The gallbladder, gallstones, and beyond….

The gallbladder, gallstones, and beyond….

The gallbladder, gallstones, and beyond. Leslie Kobayashi, MD January 31, 2012 Anatomy Liver Bile ducts Pancreas Duodenum Transverse colon

Anatomy Fundus Body Infundibulum/Neck Cystic duct Spiral Valves of Heister

Anatomy Triangle of calot Borders: CHD, cystic duct, liver edge Contents: Cystic artery, node of Calot Ductal Anatomy

Right and Left Hepatic Common Hepatic duct Cystic duct Common bile duct ducts Aberrant anatomy Vascular Normally (>90%)

cystic a. arises from RHA Replaced right hepatic a. Replaced left hepatic a. Bile 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 Bile 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 GB 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 Significance

Do gallbladder problems create a significant healthcare burden? YES! Health burden

6.2 Billion$ in US 1.8 million ambulatory care visits Increased 20% since 1980s Cholecystectomy most common elective abdominal procedure in the US 750,000 annually Why does that happen? Stones

Types of stones Cholesterol stones (75%) Female fat fertile Black stones (20%) Hemolytic diseases (Sickle cell disease) Cirrhosis

Brown stones (5%) Infection PSC *primarily form in the ducts Cholesterol stones

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, TGs, HDL, Spinal cord injury Cholesterol stones 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 Cholesterol stones Increase risk of stone formation

TPN Octreotide Ceftriaxone Decrease Statins ?ursodiol risk of stone formation Pigmented stones Often

radiopaque due to calcium bilirubinate, calcium fatty acid soaps and inorganic calcium salts Two types Black Brown

Pigmented stones Black Form in GB Bile sterile Associated with age, hemolytic DOs, alcoholism, cirrhosis, Gilberts syndrome, Cystic fibrosis, pancreatitis and TPN Cholecystectomy curative Pigmented stones

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 Stones: Where do they

go? And what do they do? Biliary colic Cholecystit is GS

P Choledocho Cholangitis In the gallbladder Incidence: 10-30% of the population Asymptomatic Symptomatic

(80%) (1-3% per year) No inflammation: Biliary colic +inflammation: acute cholecystitis +obstruction : choledocholithiasis, GSP +obstruction+inflammation: cholangitis Biliary colic History

Transient abdominal pain Occurs after fatty meals Exam Benign Labs Normal Ultrasound GS

Hyperechoic masses, dependent in location Acoustic shadowing Cholecystitis History Prolonged pain Fevers

Nausea/emesis Exam Fever, tachycardia RUQ TTP, Murphys sign Labs Leukocytosis Mild LFTs Imaging

Ultrasound HIDA Cholecystitis Gallstones Obstruction of gallbladder Obstruction causes inflammation Inflamed wall is thickened

Edema or emphysema of GBW Cholecystitis Inflammation may or may not be associated with infection 50-70% of bile cultures are positive E. coli, Klebsiella,

Streptococcus, Enterobacter Ultrasound 95% sensitivity/specificity Signs of cholecystitis Gallstones

GBW >3mm Pericholecystic fluid GBW striations or air within GBW Sonographic Murphys sign GS with GBW thickening Normal GBW <3mm Pericholecystic fluid

HIDA Cholescintigraphy: Injection of Tc99 labeled hydroxyl iminodiacetic acid HIDAhepatocytessecreted into bile Normal visualization of GB, CBD

and SB within 30-60 min +scan if no visualization of GB HIDA Normal HIDA Positive HIDA Rim sign *Sphincter, CBD

HIDA 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 Cholecystitis: Complications 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 Gallstone ileus Complications Cystic duct obstruction Hydrops Bile is absorbed but GB

mucosa continues to secrete mucus GB tense, filled with mucinous fluid Complications Mirrizis 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 What if the stones escape the GB? Stones in the CBD Choledocholithiasis

History: jaundice, icterus, pruritis, dark urine, steatorrhea, acholic stools, bleeding Exam: jaundice, icterus, RUQ pain, Murphys sign Labs Elevated LFTs, INR Elevated bilirubin highest PPV 25-50% May be normal in up to 30% of patients

Choledocholithiasis 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 Cholangitis History/Exam: similar to choledocholithiasis with sepsis, septic shock Labs/Imaging:

similar to choledocholithiasis with leukocytosis, RUQ pain, fevers, bactermia, MSOF jaundice Triad + MS, shockMS, shock Charcots triad Reynolds

pentad Beyond the CBD Gallstone pancreatitis History: epigastric pain, nausea/emesis Exam: RUQ/epigastric TTP, SIRS Labs: amylase/lipase 3x nl,

LFTs, leukocytosis Imaging: CBD dilation, pancreatic edema, necrosis, fluid collection Ransons criteriaAlcoholic First 24hours: 48 hours

