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CHAPTER 32 - GALLBLADDER 2.

sympathetic branches that pass through the celiac plexus


ANATOMY
 pear-shaped sac  Preganglionic sympathetic level: T8 & T9
 7-10cm long  Impulses from the liver, gallbladder, & bile ducts pass by means of
 average capacity: 30-50mL sympathetic afferent fibers through the splanchnic nerves &
o obstruction: can distend markedly & contain up to 300mL mediate the pain of biliary colic
 location: fossa on the inferior surface of the liver
o divides the liver into right & left liver lobes Bile Ducts
 4 anatomic areas o R + L hepatic duct = CHD + cystic duct = CBD/choledochus
1. fundus: consist of:
a. rounded, blind end 1. Right & left hepatic ducts
b. normally extends 1-2cm beyond the liver's margin a. LHD longer than the right
o greater propensity for dilatation as a consequence of
c. contains most of the smooth muscles of the organ distal obstruction
2. corpus (body): 2. CHD
a. main storage area & contains most of the elastic tissue a. 1-4cm in length
b. extends from the fundus and tapers into the neck b. Diameter: 4mm

3. infundibulum: c. lies in front of the portal vein & to the right of the hepatic artery
a. convexity of neck 3. Cystic duct
b. a.k.a. Hartmann's pouch a. joins CHD at an acute angle to form CBD
4. neck: b. length is quite variable
a. funnel-shaped area that connects with the cystic duct c. Variations of its point of union with the CHD: surgically impt
b. lies in the deepest part of the gallbladder fossa d. spiral valves of Heister: variable # of mucosal folds at a
c. extends into the free portion of the hepatoduodenal ligament segment of the cystic duct adjacent to the gallbladder neck
o NO valvular fxn
o may make cannulation of the cystic duct difficult

 Same peritoneal lining that covers the liver covers the fundus &
4. CBD or choledochus
inferior surface of the gallbladder.
 intrahepatic gallbladder: when gallbladder is embedded deep
a. enters the 2nd portion of the duodenum through the sphincter
of Oddi
inside the liver parenchyma b. 7-11cm in length
 lined by a single, highly folded, tall columnar epithelium  c. 5-10mm in diameter
Upper 3rd Middle 3rd Lower 3rd
contains cholesterol & fat globules supraduodenal portion retroduodenal portion pancreatic portion
o tubuloalveolar glands: passes downward in the curves behind the 1st portion curves behind the head of
 secretes mucus free edge of the of the duodenum the pancreas in a groove, or
 found in mucosa lining infundibulum & neck hepatoduodenal ligament to traverses through it
the right of the hepatic diverges laterally from the
 absent: body & fundus artery portal vein & hepatic arteries enters the 2nd part of the
 Muscle layer: circular longitudinal & oblique fibers without well- duodenum
developed layers anterior to the portal vein

 perimuscular subserosa contains: CT, nerves, vessels, d. runs obliquely downward within the wall of the duodenum for 1-
lymphatics, and adipocytes. 2cm before opening on the ampulla of Vater

 covered by the serosa except where the gallbladder is embedded o 10cm distal to the pylorus
in the liver e. 3 configurations of the union of CBD & main pancreatic duct
 lacks a muscularis mucosa & submucosa o 70%: unite outside the duodenal wall & traverse the
 cystic artery: usually a branch of the RHA (>90% of the time) duodenal wall as a single duct
o nearly always found within the hepatocystic triangle (triangle of o 20%: join within the duodenal wall and have a short or no
Calot): common duct, but open through the same opening into the
o cystic duct duodenum
o CHD o 10%: exit via separate openings into the duodenum
o liver margin f. sphincter of Oddi:
o When cystic artery reaches the neck of the gallbladder, it o thick coat of circular smooth muscle, surrounds the CBD at
divides into anterior & posterior divisions the ampulla of Vater
 Venous return: o controls the flow of bile into the duodenum
1. small veins that enter directly into the liver
2. large cystic vein  portal vein
 Lymphatics drain into nodes at the neck of the gallbladder
 Nerves of the gallbladder arise from:
1. vagus
o hepatic branch: supplies cholinergic fibers to the
gallbladder, bile ducts, & liver
o peptide-containing nerves containing agents
g. lined by a columnar mucosa with numerous mucous
glands in the CBD
h. A distinct muscle layer is not present in the human CBD
i. arterial supply to the bile ducts:
o GdA & RHA
o with major trunks running along the medial & lateral walls (3
o'clock and 9 o'clock)
o anastomose freely within the duct walls
j. density of nerve fibers & ganglia ↑ near the sphincter
of Oddi
k. nerve supply to CBD & sphincter of Oddi: same as for
the gallbladder

