ▪ Gallstone ileus Cystic duct obstruction→ Hydrops Bile is absorbed but GB mucosa continues to secrete mucus GB tense, filled with mucinous fluid Mirrizi’s syndrome Impacted stone in infundibulum or CD →External compression of the CBD 0.7-1.4% of patients Assc with ↑risk of CBD injury, GB cancer Stone in CBD No obstruction Symptomatic Asymptomatic + obstruction No infection +Infection History: jaundice, icterus, pruritis, dark urine, steatorrhea, acholic stools, bleeding Exam: jaundice, icterus, RUQ pain, Murphy’s sign Labs Elevated LFT’s, INR Elevated bilirubin highest PPV 25-50% May be normal in up to 30% of patients Imaging Dilated CBD on UTZ ▪ CBD <5mm risk of stone ~1% ▪ CBD >5mm risk of stone 58% MRCP Sensitivity 95% Specificity 89% CBD dilation Stones within the bile duct History/Exam: similar to choledocholithiasis with sepsis, septic shock Labs/Imaging: similar to choledocholithiasis with leukocytosis, bactermia, ±MSOF Charcot’s triad RUQ pain, fevers, jaundice Reynolds pentad Triad + ΔMS, shock History: epigastric pain, nausea/emesis Exam: RUQ/epigastric TTP, SIRS Labs: amylase/lipase ↑3x nl, ±↑LFT’s, leukocytosis Imaging: ±CBD dilation, pancreatic edema, necrosis, fluid collection First 24hours: 48 hours Glucose >200 Ca <8 Age >55 Hct↓>10 LDH>350 PaO2 <60 AST>250 BUN↑>5 WBC>16k Base Deficit >4 Sequestration >6L First 24hours: 48 hours Glucose >220 Ca <8 Age >70 Hct↓>10 LDH>400 PaO2 <60 AST>440 BUN↑>2 WBC>18k Base Deficit >5 Sequestration >6L Each category 0 or 1 Add up total points Mortality 0-2 <5% 3-4 15% 5-6 40% 7-8 ~100% Medical sphincterotomy, Surgical Lap Open CBDE ERCP stent Percutaneous Cholecystostomy tube Preparation Eat a diet high in alkaline-forming foods and low in fats for at least 3-5 days before the cleanse. Help to gently prepare the liver by having a glass of fresh apple juice every day for 1 week prior to the cleanse. Apple juice helps to dissolve the stones Ingredients •Epsom salts (Magnesium Sulfate): 4 tablespoons •Olive oil: 1/2 cup or 125 ml •Fresh pink grapefruit: squeeze 1/2 cup (125 ml) juice •Or use 7-8 fresh lemons/limes: squeezed into 1/2 cup •1 liter jar with lid juice Or you could try: IVF hydration Antibiotics Bowel rest Ursodiol: used as Mechanism: supplemental bile acid decreases lithogenicity of bile, dissolve existing stones Indications: bridge to LC/OC, too sick for OR, cirrhotics, PSC, TPN Efficacy: may ↓LFT’s in PSC/cirrhotics, may ↓stones/sludge on UTZ, does not ↓symptoms, prevent need for OR, stones recur after cessation of medication Diet: Cholesterol/Fatty acids Carbohydrates Legumes Unsaturated fats Coffee, Fiber Vitamin C, Alcohol Failure of medical management in acute cholecystitis 32% Recurrence rate of GSP 29-63% Surgical management results in reduced HLOS Timing of surgery for acute cholecystitis Within 48hrs vs >72hrs no difference in conversion rates, OR time, LOS Comparing first hospitalization (<7d) vs delayed (>6wks) ▪ 17.5% rqr emergent cholecystectomy for recurrent/unresolving sx’s ▪ No difference in conversion rates or CBD injury Timing of surgery for GSP Early operation safe with mild pancreatitis Rason’s criteria <3 Increased conversion rate, HLOS, and operative complications in early operation in severe pancreatitis Ranson’s criteria ≥3 Port placement Umbilicus Subxiphoid just to the right of the falciform at the level of the inferior liver edge 2-3cm below costal margin in midclavicular line Anterior axillary line, below the fundus of gallbladder Retraction and dissection of Triangle of Calot prior to Gallbladder removal from fossa CD may be clipped, sutured, tied, stapled Remove gallbladder in fundus→dome direction Right subcostal incision Mini-cholecystectomy (5-8cm) incision associated with equivalent outcomes/complications and less post-op pain, decreased LOS Dome down dissection technique Isolate cystic artery/duct and suture ligate Conversion rate: 0.18-35% ave 4.7% CBD injury rates Lap 0.2-0.6% Open 0-0.3% Complication rate Lap ~1.2% Open (bile leak 1%) LOS: shorter for Lap RF’s for conversion Male sex Obesity ↑age Wide short cystic duct Low surgeon case load Gangrenous or emphysematous chole ↑risk of conversion RR 3.2 (CI 2.5-4.2) No ↑risk of local complications or CBD injury Can be transhepatic or transperitoneal no difference in outcomes Technical success 96-98% Resolution of symptoms 68-96% Mortality 3-14% Complications Dislodged catheter 16-33% Bleeding 1.5-1.8% Recurrent cholecystitis 7-41% Choledocholithiasis Stones in CBD in 10-15% of symptomatic pt’s 55-70% pass spontaneously GSP20-30% of patients have CBD stones 85-90% pass spontaneously Symptomatic cholecystitis 4.6% +IOC at the time of LC 97.8% pass spontaneously CBDE Can be performed lap or open Transcystic or via choledochotomy CBDE Imaging duct ▪ Fluorscopic guidance ▪ Choledochoscopy Clearing duct ▪ Basket, snare, flush ▪ +/- glucagon to relax sphincter CBDE Completion cholangiogram Clip, tie or staple cystic duct stump Close choledochotomy over T-tube +/-drain external Success rate of duct clearance 75-95% Efficacy 1 procedure: 71-75% Multiple procedures: 84-95% Mortality 0.2-0.5% Complication rate 5-8% Perforation Bleeding Pancreatitis Cholangitis 1-2% of patients will represent with CBD stone following cholecystectomy Dx <2yrs post-op = retained stone Dx > 2yrs post-op =recurrent stone Ileus Incisional/port site hernia Wound infection Abscess Biloma/bile leak Strasberg-Bismuth classification A-CD stump, fossa B/C-aberrant RHD D-lateral injury E-circumferential injury to major duct Increased risk of stones 2-12% have stones 0.05-1.2% symptomatic during pregnancy Risk of stones increased in: Hispanic Pre-pregnancy obesity (4x) Decreased by EtOH consumption Biliary disease the most common nonobstetrical cause of maternal hospitalization Cholecystitis most common 40% GSP 30% CBD stone 20% Biliary colic 10% If symptomatic risk of recurrence high 40%-70% recur prior to delivery If symptomatic risk of fetal loss high 10-20% Treatment goals Treat infection Maintain nutrition Prevent contractions/preterm labor Prevent fetal loss Prevent maternal morbidity/mortality Surgical management associated with fewer complications than medical management Contractions equivalent (~30%) Decreased preterm delivery, need for c- section, and recurrent symptoms Fetal loss with LC 0-5% Ideal timing LC/OC 2nd trimester ↓preterm labor (0% vs. 40%) ↓ fetal loss ↓ risk of fetal malformation Technically easier 1st delay to 2nd, 3rd delay to postpartum ERCP can be performed safely with: Low radiation exposure ▪ Fluoro time 14sec-3.2min ▪ Radiation exposure 40-310 mrad Few complications ~7% Operative considerations Port placement to accommodate uterus Hassan vs. Veress likely equivalent ↓insufflation pressure 10-12 Stones more common in cirrhotics (2x) Diagnosis difficult Pain nonspecific Elevated LFT’s nonspecific Leukocytosis nonspecific GBW thickening nonspecific ▪ HIDA may be helpful Management differences Increased operative risk ▪ Morbidity 3x ▪ Conversion 2x ▪ Bleeding 8x Increased risk with cholecystostomy ▪ Bleeding ▪ Ascites/Leak Mortality Overall acceptable 0.6-0.8% Significantly increased in Child’s C patients (17%) LC safer than OC Less bleeding Shorter OR time Shorter HLOS Possibly lower mortality (open mortality 8-25%) Acalculous cholecystitis M>F 1.5:1 4-8% of all cholecystitis Dx with UTZ/HIDA Gallbladder polyps Gallbladder cancer