Glucose >200 Age >55 Ca <8 Hct>10 LDH>350 PaO2 <60 AST>250

BUN>5 WBC>16k Base Deficit >4 Sequestration >6L Ransons criteria-NonAlcoholic First 24hours:

48 hours Glucose >220 Age >70 Ca <8 Hct>10 LDH>400

PaO2 <60 AST>440 BUN>2 WBC>18k Base Deficit >5 Sequestration >6L

Ransons criteria Each category 0 or Add up total points Mortality 0-2 <5% 3-4 15% 5-6 40% 7-8 ~100% 1 Treatments

Treatment Medical Surgical Lap Open CBDE ERCP sphincterotom y,

stent Percutaneous Cholecystosto my tube Treating the gallbladder Gallstone Cleanse 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 juice 1 liter jar with lid

Medical Or you could try: IVF hydration Antibiotics Bowel rest Medical 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 LFTs in PSC/cirrhotics, may stones/sludge on UTZ, does not symptoms, prevent need for OR, stones

recur after cessation of medication Medical Diet: Treatment Failure of medical management in acute cholecystitis 32% Recurrence

Surgical rate of GSP 29-63% management results in reduced HLOS Treatment 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 sxs No difference in conversion rates or CBD injury Treatment Timing

of surgery for GSP Early operation safe with mild pancreatitis Rasons criteria <3 Increased conversion rate, HLOS, and operative complications in early operation in severe pancreatitis Ransons criteria 3 Surgical approaches

Laparoscopic 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 Laparoscopic Retraction and dissection of Triangle of Calot prior to Gallbladder removal from fossa CD

may be clipped, sutured, tied, stapled Remove gallbladder in fundusdome direction Open 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 Lap vs. open

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 Difficult Cholecystectomy RFs 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

Other options Cholecystostomy tube 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% Clearing the duct Natural history of CBD stones Choledocholithiasis Stones in CBD in 10-15% of symptomatic pts 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

Surgical approaches CBDE Can be performed lap or open Transcystic or via choledochotomy

Surgical approaches CBDE Imaging duct Fluorscopic guidance Choledochoscopy Clearing duct Basket, snare, flush +/- glucagon to relax sphincter Surgical approaches

CBDE Completion cholangiogram Clip, tie or staple cystic duct stump Close choledochotomy over T-tube +/-drain external Success rate of duct clearance 75- 95% ERCP Efficacy

1 procedure: 71-75% Multiple procedures: 84-95% Mortality 0.2-0.5% Complication Perforation Bleeding Pancreatitis Cholangitis

rate 5-8% Complications Complications 1-2% of patients will represent with CBD stone following cholecystectomy Dx <2yrs post-op = retained

stone Dx > 2yrs post-op =recurrent stone Other Complications Ileus Incisional/port site Wound infection Abscess hernia

Biloma/bile leak CBD Injury Strasberg-Bismuth classification A-CD stump, fossa B/C-aberrant RHD D-lateral injury

E-circumferential injury to major duct Special circumstances Pregnancy 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 Pregnancy

Biliary disease the most common non-obstetrical cause of maternal hospitalization Cholecystitis most common 40% GSP 30% CBD stone 20%

Biliary colic 10% Pregnancy If symptomatic risk of recurrence high 40%-70% recur prior to delivery If symptomatic risk of fetal

loss high 10-20% Pregnancy Treatment goals Treat infection Maintain nutrition Prevent contractions/preterm labor Prevent fetal loss Prevent maternal

morbidity/mortality Pregnancy 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% Pregnancy 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 Pregnancy ERCP can be performed

safely with: Low radiation exposure Fluoro time 14sec-3.2min Radiation exposure 40-310 mrad Few complications ~7% Pregnancy Operative considerations

Port placement to accommodate uterus Hassan vs. Veress likely equivalent insufflation pressure 10-12 Cirrhotics Stones more common in cirrhotics

(2x) Diagnosis difficult Pain nonspecific Elevated LFTs nonspecific Leukocytosis nonspecific GBW thickening nonspecific HIDA may be helpful Cirrhotics Management differences

Increased operative risk Morbidity 3x Conversion 2x Bleeding 8x Increased risk with cholecystostomy Bleeding Ascites/Leak

Cirrhotics Mortality Overall acceptable 0.6-0.8% Significantly increased in Childs C patients (17%) LC safer than OC Less bleeding Shorter OR time

Shorter HLOS Possibly lower mortality (open mortality 8-25%) Other pathology Acalculous cholecystitis M>F 1.5:1 4-8% of all cholecystitis

Dx with UTZ/HIDA Gallbladder polyps Gallbladder cancer Thank You

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