ANOMALIES
 Isolated congenital absence of the gallbladder:
o very rare → reported incidence: 0.03%
o before making Dx: r/o presence of an intrahepatic bladder or
anomalous position
 Duplication of the gallbladder with 2 separate cavities & 2
separate cystic ducts:
o Incidence: 1:4000 persons
o 2 major varieties:
1. each gallbladder has its own cystic duct that empties
independently into the same or different parts of the
extrahepatic biliary tree (more common)
2. 2 cystic ducts that merge before they enter the CBD
 Left-sided gallbladder with a cystic duct emptying into the
LHD or the CBD & a retrodisplacement of the gallbladder
o both extremely rare PHYSIOLOGY
 Partial or totally intrahepatic gallbladder Bile Formation & Composition
o asso with an ↑ incidence of cholelithiasis  liver  produces (normal adult: 500-1000mL/day) bile
 Small ducts (of Luschka) continuously and excretes  bile canaliculi
o may drain directly from the liver into the body of the gallbladder  Bile secretion: responsive to neurogenic, humoral, & chemical
o If present, but not recognized at the time of a cholecystectomy, a bile stimuli
leak with the accumulation of bile (biloma) o Vagal stimulation: ↑ secretion of bile
 Accessory RHD o Splanchnic nerve stimulation: ↓ bile flow
o 5% of cases
 Anomalies of the hepatic artery & cystic artery:  HCl, partly digested proteins, & FA in the duodenum  stimulate
o Common - 50% secretin release  ↑ bile production & bile flow
o 5%: 2 right hepatic arteries  intact sphincter of Oddi: bile flow is directed into the gallbladder
 1 from the common hepatic artery  BILE
 1 from the SMA o mainly composed of water, electrolytes, bile salts, proteins, lipids, and
o 20%: RHA comes off the SMA bile pigments.
o Na, K, Ca, & Cl: same conc in bile as in plasma or ECF
 may course anterior to the common duct. o pH of hepatic bile:
 may be vulnerable during surgical procedures when it runs  usually neutral or slightly alkaline but varies with diet
parallel to the cystic duct or in the mesentery of the
gallbladder  ↑ in protein: more acidic
o 90%: cystic artery arises from the RHA  Primary bile salts: Cholate & Chenodeoxycholate
 but may arise from the left hepatic, common hepatic, o synthesized from cholesterol
gastroduodenal, or SMA o Conjugated with taurine & glycine
o act within the bile as anions (bile acids) that are balanced by Na
o excreted into the bile by the hepatocyte
o aid in the digestion & absorption of fats in the intestines
 about 80% of the conjugated bile acids: absorbed in the
terminal ileum
 Remainder: dehydroxylated (deconjugated) by gut bacteria 
2⁰ bile acids: Deoxycholate & Lithocholate  absorbed in the
colon  transported to the liver, conjugated  secreted into
the bile
 95% of the bile acid pool: reabsorbed & returned via the
enterohepatic circulation
 5%: excreted in the stool
 Cholesterol & phospholipids: principal lipids found in bile
o synthesis: in part, regulated by bile acids
 color of the bile: d/t presence of the pigment bilirubin
diglucuronide
o metabolic product from the breakdown of Hb
o present in bile in conc 100x greater than in plasma
o bacteria convert it into urobilinogen

Gallbladder Function
 regulate the flow of bile  prevents the regurgitation of duodenal contents into the biliary tree
 main fxn:  diverts bile into the gallbladder.
o to concentrate & store hepatic bile
 complex structure that is fxnally independent from the duodenal
o to deliver bile into the duodenum in response to a meal musculature
1. Absorption & Secretion  creates a high-pressure zone between the bile duct & duodenum.
 fasting state: ~80% of the bile  stored in the gallbladder


4-6mm in length
basal resting pressure of about 13 mmHg above the duodenal pressure.
o Storage: made possible because of the remarkable absorptive
o Manometry: shows phasic contractions
capacity of the gallbladder
o gallbladder mucosa: greatest absorptive power per unit area of any
 Frequency: 4/min

structure in the body  Amplitude: 12-140mmHg


 rapidly absorbs Na, Cl, & water against significant conc
gradients
 spontaneous motility: regulated by the ICC

o rapid absorption: 1 of the mechanisms that prevent a rise in pressure


o Relaxation: ↑ in CCK  diminished amplitude of phasic contractions
& ↓ basal pressure  ↑ flow of bile into the duodenum
within the biliary system under normal circumstances. o During fasting: activity is coordinated with:
 Gradual relaxation + emptying of the gallbladder during the fasting period 1. the periodic partial gallbladder emptying
 maintaining a relatively low intraluminal pressure in the biliary tree. 2. an ↑ in bile flow: during phase II of the migrating myoelectric
 epithelial cells of the gallbladder: secrete at least 2 impt products: motor complexes
1) glycoproteins
2) H+ ions
 mucosal glands in the infundibulum & neck: secrete mucus glycoprotein
o protect the mucosa from the lytic action of bile
o facilitate the passage of bile through the cystic duct
o makes up the colorless "white bile" seen in hydrops of the gallbladder

 transport of H+ ions  ↓ in the gallbladder bile pH  acidification


promotes calcium solubility
2. Motor Activity
 Gallbladder filling: tonic contraction of the sphincter of Oddi creates a
pressure gradient between the bile ducts & gallbladder
 Fasting: In association with phase II of the interdigestive migrating
myenteric motor complex, gallbladder repeatedly empties small volumes of
bile into the duodenum.
o mediated in part by motilin
 In response to a meal: gallbladder empties by a coordinated motor
response of:
1) gallbladder contraction
2) sphincter of Oddi relaxation
 CCK DIAGNOSTIC STUDIES
o 1 of the main stimuli to gallbladder emptying - 1924 - oral cholecystography
o released endogenously in response to a meal - 1950s - biliary scintigraphy & ERC
o peptide that comes from epithelial cells of the upper GIT - Present – UTZ, CT, & MRI
o highest conc: duodenum
Blood Tests
o released into the bloodstream by acid, fat, & AA in the duodenum
- Routine CBC & liver fxn tests
o plasma t1/2: 2-3 mins Cholecystitis ↑ WBC
o metabolized by both the liver & kidneys. Cholangitis ↑ WBC, ↑ bilirubin, ALP, & aminotransferase
o acts directly on smooth muscle receptors of the gallbladder and Cholestasis ↑ bilirubin, ↑ ALP
stimulates gallbladder contraction Serum aminotransferases – N/mildly ↑
o relaxes the terminal bile duct, sphincter of Oddi, & duodenum. Biliary colic or chronic blood tests will typically be normal

