| What is biliary pain? | Most common presenting symptom of cholelithiasis, 75% of symptomatic gall stone pts seek medical attention for episodic abdominal pain |
| How is the pathogenesis of biliary pain? | Caused by intermittent obstruction of bile duct by 1 more more stones.
Most common histologic changes are fibrosis of gall bladder wall, chronic inflammatory cell infiltrate, and intact mucosa.
Recurrent episodes can be associated with scarred shrunken gall bladder and Rokitansky-Aschuff sinus (intramural diverticula) |
| What are the clinical features of biliary pain? | Biliary colic since pain is steady and not intermittent.
Increases gradually over a period of 15 minutes to an hour, then resolves slowly.
If it lasts more than 6 hours we have acute cholecystitis instead of simple biliary pain.
Felt maximally at epigastrum , RUQ, LUQ, and precordium/ lower abdomen.
May radiate to scapula/ right shoulder/ lower abdomen. and accompany diaphoresis/ nausea/ vomit. |
| What are the physical exam findings of biliary pain? | Normal, mild to moderate gallbladder tenderness during attack and mild residual tenderness after attack for several days. |
| How is the dx of biliary pain? | For uncomplicated biliary pain (first time) usually labs are normal.
Imaging needed is US of RUQ |
| What is the differential dx of biliary pain? | GERD, peptic ulcer, pancreatitis, renal colic, diverticulitis, colon carcinoma, IBS, radiculopathy, angina pectoris. |
| What is the treatment of biliary pain? | Aspirin prophylaxis prevents gall stone formation and pain.
Recurrent episodes pt get elective laparoscopic cholecystectomy. |
| What is acute cholecystitis? | Most common complication of gallstone disease |
| How is the pathogenesis of acute cholecystitis? | When stone is embedded in cystic duct, and causes chronic obstruction rather than transient biliary pain.
Stasis of bile results in damage of gall bladder mucosa, and release of intracellular enzymes and inflammatory cascades.
Enteric bacteria can be cultured from gall bladder bile in half of pt w/acute cholecystitis.
Cause of obstruction is stone in cystic duct/ gall bladder neck/ Hartman's pouch (90%).
It is a disease of the young, healthy women w/ good prognosis.
remaining 10% have absence of gall stones (acalculous cholecystitis) and occurs more for critically ill pts. |
| What is the pathology caused by acute cholecystitis? | Usually gallbladder distention, stone in cystic duct, after opened we see inflammatory exudate and pus (rarely)
Later disease, bile pigments are replaced by thin mucoid pus/blood.
If left untreated, and cystic duct still obstructed, lumen of gall bladder is distended and w/clear mucoid fluid (hydrops of gallbladder)
If resected and no gall stones, we should look for vasculitis/ cholesterol embolus. |
| What are the clinical features of acute cholecystitis? | 75% report prior biliary pain, for more than 6 hours (sus of cholecystitis)
Resolves w/out complications in 84% of pt, but get gangrenous cholecystitis (7%) empyema (6%), perforation (3%) and emphysema (<1%) |
| What are physical exam findings in acute cholecystitis? | Fever (common), serum bilirubin <4, right subcostal tenderness w/palpable gall bladder, and murphy's sign (specific)
Leukocytosis is common for dx. |
| How is dx of acute cholecystitis? | Leukocytosis (lab)
Radio: US most useful, murphy's sign (focal bladder tenderness under sonography 90% acute cholecystitis)
US also detects nonspecific findings suggesting it, such as pericholecystic fluid/ wall thickness (>4mm) but they lose their specificity if pt has ascites or hypoalbuminemia (suggesting liver disease)
CT: for detection of complications |
| How is the treatment of acute cholecystitis? | Hospitalization, fluids and electrolytes IV, broad-spectrum Abx (pipercillin-tazobactam, ceftriaxone, metronidazole, levofloxacin)
Cholecystectomy is definitive therapy (laparoscopic) |
| What is Choledocolithiasis? | Life-threatening complications like cholangitis and acute pancreatitis (if symptomatic) so needs direct intervention. |
| How is pathogenesis of choledocholithiasis? | Gall stones pass to bile duct, or de novo form in duct.
All of one type (cholesterol or pigment), cholesterol stones form only in gall bladder (not de novo) black pigment stones rarely merge to duct from gall bladder, majority are soft brown pigment stones (de novo from bacterial actions on phospholipids and bilirubin in bile).
15% of pt w/gall bladder stones also have bile duct stones, but pt w/ductal stones 95% also have gallstones |
| What are the clinical features of choledocholithiasis? | Acute obstruction causes biliary pain and jaundice, gradual obstruction causes pruritis and jaundice alone w/out pain.
If bacteria enter, we might see cholangitis, long standing obstruction can cause secondary biliary cirrhosis, thus chronic liver disease.
Serum bilirubin 2-5 mg/dl, rarely exceed 12mg/dl.
Transient spikes of ALT/amylase suggest bile stone went to duodenum, liver biochemical tests sensitivity is 94% to detect choledocholithiasis. |
| How is the dx of choledocholethiasis? | US (visualizes stones in only 50% cases, but can see dilation of duct 75%, cannot exclude it definitely)
MRCP (non invasive, visualizes duct more accurately, can exclude or confirm choledocholithiasis)
EUS (more invasive than US, visualizes duct more accurately, sensitivity 98% compared w/ERCP)
If low probability we use EUS/MRCP (less invasive than ERCP)
ERCP (sensitive and specific 95%, but only therapeutic usually) |
| What is the tx of choledocholithiasis? | ERCP remove stone, cholecystectomy needed to stop recurrent episodes in only 10% of cases, high risk pt we may use endoscopic removal of stones w/out cholecystectomy |
| What is cholangitis? | Of all the common complications of gallstones, the most serious and lethal is acute bacterial cholangitis. |
| What are etiologies causing cholangitis? | 85% stone in bile duct causing bile stasis, other causes are neoplasms, strictures, parasitic infection, congenital abnormalities of duct.
Degree of bacterial entry into hepatic venous blood is indicator of the degree of obstruction and biliary pressure.
Bacteria in bile are E.coli, Klebsiella, Pseudomonas, Proteus, Enterococci, anaerobics (15% ONLY) C.perfingens and Bacteroides |
| What are the clinical features of cholangitis? | Charcot's triad (RUQ pain, Jaundice and Fever- present in only 70%)
Pain can be mild and transient (w/ chills and rigors maybe)
Bilirubin 2mg/dl in 80% of cases, WBW elevated 80% of cases, ALP elevated, culture positive of enteric bacteria |
| How is the dx of cholangitis? | EUS and MRCP (better than CT), ERCP therapeutic drainage of infected bile (life saving), if ERCP unsuccessful use THC |
| What is the tx of cholangitis? | Culture is needed to determine needed Abx, improvement in 6-12 hours if infection under control, use ERCP/ decompress bile duct using intrabiliary stent.
Relief of symptoms and leukocytosis w/in 2-3days |
