Tieman Hepatobiliary DSA Flashcards
Asymptomatic Stones
found incidentally on ultrasound
Chronic cholecystitis (calculous and acalculous)
Biliary Colic
Visceral pain, self-limiting (< 6-8 hours), associated with fats or rich meals,
Few, if any, physical findings or lab abnormalities
Acute cholecystitis (calculous and acalculous)
Often starts out as biliary colic, but pain becomes parietal, persistent and escalating, N&V
PE: Systemic signs of inflammation, localized RUQ tenderness (Murphy’s sign)
Lab: mildly elevated WBC, normal or slightly elevated bilirubin, LFT’s and amylase
Acute acalculous usually in patients very ill with co-existing disease process
Usually a low-flow, ischemic condition
GALLBLADDER DISEASE—DIFFERENTIAL DIAGNOSIS
Chronic: PUD GERD Pancreatitis Kidney pathology Intestinal pathology Lower chest pathology—Cardiac, pulmonary Herpes Zoster
Acute: Appendicitis PTE Perforated duodenal ulcer Diverticulitis Pancreatitis Nephritis, Nephrolithiasis
Ultrasound
Stones vs. no stones
> 90% sensitivity and specificity for cholelithiasis > 2mm
Associated findings, eg. Wall thickness, fluid, dilated CBD, polyps, areas suspicious for CA
Cholescintigraphy (bile duct scan, HIDA scan)
Useful in ? Cases of acute calculous cholecystitis
Non-visualization of GB
Combined with CCK ejection fraction
CCKEF < 35% and producing biliary colic diagnostic for chronic acalculous cholecystitis
CT scan
may be useful to eliminate other conditions in differential diagnosis
treatment of asymptomatic gallbladder disease
and, to whom might we offer surgery?
No treatment—only 2-3%/year become symptomatic, rarely with complications
May offer surgery to: Sickle cell patients Native americans with large stones (risk of CA) Porcelain Gallbladder (risk of CA) Gallbladder polyps > 1cm (risk of CA) Pt. with abnormal pancreatic duct drainage (risk of CA) Transplant patients (Immunosupression) People traveling to remote areas
GALLBLADDER DISEASETREATMENT- Chronic acalculous and calculous
Biliary Colic
30% may have only one attack
70% will have recurrent attacks, usually more frequent and severe
1-2%/year will develop complications
This group clearly benefits from laparoscopic cholecystectomy
GALLBLADDER DISEASETREATMENT- Acute calculous cholecystitis
Hospitalization Pain control Rehydration Broad-spectrum antibiotics Laparoscopic cholecystectomy
GALLBLADDER DISEASETREATMENT - Acute acalculous cholecystitis
Usually already hospitalized for another reason
Broad-spectrum antibiotics
Laparoscopic cholecystectomy, if acceptable surgical risk
Percutaneous GB drainage, if unacceptable risk
CHOLEDOCHOLITHIASIS AND CHOLANGITIS- clinical picture
15% of patients with cholelithiasis also have choledocholithiasis
Routine vs. selective intraoperative cholangiogram debated among surgeons
Retained or recurrent stone
Clinical picture may range from asymptomatic to life-threatening
Major complications are obstruction, pancreatitis and ascending (suppurative) cholangitis
CHOLEDOCHOLITHIASIS AND CHOLANGITIS- SIGNS AND SYMPTOMS
Choledocholithiasis
- Abdominal pain
- Jaundice
- Pruritis
- Acholic stools
Ascending (suppurative) cholangitis
- Charcot’s Triad—RUQ abd. pain, jaundice and fever with shaking chills
- Reynold’s pentad—Charcot’s triad + hypotension and altered sensorium
CHOLEDOCHOLITHIASIS AND CHOLANGITIS - DIAGNOSIS
LAB: Bili > 4.0, elevated amylase, elevated AP and GGTP, WBC elevated in cholangitis
US—only 50% accurate in identifying choledocholithiasis, may show ductal dilatation
MRCP
ERCP—advantage of being diagnostic and therapeutic
CHOLEDOCHOLITHIASIS - TREATMENT
CHOLEDOCHOLITHIASIS
Most, if not all, common duct stones should be removed because of the risk and severity of complications
At surgery, stones may be removed laparoscopically or by open surgery
ERCP with sphincterotomy and stone removal by balloon or basket
cholangitis treatment
Hydration, broad-spectrum antibiotics, ductal drainage (urgent, if Reynold’s Pentad present)
ERCP
PTC
Open surgery
CHOLESTASIS- definition
The systemic retention of biliary constituents as a result of failure of formation and (or) the flow of bile
intrahepatic vs extrahepatic cholestasis
INTRAHEPATIC
Usually a failure of formation of bile at the hepatocyte level
Elevated transaminases and unconjugated bilirubin
Can also be an obstructive process confined to the intrahepatic bile ducts
EXTRAHEPATIC
Obstructive process of the extrahepatic bile ducts
Elevated AP, GGTP and conjugated bilirubin
Neonatal obstructive jaundice
Must be considered in any newborn jaundice presenting or persisting after 14 days old
Elevated conjugated bilirubin, AP, GGTP
Often, but not always, with acholic stools
Most common causes are
Biliary atresia
Less common causes are congenital biliary tract anomalies, choledochal cysts, and infections
BILIARY ATRESIA
Post-natal destruction of EH bile ducts with resultant injury and fibrosis of IH bile ducts
Unknown etiology
~30% of neo-natal cholestatic jaundice
Females > males
Associated with extra-hepatic anomalies
Most common cause of hepatic death and reason for liver transplantation in children
Diagnosed by lab, US, MRC and liver bx
Treated by Porto-enterostomy (Kasai procedure)
Best results if done at < 60 days of age
If Kasai procedure fails, liver transplant
CHOLEDOCHAL CYSTS
Less common cause of pediatric obstructive jaundice (2-4%)
5 types—type V (intrahepatic) called Caroli’s disease
60-70% are found at age <10
Present with obstructive jaundice, acholic stools, pruritis, abd. pain, and/or fever
Diagnosed by typical lab pattern of obstructive jaundice, US, MRCP, and ERCP
Should usually be surgically resected because of risk of malignancy and cholangitis
PRIMARY SCLEROSING CHOLANGITIS
Auto-immune disease
Patchy inflammation, fibrosis and destruction of IH and EH bile ducts
Obstruction—cirrhosis—liver failure
Young patient (25-45 year olds)
2:1 men:women
*** 80% have IBD (2-4% of IBD patients develop PSC)
PRIMARY SCLEROSING CHOLANGITIS– things we must differentiate it from
Must differentiate from Primary Biliary Cirrhosis (women ages 20-60, intrahepatic ductal fibrosis)
Antibodies somewhat helpful
Anti-nuclear and anti-smooth muscle + in ~20%
Anti-mitochondrial rarely +, if + that suggests PBC
pANCA + if colitis present, but doesn’t distinguish from colitis w/o PSC
Usually requires MRCP or ERCP and liver biopsy for definitive diagnosis
Must be differentiated from Secondary Sclerosing Cholangitis Post-surgical trauma Infection Toxins Cholangiocarcinoma Aids-associated cholangiopathy
PRIMARY SCLEROSING CHOLANGITIS- treatment
Asymptomatic
- No specific treatment
Mild-moderate symptoms
- Medical treatment of jaundice, pruritis, cholangitis
- Monitor for colonic neoplasia and IBD
- Monitor for cholangiocarcinoma (6-11% in PSC)
Severe symptoms or liver failure
- Liver transplant
- – Excellent survival unless cholangiocarcinoma has developed