o CCK stimulation of the gallbladder & biliary tree: mediated by cholecystitis


cholinergic vagal neurons.
o Vagotomy: ↓ response to CCK stimulation  ↑ size & volume of the Ultrasonography
gallbladder - initial investigation of any px suspected of dse of the biliary tree
 When stimulated by eating: empties 50-70% of its contents w/i 30-40 mins
-
-
noninvasive, painless
operator dependent
 Over the next 60-90 mins: gallbladder gradually refills  ↓ CCK level - Adjacent organs can frequently be examined at the same time.
- difficult to examine satisfactorily:
 Defects in the motor activity  role in cholesterol nucleation & gallstone o Obese
formation o Ascites
3. Neurohormonal Regulation o distended bowel
 vagus nerve: stimulates contraction of the gallbladder - show stones in the gallbladder with sensitivity & specificity of >90%.
 splanchnic sympathetic stimulation: inhibitory to motor activity Stones Polyps
 Parasympathomimetic drugs: contract the gallbladder acoustically dense calcified & reflect shadows
move with changes in position Don’t move with change in posture
o Atropine  relaxation

 Antral distention of the stomach causes both gallbladder contraction and


relaxation of the sphincter of Oddi.
 Hormonal receptors: located on the smooth muscles, vessels, nerves, and
epithelium of the gallbladder.
 VIP:
o inhibits contraction → gallbladder relaxation

 Somatostatin & its analogues: potent inhibitors of GB contraction


- thickened gallbladder wall & local tenderness  cholecystitis
 Other hormones - substance P & enkephalin: physiologic role is unclear Acute cholecystitis Chronic cholecystitis
layer of edema w/i the wall of the GB or contracted, thick-walled gallbladder
between the GB and the liver in
Sphincter of Oddi association with localized tenderness
 regulates flow of bile (& pancreatic juice) into the duodenum
- extrahepatic bile ducts are also well visualized, except for the
retroduodenal portion
- Dilation of the ducts in a px with jaundice  extrahepatic obstruction
- site & cause of obstruction can be determined
- helpful in evaluating tumor invasion & flow in the portal vein
- impt guideline for resectability of periampullary & pancreatic head tumor

Oral Cholecystography
- Once considered the Dx procedure of choice for gallstones
- replaced by UTZ
- oral administration of a radiopaque compound that is absorbed, excreted
by the liver, and passed into the gallbladder
- Stones are noted on a film as filling defects in a visualized, opacified
gallbladder
- No value in px with:
o intestinal malabsorption
o vomiting
o obstructive jaundice
o hepatic failure

Biliary Radionuclide Scanning (HIDA Scan) MRI


- noninvasive evaluation of the liver, gallbladder, bile ducts, and duodenum - provides anatomic details of the liver, gallbladder, & pancreas similar to
with both anatomic & fxnal info those obtained from CT
- 99mTechnetium-labeled derivatives of dimethyl iminodiacetic acid (HIDA) - generate high resolution anatomic images of the biliary tree & pancreatic
are injected IV, cleared by the Kupffer cells in the liver → excreted in bile duct
-
- Dx acute cholecystitis: nonvisualized gallbladder, with prompt filling of the
sensitivity 95% & specificity 89%, at detecting choledocholithiasis
CBD & duodenum. - MRCP - offers a single noninvasive test for the Dx of biliary tract and
- Evidence of cystic duct obstruction on biliary scintigraphy  highly
pancreatic disease
Dx for acute cholecystitis
- sensitivity & specificity for the Dx: 95%
- False (+) results  gallbladder stasis (critically-ill px & px receiving
parenteral nutrition)
- Filling of the gallbladder & CBD with delayed or absent filling of the
duodenum  obstruction at the ampulla
- Confirms biliary leaks (complication of surgery)

Computed Tomography
- inferior to UTZ in diagnosing gallstones
- define course & status of the extrahepatic biliary tree & adjacent structures
- TOC in evaluating the px with suspected malignancy of GB,
extrahepatic biliary system or head of pancreas ERCP
- integral part of the DDx of obstructive jaundice - requires IV sedation
- Spiral CT - provides additional staging info, including vascular involvement - advantages of ERC:
in px with periampullary tumors o direct visualization of the ampullary region
o direct access to the distal CBD, with the possibility of
therapeutic intervention
- ERC – Dx & often therapeutic procedure of choice
o stones in the CBD when asso with obstructive jaundice
o cholangitis
o gallstone pancreatitis
- (+) ductal stone  sphincterotomy & stone extraction & CBD cleared of
stones
o success rate of CBD cannulation & cholangiography: >90%
- Complications of Dx ERC: (5%)
o Pancreatitis
o Cholangitis
- small fiber-optic cameras
o provide direct visualization of the biliary and pancreatic ducts
o ↑ the effectiveness of ERCP in the Dx of certain biliary & pancreatic
dses
- Intraductal endoscopy - therapeutic applications that include biliary stone
lithotripsy and extraction in high-risk surgical px
o Typical complications:
Percutaneous Transhepatic Cholangiography  bile duct perforation
- little role in the mgnt of px with uncomplicated gallstone dse  minor bleeding from sphincterotomy or lithotripsy
- particularly useful in px with bile duct strictures & tumors
 cholangitis

