Lecture 5: Diseases of the Biliary Tract

Osteopathic findings in gallbladder disease

Referred pain (mid-thoracic region; R shoulder and tip of the R scapula)

Somatic dysfunction T5-9 on the R

Restriction of the celiac ganglion

If the diaphragm is significantly irritated, findings at C3-5

Suspect Acute Cholecystitis if at least one in each category is present

Signs of local inflammation: Murphy sign, RUQ mass, pain or tenderness

Signs of systemic inflammation: Fever, ↑ WBC, ↑ C-reactive protein

Characteristic imaging findings

Cholelithiasis

Gallstones

Cholecystitis

Gallbladder Inflammation

Choledocholithiasis

Common bile duct stones

Cholangitis

Inflammation/infection of the biliary tree

Biliary colic

Pain due to gallbladder contraction or stones/sludge

Most accurate predictor of gallstone disease

Functional gallbladder disorder

Biliary pain in the absence of gallstones/sludge

LFT’s are normal

May have low ejection fraction of the GB

Cholecystectomy

Removal of the GB

Cholelithiasis Pathogenesis

Bile produced in liver; secreted into hepatic duct; stored in gallbladder; released into duodenum to digest fats

Bile= cholesterol + lecithin + bile acids

Cholesterol insoluble so lecithin & bile acids make micelles to keep it soluble

If too much cholesterol or too little bile acids/salts, → Cholesterol supersaturation → crystals → gallstones

Decrease gallbladder motility → sludging

In the cystic duct, cause biliary colic or cholecystitis

In common bile duct, cause cholangitis and/or pancreatitis

Cholelithiasis Risk Factors

Obesity → Increase Cholesterol secretion

Increasing age

Women

Genetics

NAFLD, Hepatitis B + C, Cirrhosis → ↓ synthesis of bile salts

Postmenopausal hormone therapy or pregnancy (estrogen ↑ chol; progesterone ↓ bile salts & slows emptying)

Bariatric surgery- gallbladder stasis

Diabetes (↑l ipids; neuropathy→ gb hypomotility and biliary stasis)

Crohn’s (bile salts not resorbed)

Drugs: Ceftriaxone

Spinal cord injuries (gallbladder less motile; bile stasis occurs

Cholesterol Stones

Most common stone in adults

Cholesterol > bile acid

Common in adults with diabetes, obesity, hyperlipidemia, or multiparity

Pigment Stones

Black:

Most common stone in children

Due to hemolytic states; unconj. bilirubin precipitates; primarily made of Ca bilirubinate

Sickle cell patients

Radiopaque (Fe from the hemolyzed RBC’s shows up)

Brown: Radiolucent; infection

Symptomatic Cholelithiasis

Transient obstruction of cystic duct

Biliary colic

Epigastric/RUQ dull pressure/pain; typically lasts ~30 mins, but can last a few hrs

Usually occurs 1-2 hrs postprandial OR nocturnal

Can be triggered by a fatty meal

May radiate to the back & be assoc. with N/V

Can go hrs or years between attacks; most within 2 yrs

Not relieved or exacerbated by movement or flatus/Bowel movements

Abdominal Ultrasound most accurate if fasting >8 hrs, as stones are best seen in a distended GB filled with bile

Stones cast shadow + move around

Cholelithiasis

Cholelithiasis

Cholelithiasis

Cholelithiasis

Calcified gallstones in gallbladder, cystic duct, and common bile duct

If no stones on US, but biliary colic

Endoscopic ultrasound

Transducer on tip of endoscope

More sensitive for sludge & small stones

Can exclude PUD

Magnetic Resonance Cholangiopancreatography (MRCP)

Noninvasive

Alternative if US negative

Common bile duct stone

Therapy for cholelithiasis

Symptomatic:

Acute episode: IM NSAID (diclofenac), hydration, antiemetics, followed by po NSAIDS

Diclofenac ↓ progression to cholecystitis

Definitive: Laparoscopic Cholecystectomy

Asymptomatic:

Observe

Surgery in Hemolytic/sickle cell anemia, organ transplant, ↑ risk of cancer (porcelain gallbladder, large/growing polyps)

Cholelithiasis Therapy

Oral bile acid litholysis with urso-deoxycholic acid (UDCA)

Reserved for those who can’t tolerate or refuse surgery

Complications of Gallstones

Acute Cholestasis/cholecystitis/cholangitis

Chronic cholecystitis

Gallstone Ileus- Large stone erodes through GB wall into duodenum → obstructs small bowel → Enterolithotomy

Choledocholithiasis (common bile duct stone)

Gangrene of gallbladder, perforation

Pancreatitis

Gallstone Ileus

Gallstone Ileus

When do you hospitalize a patient with biliary disease?

