CHOLELITHIASIS

INTRODUCTION DEFINITIONS

Colic: temporary blockage by a stone Cholecystitis: inflammation of the gallbladder Cholangitis: inflammation of the biliary tree Choledocholithiasis: stones in the common bile duct not necessarily obstructive

PATHOPHYSIOLOGY

3 types of stones: formation is caused by crystallization of bile (bile acids, lethicin & phospholipids) Cholesterol (70%): excess cholesterol secretion & inadequate bile secretion Pigment (15%): calcium bilirubinate; with hemolytic disorders, cirrhosis & parasitic infections Mixed

Impaired motility can predispose to stone formation Sludge is crystals without stones. It may be a first step in stone formation, or independent of it. It can be seen on U/S.
EPIDEMIOLOGY

20 million have GS 1-2% develop GS each year Asymptomatic stones are not associated with fatalities

ETHNICITY

Highest in fair skinned people i.e. of Northern European descent & Hispanic populations Asians are more likely to develop pigmented stones African descent with sickle cell anemia

GENDER

More common in women Internationally: 20% of women, 14% of men May be due to estrogen effect of cholesterol production/progesterone effect on cholesterol stasis Pregnant are more likely to be symptomatic Higher risk with multiple pregnancies, OCP, hormone replacement therapy

AGE

Uncommon in children, unless with congenital anomalies/hemolytic disease Incidence increases with age (1-3% per year)

ETIOLOGY/RISK FACTORS

Fair, fat, female, fertile High fat diet Obesity Rapid weight loss TPN (NPO) Ileal disease Increases with age, alcoholism Diabetics have more complications Hemolytics

DIAGNOSIS HISTORY

3 clinical stages: Asymptomatic silent (60-80%); discovered accidently on U/S Symptomatic o Severe colic pain, lasting 1-5 hours, wakes patient up at night o Classic: RUQ pain (esp. once peritoneum is irritated) o Epigastric pain (visceral pain & GB wall distension) o Radiation to shoulder o Small stones are more symptomatic o Severe symptoms develop in 3-9% - cholecystectomy rate of 3-8%/year
Indigestion, bloating, and fatty food intolerance occur in similar frequencies in patients without gallstones, and are not cured with cholecystectomy.

Complicated (20% of symptomatic): Cholecystitis (acute or chronic), cholangitis, CBD stones, pancreatitis, ileus GS Gallstones increase the risk of GB carcinoma

PHYSICAL EXAMINATION

If asymptomatic: vital signs are completely normal Symptomatic: Murphys sign Fever, tachycardia and hypotension suggest more sever conditions; cholangitis, cholecystitis etc.

DIFFERENTIAL DIAGNOSIS

 WORK

AAA Appendicitis Diverticulitis Cholangitis Gastroenteritis Hepatitis UP

IBD Mesenteric ischemia Small bowel obstruction Pancreatitis Renal colic Pneumonia

LAB TESTS

o Asymptomatic: all normal o WBC is not reliable (>11,000 only in 60%) >15,000 suggests perforation o ALT, AST, ALP suggest CBD stones o Amylase elevation suggest GS pancreatitis
IMAGING

o U/S & HIDA (scintigraphy): Best. Plain x-ray, CT & ERCP: adjuncts. o U/S Sensitive & specific (94%, 80%) Wall thickening 2-4 mm (false positives) Sonographic Murphys Distension Pericholecystic fluid Dilated CBD 7-8 mm o HIDA scan: cystic duct patency Very sensitive, specific (94%, 85%) GB should be visualized 30 minutes after injection, if not: Cholecystitis Cystic duct obstruction CBD obstruction if small intestines are not visualized False positives (high bilirubin) o ERCP (endoscopy + fluoroscopy) Diagnostic & therapeutic Visualizes biliary tree Indications: Jaundice. Elevated LFT + dilated CBD Complications: bleeding, perforation, pancreatitis, cholangitis o CT (best?) Misses 20% of stones For complications Ductal dilatation Surrounding organs If Dx uncertain

EMERGENCY

o Suspect GB colic if: RUQ pain, 4-6 hrs, radiating to back o Acute cholecystitis if pain is of longer duration +/- fever o After assessment of ABCs, perform standard IV, pulse oximetry, EKG, and monitoring. Send labs immediately Include cultures if febrile o Elderly and diabetics cannot tolerate delay in diagnosis and can rapidly progress to sepsis PRIMARY GOAL OF ER CARE IS DIAGNOSIS OF ACUTE CHOLECYSTITIS WITH LABS, US, AND/OR HIDA. Acute cholecystitis & hypotension: admit to ICU and give inotrops (stabilize) then relieve obstruction o Once diagnosed, admission is usually necessary If unstable or in severe pain consider bedside U/S to rule out AAA and confirm diagnosis of acute cholecystitis Replace volume with IVF, NPO +/- NGT Administer pain control early
MEDICATIONS

o Anticholinergics such as Bentyl (dicyclomine hydrochloride) to decrease GB and biliary tree tone. o Demerol o Antiemetics (phenergan, compazine). o Antibiotics (Zosyn) need to cover E. coli (39%), Klebsiella (54%), Enterobacter (34%), Enterococci, group D strep.
CHOLECYSTECTOMY

o Cholecystectomy can be performed after the first 24-48 hours or after the inflammation has subsided. o Unstable patients may need more urgent interventions with ERCP, percutaneous drainage, or cholecystectomy. o Laparoscopic cholecystectomy: very effective with few complications (4%). 5% convert to open. In acute setting up to 50% open.

OUTPATIENT

Afebrile, normal VS Minimal pain and tenderness No markedly abnormal labs, normal CBD, no pericholecystic fluid No underlying medical problems. Next day follow-up visit Discharge on oral antibiotics & pain medications

COMPLICATIONS

Cholangitis: Charcots triad (RUQ pain, jaundice and fever) Sepsis Pancreatitis Perforation (10%) GS ileus (mortality 20% as diagnosis difficult) Hepatitis Choledocholithiasis

PROGNOSIS

Uncomplicated cholecystitis as a low mortality Emphysematous GB mortality is 15% Perforation of GB occurs in 3-15% with up to 60% mortality Gangrenous GB 25% mortality.