- defines the anatomy of the biliary tree proximal to the affected segment.
- potential risks:
o bleeding
o Cholangitis
o bile leak
o other catheter-related problems
- Both stones are common in Asians

1. CHOLESTEROL STONES
- Mostly radiolucent; 10% are radiodense
- SUPERSATURATION OF BILE WITH CHOLESTEROL - COMMON
PRIMARY EVENT IN FORMATION OF ALL CHOLESTEROL STONES
- High bile cholesterol + cholesterol gallstones  1 DSE ENTITY
- Cholesterol is insoluble in bile  solubility depends on the relative conc of
cholesterol, bile salts & lecithin  ↑ cholesterol, ↓ solubility
- Supersaturation - ALWAYS caused by HYPERSECRETION of
CHOLESTEROL not by ↓ production of bile salts and lecithin
- LECITHIN – MAIN PHOSPHOLIPID IN BILE
Endoscopic UTZ PURE CHOLE STONES MIXED CHOLE STONES
- Operator dependent - uncommon - Most cholesterol stones have variable
- noninvasive imaging of the bile ducts and adjacent structures. - <10% of all stones amounts of bile pigments and calcium
- Always >70% cholesterol by wt
- value in the evaluation of tumors & their resectability - single large stones with smooth surfaces - usually multiple, of variable sizes and may
- Allow needle biopsies of a tumor under ultrasonic guidance be hard and faceted OR irregular,
- used to ID bile duct stones mulberry-shaped and soft
- Colors: whitish yellow & green-black
- less sensitive than ERC, the technique is less invasive.

GALLSTONE DISEASE
Prevalence and Incidence
- 1 of the most common problems in the GIT
- Autopsy reports: 11-36% prevalence
- Prevalence r/t:
a. Age
b. Gender – ♀ 3x more affected
c. Ethnic & family background – 1st degree relatives have 2x prevalence
- Conditions predisposing to gallstones:
a. Obesity 2. PIGMENT STONES
b. Pregnancy - Contain <20% cholesterol
c. Diet - Dark d/t CALCUM BILIRUBINATE
d. CD BLACK PIGMENT BROWN PIGMENT
e. Terminal ileal resection -
f. Gastric surgery -
small, brittle, black & may be speculated
formed by SUPERSATURATION of - typically found in the BILIARY TREE of
calcium bilirubinate, carbonate and asian people
g. HS
phosphate - asso with PARASITIC infxn in Asians
h. SCD - WESTERN COUNTRIES: occur as
i. Thalassemia - mostly 2⁰ to hemolytic dses such as HS, PRIMARY BILE DUCT STONES IN
SCD, & in those with CIRRHOSIS BILIARY STRICTURES OR BILE STATIS
- Like cholesterol stones, FORMED IN THE - <1cm, brownish-yellow, soft and mushy
Natural History GALLBLADDER - form in either the gallbladder or bile ducts
- Most are asymptomatic - Unconjugated bilirubin is LESS soluble in - 2⁰ to bacterial infxn
- Some are symptomatic d/t unknown reasons bile + slow unconjugation of bilirubin in
bile + CALCIUM  STONE FORMATION - MAJOR COMPOSITION  calcium
- Symptoms r/t obstruction of the cystic duct
- Complications of symptomatic gallstones: - higher prevalence in asian countries
bilirubinate + bacterial cell bodies

a. Acute cholecystitis - B-Glucuronidase from bacteria like E.coli 


b. Choledocholithiasis ± cholangitis converts conjugated to unconjugated
bilirubin  unconjugated bilirubin
c. Gallstone pancreatitis
precipitates with calcium and bacteria 
d. Cholecystocholedochal fistula BROWN PIGMENT STONES formation
e. Cholecystoduodenal or cholecystoenteric fistula → gallstone
ileus SYMPTOMATIC GALLSTONES
f. Gallbladder carcinoma
- RARELY, complications are the presenting symptoms 1. CHRONIC CHOLECYSTITIS (Biliary Colic)
- Commonly diagnosed incidentally - 2/3 with gallstone dse presents as chronic cholecystitis
- Every year, 3% of asymptomatic become SYMPTOMATIC
- Every year, 3-5% have complications - Characterized as RECURRENT BOUTS OF PAIN known as biliary colic