Intractable pain

Intractable vomiting → dehydration

Evidence of cholecystitis, cholangitis, or pancreatitis

Acute Cholecystitis Pathogenesis

Usually caused by stones impacted in cystic duct

Obstruction→↑ intraluminal pressure & supersaturated bile

Static bile→ inflammation→ distention→ poor drainage & blood flow→ infection

Acute Cholecystitis

Begins with biliary colic and becomes steady, severe RUQ pain → radiation to R shoulder and back (>6 hrs)

Ill appearing, lying still, febrile, tachycardic

N/V

Fever

Murphy’s sign: Hand placed under ribcage & pt. asked to take deep breath → as GB descends & contacts hand, pain is elicited, and breath is held

Can also be elicited sonographically

Leukocytosis, ↑ CRP (>3 mg/dl)

US—distended GB & cystic duct w/ stones, thickened wall, sonographic Murphy’s, pericholecystic fluid

Acute Cholecystitis

Thickened wall, double wall sign, sludge & stones with acoustic shadowing

HIDA

HIDA (99m technetium-labeled hepatobiliary imaging using iminodiacetic acid) / Cholescintigraphy / hepatobiliary scintigraphy

Demonstrates obstructed cystic or common bile duct

Performed if clinically cholecystitis and US is nondiagnostic

IV injected isotope “follows” bile

Liver is not visualized → liver disease

Gallbladder not visualized → cystic duct obstructed

Small bowel not visualized → common duct obstructed

If both gallbladder and small bowel are visualized with the HIDA scan, CCK can be injected to see if it functions well

Ejection fraction <35% =poorly functioning GB

Acute Cholecystitis Treatment

NPO

IV fluids/correct electrolytes

Analgesics

Antiemetic & NG tube if vomiting

Empiric antibiotics if suspected infection

Early cholecystectomy (<72 hrs)

Complications of Acute Cholecystitis

Gangrene

Perforation

Cholecystoenteric fistula—Perf into bowel

Gallstone ileus

Emphysematous cholecystitis—Crepitus in abdominal wall next to gallbladder

Caused by gas-forming Clostridium welchii

Chronic Cholecystitis

Multiple episodes of acute disease or chronic irritation by stones leads to thickening and fibrosis

Choledocholithiasis

Past history of colicky pain-now sudden onset severe pain RUQ w/ radiation

N/V

Fever if cholangitis

Obstructive jaundice → pale stools, dark urine

May develop pancreatitis

Elevated conjugated (direct) bilirubin

Elevated alkaline phosphatase

Amylase/lipase elevated if pancreatitis

Leukocytosis if also cholangitis

GGT must be elevated

Choledocholithiasis Imaging

US: Dilated ducts and possibly stones

CT: Dilated ducts, but stones are isodense with bile so can’t be seen

MRCP

Endoscopic US

Endosonographic image of stone in common bile duct (with acoustic shadow)

ERCP (endoscopic retrograde cholangiopancreatography)

With endoscope, cannulate duodenal papillae and view biliary & pancreatic tree

If stones present, can be removed

Allows treatment at same time as dx

Often done intraoperatively during a lap chole

Potential complication: Pancreatitis

MRCP or endoscopic US can be done first for dx, only doing ERCP if needed for stone removal

ERCP

Choledocholithiasis Treatment

IV fluids

Bedrest

Control N/V

Pain control

lap chole with intraoperative ERCP

Even if the patient is asymptomatic (unlikely), the stones must be removed

Acute Cholangitis

Ascending infection

From any obstruction of flow of bile

Serious (hypotension altered mental status); can be fatal

Infection in the biliary tree, obstruction from stones, strictures, cancer

Can lead to sepsis & death

Organisms are usually colonic origin- bacteria from duodenum can ascend through the sphincter of Oddi area after sphinterotomy, stent, or other disruption

Some bacteria passes through on its own and a stone in the common duct then acts as a nidus for infection

Charcot’s Triad

RUQ pain

Fever + Chills

Jaundice

Reynold’s Pentad

Obstructive cholangitis/high mortality

Charcot’s Triad PLUS

Mental status changes

Hypotension

Cholangitis Labs and Imaging

Leukocytosis, elevated alkaline phosphatase, GGT, & direct bilirubin; blood cultures

US: Common bile duct dilation & stones

CT with IV contrast or MRCP: Determine level & cause of obstruction

Cholangitis Treatment

ERCP with sphincterotomy (severing muscle fibers of sphincter of Oddi to enlarge outlet of biliary tree), stone removal, and biliary drainage/stent

Antibiotics

IV fluids

NPO

Common Bile Duct Stones

Primary Sclerosing Cholangitis

Primary Sclerosing Cholangitis

Rare, immune-mediated, men

Ulcerative colitis

Fibrosis of extra & intrahepatic bile ducts → obstructive jaundice

String of beads

Primary Biliary Cholangitis

Chronic autoimmune disease

Women >45

Inflammation/destruction/fibrosis of bile ducts (intrahepatic only)

Leads to scarring & cirrhosis

Porcelain (calcified) gallbladder

Porcelain (calcified) gallbladder

Chronic cholecystitis

Small risk for cancer

Fitz-Hugh-Curtis syndrome

Perihepatitis (inflammation of the liver capsule

Gynecologic pain