- In a 20-year period, 2/3 are ASYMPTOMATIC  Thus, DO NOT DO - Stones chronically obstructs cystic duct  gallbladder wall ↑ in tension
PROPHYLACTIC CHOLECYSTECTOMY, except in the ff:
a. Elderly with DM
- Initially, epithelium is normal or hypertrophied  eventually, becomes
b. Those who will be isolated from medical care for long periods of atrophied  atrophied epithelium protrudes into muscle coat  ASCHOFF-
time ROKITANSKY SINUSES
Clinical presentation
c. Populations w/ ↑ risk of gallbladder CA - CHIEF SYMPTOM: PAIN
d. Porcelain gallbladder  ABSOLUTE INDICATION FOR - Onset: Gradually ↑ over the 1st 30 mins
PROPHYLACTIC CHOLECYSTECOMY → high possibility of
malignancy - Location: RUQ or epigastric area
- Duration: 1-5 hrs
Gallstone Formation
- Characteristic: Constant Episodic
- form as a result of solids settling out of solution - Aggravating factor: Fatty meal or abruptly during the night
- solutes in bile: - Scale: SEVERE PAIN
a. bilirubin
b. bile salts
c. phospholipids
d. cholesterol
- 2 classifications of gallstones:
A. CHOLESTEROL – 80% of stones in western countries are cholesterol
B. PIGMENT – 15-20% of stones in western countries are pigment stones
- Pregnant: DO CONSERVATIVE MGMT  if ineffective, LAPAROSCOPIC
CHOLECYSTECTOMY during the 2nd trimester
- 90% of px after cholecystectomy are already symptom free
- Px with atypical symptoms  results of cholecystectomy are not as
favorable

2. ACUTE CHOLECYSTITIS
Pathogenesis
- 90-95%→ d/t gallstones
- Acalculous cholecystitis  px with systemic dses
- <1%  d/t tumors obstructing the cystic duct
- INITATING EVENT: OBSTRUCTION → distension, inflammation & edema
of GB
- ONLY DEVELOPS IF ONLY THE CYSTIC DUCT IS OBSTRUCTED 
Reason: UNKNOWN
- Duration of obstruction is impt
- Mucosal inflammation d/t lysolecithin, bile salts, & platelet-activating factor
 ↑ PG  inflammatory response is amplified
- 15-30% of cases have 2⁰ bacterial contamination r/t cholecystectomy
PE & Lab findings - PATHOLOGY:
 GB wall - thickened & reddish with subserosal hemorrhages with possible
- Palpation: RUQ tenderness
- If px is pain-free, PE is UNREMARKABLE pericholecystic fluid

- WBC & LIVER FXN TESTS - USUALLY N⁰ in UNCOMPLICATED


 Mucosa - hyperemia and patchy necrosis.

GALLSTONES - 5-10% of cases: inflammation results in ischemia & necrosis.


Note: 50% may have ATYPICAL FINDINGS - If stone is dislodged, inflammation subsides.
- milder pain in relation to meals - ACUTE GANGRENOUS CHOLECYSTITIS  if infxn supervenes!
- pain may be located in the back or LUQ
- bloating and belching with pain - EMPHYSEMATOUS GALLBLADDER  If gas-forming organisms are part
- IMPORTANCE: RULE OUT OTHER CAUSES OF ABDOMINAL PAIN: of the infecting bacteria → Gas is seen in the lumen & walls on CT scan
A. PUD - Perforation may occur but RARE!
B. GERD Clinical manifestations
C. Abdominal wall hernias
D. IBD - 80% of px have Hx of CHRONIC CHOLECYSTITIS
E. diverticular diseases - Presents with BILIARY COLIC but PAIN DOES NOT SUBSIDE,
F. Liver diseases
REMITTING AND PERSISTS FOR DAYS
G. Renal calculi
H. Pleuritic chest pain - Same location & radiation as chronic cholecystitis.
J. Myocardial pains - MORE SEVERE PAIN
- IF PAIN IS >24 HRS, SUSPECT ACUTE CHOLECYSTITIS - Often febrile with anorexia, N/V, & presents with PERITONEAL
HYDROPS OF THE GALLBLADDER INFLAMMATION as manifested by reluctant to move
o Impacted stone without inflammation  gallbladder excretes PE & Lab findings
excessive mucus  becomes distended - focal tenderness & guarding on RUQ
o Palpable but NOT TENDER - Gallbladder may be palpable
o May warrant EARLY CHOLECYSTECTOMY to avoid complications - (+) MURPHY’S SIGN  HIGHLY CHARACTERISTIC OF ACUTE
Diagnosis CHOLECYSTITIS
- depends on presence of typical symptoms & imaging of stones - LEUKOCYTOSIS (12-15k); Some may be normal.
- UTZ  STD Dx TESTS FOR STONES - WBC count >20k– HIGHLY SUGGESTIVE OF COMPLICATED FORM OF
CHOLECYSTITIS SUCH AS GANGRENOUS CHOLECYSTITIS,
- If symptomatic and incidentally found during a CT, DO UTZ BEFORE
PERFORATION OR CHOLANGITIS!
SURGERY
- If ASMYPTOMATIC & (+) for stones during UTZ → DO NOTHING
- Liver chemistries are usually normal but may have slight ↑ of bilirubin

- Sometimes, no stones are found but only biliary sludge (<4mg/mL) along with mild ↑ in ALP, transaminases and amylase

- ≥2 RECURRENT ATTACKS OF TYPICAL BILIARY PAINS & SLUDGE  - SEVERE JAUNDICE  highly suggestive of CBD stones or obstruction of
CONSIDER CHOLECYSTECTOMY the bile ducts d/t pericholecystic inflammation 2⁰ to impaction of stone in
Other causes of biliary pain: the INFUNDIBULUM  MIRIZZI’S SYNDROME
1. Cholesterolosis or “STRAWBERRY GALLBLADDER: - DIABETICS & ELDERLY: subtle presentation  DELAY IN Dx  10x ↑ in
- accumulation of cholesterol in macrophages within the mucosa or in a
polyp mortality rate VS young and healthy px
DDx:
- TMX: if symptomatic → CHOLECYSTECTOMY 1. PUD ± perforation
2. Adenomyomatosis or CHOLECYSTITIS GLANDURALIS 2. Pancreatitis
PROLIFERANS 3. Appendicitis
4. Hepatitis
- hypertrophic smooth muscle fibers and in-growth of mucosa into the 5. Perihepatitis
muscle layer (epithelial sinus formation) 6. MI
- adenomatous polyps develop in the lumen of the FUNDUS 7. Pneumonia
- wall is thickened 8. Pleuritis
- septae or strictures may be found
9. Herpes Zoster involving the intercostals nerve
- TMX: if symptomatic → CHOLECYSTECOMY Diagnosis
Management
UTZ HIDA Scan CT
- Elective laparoscopic cholecystecomy - MOST USEFUL
- helpful in ATYPICAL - LESS sensitive than UTZ
- While waiting surgery, avoid large & fatty meals - Sensitivity & specificity: cases - Performed in px with an
- DM px: cholecystectomy ASAP → more prone to devt of acute cholecystitis 95% acute abdomen
- -
Shows GB wall
thickening & the
- LACK OF FILLING OF
Findings in acute
cholecystitis:
d. secondary stones
Clinical manifestations
pericholecystic fluid GALLBLADDER after 4 a. Thickening of the GB wall
hrs  indication of an b. Pericholecystic fluid - May be silent
- SONOGRAPHIC obstructed gallbladder  c. Presence of gallstones - Pain - similar to biliary colic
MURPHY’S SIGN  combined with clinical d. Air in the gallbladder wall - MILD jaundice, N/V - common
Focal tenderness over findings of acute - Mild epigastric or RUQ pain but PE may be normal
the gallbladder when
compressed by the
cholecystitis, HIGHLY
SPECIFIC & SENSITIVE
- If stone temporarily impacts the ampulla of Vater  symptoms may be
INTERMITTENT
sonographic tube
- NORMAL  EXCLUDES
acute cholecystitis
- If stone passes  resolution of symptoms
- If stone is completely impacted  SEVERE jaundice
- 1/3 of px have NORMAL liver chemistries
- 2/3 have mild elevation of bilirubin, ALP, AST and ALT
Diagnosis
- Must be FIRST TEST!
- Determines size of CBD

- If stone is in the retroduodenal part of the duct, bowel gas may


hinder its detection.
UTZ
- The ff if all present is highly suggestive of choledocholithiasis
a. Dilated bile duct of >8mm
b. Presence of gallstones
Medical treatment c. Jaundice
d. Biliary pain
- IV FLUIDS, Abx & ANALGESIA - Excellent anatomic detail
- Abx should cover G (-) aerobes & anaerobes. Either one of the ff: MRC - sensitivity of 95% & specificity of 89%, in detecting stones
a. 3rd-generation cephalosporin with good anaerobic coverage >5mm
Endo - GOLD STD FOR DIAGNOSING CHOLEDOCHOLITHIASIS
b. nd
2 -generation cephalosporin + metronidazole Cholangiograph - Both THERAPEUTIC and DIAGNOSTIC!

c. AG + metronidazole  allergy to PCN y


- Inflammation in acute cholecystitis is sterile in MORE THAN HALF of px - Sensitivity of 91% and specificity of 100%
- Difficult to determine who is secondarily infected  Thus, Abx mgnt - - Disadvantages:
Endo UTZ 1. No therapeutic capabilities. Only diagnostic.
mainstay in medical tmx of acute cholecystitis 2. Requires expertise
Surgical Treatment 3. Less available
- CHOLECYSTECTOMY  DEFINITIVE TMX OF ACUTE PTHC
- NOT USED IN 2⁰ STONES
- PRIMARY STONES - both therapeutic & Dx
CHOLECYSTITIS
Treatment
- Early cholecystectomy after 2-3 days of symptoms  PREFERRED But not
DEPENDS ON WHAT IMAGING MODALITY IS USED TO DOCUMENT THE
done if the px is surgically unfit STONES:
- Advantages of early cholecystectomy 1. If Endoscopic Cholangiography is used:
a. Definitive solution in just 1 hospital stay SPHINCTERECTOMY and DUCTAL CLEARANCE followed by LAPARASCOPIC
b. Quicker recovery times CHOLECYSTECOMY
c. Earlier return to work
- LAPAROSCOPIC CHOLECYSTECOMY Procedure of choice 2. If intraoperative cholangiogram is used:
Either the ff can be used:
- 10-15% of laparascopic cholecystectomy converts into open a. CBD exploration via the cystic duct

-
cholecystectomy & higher in acute cholecystitis than chronic cholecystitis
More tedious & takes longer in the setting of ACUTE CHOLECYSTITIS
- If expertise or equipments is lacking, a drain should be left adjacent to the
cystic duct. A DAY AFTER, perform endoscopic sphincterectomy
- Early operation  carries the same complication rate b. Formal choledochotomy
- T-tube should be placed
- Px who present 3-4 days after illness and unfit for surgery  Abx  2 mos
later, do CHOLECYSTECTOMY!
- In px mentioned above, laparoscopic cholecystectomy can be attempted
but keep in mind that conversion rate to open cholecystectomy is high.
- Unfit for surgery  DO CHOLECYSTOSTOMY!
 Either percutaneous or open cholecystostomy!
- If failure to improve after cholecystostomy  SUSPECT GANGRENOUS
CHOLECYSTITIS
- If improving, it can be removed and schedule a cholecystectomy
afterwards.
- Those who can’t tolerate surgery  remove stones via the
cholecystostomy tube!

3. CHOLEDOCHOLITHIASIS
 Stones in the CBD
 6-12% prevalence among those who have gallstones - Stones impacted in the ampulla  DIFFICULT TO REMOVE  usually,
 20-25% of px who are >60yo have choledocholithiasis  THUS, CBD is dilated to about 2cm  If this happens, a
CHOLEDOCHODUODENOSTOMY or a ROUX-EN-Y
INCIDENCE ↑ WITH AGE
CHOLEDOCHOJEJUNOSTOMY are the best options
Types of choledochal stones
Primary Stones Secondary Stones - Retained stones  left deliberately in place or discovered after a
- Formed in the BILE DUCTS - Formed in the GALLBLADDER and cholecystectomy
- Tmx of retained stones:
- Usually BROWN PIGMENT
-
migrate down to the CBD
Usually CHOLESTEROL STONES 1. If CBD exploration and a T-tube is left in place, DO A T-TUBE
- COMMON IN ASIANS
- Asso with infxn & biliary stasis
CHOLANGIOGRAM!
- Causes of biliary stasis:
a. biliary strictures
2. After a t-tube cholangiogram, it can be removed endoscopically or via
b. papillary stenosis a matured T-tube tract (2-4 weeks after it has been placed)
c. tumors 3. After stones are removed, the T-tube tract can now be removed
- Px w/ indwelling stents rarely become jaundiced
- Indistinguishable from acute cholecystitis
Dx & Mgnt
- Leukocytosis, hyperbilirubinemia & ↑ ALP & transaminases
- UTZ – document presence of GB stones, dilated ducts & pinpoint site of
obstruction
- Definitive Dx test - ERC
- ERC unavailable  PTC
- ERC & PTC
o Show level & reason for obstruction
o Allow culture of bile
o Allow removal of stones & drainage of bile ducts w/ drainage catheter
or stents
- CT scan & MRI
o Show pancreatic periampullary masses + ductal dilatation
- Initially, IV Abx & fluid resuscitation
- ICU monitoring & vasopressor support
- Obstructed bile drained as soon as px is stable
- 15% will not respond to Abx & fluid resuscitation  do EMERGENCY
BILIARY DECOMPRESSION
o endoscopically w/ sphincterotomy & stone removal or by placement
of an endoscopic biliary stent  Choledocholithiasis or periampullary
malignancies
o Percutaneous transhepatic drainage:
 Proximal or perihilar obstruction
 Stricture in a biliary-enteric anastomosis
 Endoscopic rout has failed
- Recurrent stones  Discovered MOST post-cholecystectomy
- If ERC nor PTC unavailable  Emergent operation for decompression of
1. Retrieved under fluoroscopic guidance with a generous endoscopic CBD w/ T tube
sphincterotomy since recurrent stones are usually multiple and large! - Definitive operative therapy deferred until cholangitis has been tmx &
- Px >70yo  STONES SHOULD BE REMOVED ENDOSCOPICALLY
-
proper Dx established
overall mortality rate – 5%
Because of less M& M
- If asymptomatic, no need for cholecystectomy since only 15% of them will
o higher if asso w/ renal failure,  impairment, hepatic abscess &
become symptomatic. malignancies
- If symptomatic, schedule cholecystectomy.
BILIARY PANCREATITIS
- Gallstones in the CBD are asso w/ acute pancreatitis
2 main complications of choledochal stones
1. Cholangitis - Obstruction of pancreatic duct by an impacted stone or temporary
2. Gallstone Pancreatitis obstruction by a stone passing thru ampulla  pancreatitis
- UTZ of the biliary tree should be taken
CHOLANGITIS S/S Mgnt
- Ascending bacterial infxn in asso w/ partial or complete obstruction of bile (+) gallstones & severe pancreatitis ERC w/ sphincterotomy & stone extraction
ducts (acute) (+) gallstone & mild pancreatitis Cholecystectomy & intraop chlangiogram or preop
- Hepatic bile kept sterile by: ERC
o Continuous bile flow - Once pancreatitis has subsided  GB should be removed
o Antibacterial substances s/a Ig
CHOLANGIOHEPATITIS (Recurrent pyogenic cholangitis)
- Mechanical hindrance to bile flow  bacterial contamination
- Endemic to the orient
- Combined bacterial contamination + biliary obstruction  cholangitis o Chinese population in the US, Europe & Australia
- Causes of obstruction in cholangitis: - Affects both sexes equally
o Gallstones – most common - 3rd & 4th decades of life
o Benign & malignant strictures - Caused by bacterial contamination
o Parasites o E. coli
o Instrumentation of the ducts & indwelling stents o
o
Klebsiella
Bacteroides
o Partially obstructed biliary enteric anastomosis o E. faecalis
- Most common organisms cultured from bile: - Biliary parasites
o E. coli o C. sinensis
o K. pneumonia o Opisthorchis viverrini
o S. faecalis o A. lumbricoides
o Enterobacter - Bacterial enzymes  deconjugation of bilirubin, w/c precipitates as bile sludge
o B. fragilis  sludge & dead bacterial cell bodies form brown pigment stones 
Clinical Presentation partial obstruction throughout biliary tree  repeated bouts of cholangitis 
- Gallstone-induced cholangitis – older & female further stone formation, infxn, hepatic abscess, liver failure (2⁰ biliary
- Charcot’s triad – present in 2/3 of px:
-
cirrhosis)
Pain in the RUQ & epigastrium, fever, jaundice
o Fever
o Epigastric or RUQ pain - Recurrence of symptom  1 of the most characteristic feature of dse
o Jaundice - UTZ:
- Illness may progress rapidly w/ septicemia & disorientation  Reynolds
o stones in the biliary tree
pentad o pneumobilia from infxn d/t gas-forming organisms
o Fever o liver abscesses
o Jaundice o strictures
o RUQ pain o GB may be thickened, but is inflamed in 20%
o Septic shock
- MRCP & PTC – MAINSTAYS OF BILIARY IMAGING FOR
o Mental status changes CHOLANGIOHEPATITIS
- Atypical S/S – elderly o Detect obstructions
o Defines strictures & stones o ventriculoperitoneal shunt
o Allow emergent decompression of the biliary tree in septic px o cirrhosis
o previous upper abdominal procedures
o Percutaneous drain of hepatic abscess
- Long-term goal  extract stones & debris & relieve strictures - anatomic structures can’t be ID or no progress  convert to open
o May require Roux-en-Y hepaticojejunostomy to establish biliary- procedure
enteric continuity - incidence of conversion: 10-30%
- Occasionally, resection of involved areas of liver may offer the best - Conversion to an open procedure is not a failure
form of tmx - Complications for laparoscopic cholecystectomy:
- Recurrences are common o mortality rate - 0.1%.
- Poor prognosis in hepatic insufficiency o Wound infxn & cardiopulmonary complication rates are lower ff laparoscopic
cholecystectomy
o higher injury rate to the bile ducts
OPERATIVE INTERVENTIONS FOR GALLSTONE DSE
Cholecystostomy - Px undergoing cholecystectomy
- decompresses & drains the distended, inflamed, hydropic, or purulent o CBC & liver fxn tests preoperatively
gallbladder. o Prophylaxis against DVT with either LMWH or compression stockings
- For px unfit to tolerate an abdominal operation o
o
empty bladder before OR
orogastric tube is placed if the stomach is distended with gas &
- UTZ-guided percutaneous drainage with a pigtail catheter  procedure removed at the end of the operation
of choice
Open Cholecystectomy
- uncommon procedure
- conversion from laparoscopic cholecystectomy or as a 2nd procedure in px
who require laparotomy for another reason
- require open cholecystectomy because these px may not tolerate
pneumoperitoneum with carbon dioxide:
o severe obstructive pulmonary disease
- inflammation has resolved & px condition improved  remove catheter o CHF ( EF <20%)
- gallbladder removed later, usually by laparoscopy
Intraoperative Cholangiogram or UTZ
Cholecystectomy - bile ducts are visualized under fluoroscopy by injecting contrast through a
- Most common major abdominal procedure performed in Western countries. catheter placed in the cystic duct

- Open cholecystectomy was a safe & effective tmx for both acute and - evaluates size, the presence or absence of CBD stones assessed, and
chronic cholecystitis. filling defects confirmed
- do selective intraoperative cholangiogram:
o hx of AbN liver fxn tests
Laparoscopic cholecystectomy o pancreatitis
- offers a cure for gallstones with: o jaundice
o minimally invasive procedure o large duct & small stones
o minor pain and scarring o dilated duct on preoperative UTZ
o early return to full activity o if preoperative endoscopic cholangiography for the above reasons was
unsuccessful.
- TOC: symptomatic gallstones
- ABSOLUTE CONTRAINDICATIONS: - Laparoscopic UTZ - as accurate as intraoperative cholangiography in
o uncontrolled coagulopathy detecting CBD stones and it is less invasive
o end-stage liver disease

Choledochal Exploration

- Risk factors for a potentially difficult laparoscopic cholecystectomy:


o acute cholecystitis
o gangrene and empyema of the gallbladder
o biliary-enteric fistulae
o obesity
o pregnancy
or, more often,
Hepaticojejunostomy
End-to-end If CBD has been transected or injured
choledochojejunostomy

Transduodenal Sphincterotomy
- endoscopic sphincterotomy replaced open transduodenal sphincterotomy
- If an open procedure for CBD stones is being done in which the stones are
impacted, recurrent, or multiple  transduodenal

BENIGN DISEASES & LESIONS


ACALCULOUS CHOLECYSTITIS
- acute inflammation of the GB can occur w/o gallstones
- critically ill px in ICU
- R/F:
 TPN with extensive burns
 Sepsis
 major operations
 multiple trauma
 prolonged illness with multiple organs system failure
Etiology
- unknown cause
- GB distention with BILE STASIS & ISCHEMIA are implicated
Pathology
- edema of serosa and muscular layers of GB wall with patchy thrombosis of
arterioles and venules
- CBD stones that are detected intraoperatively on intraoperative S/S
cholangiography
- UTZ - managed with laparoscopic choledochal exploration as a part of the
- in alert px: similar to acute calculous cholecystitis  RUQ pain and
tenderness, fever, leukocytosis
laparoscopic cholecystectomy procedure.
- In unconscious px: fever, ↑ WBC, ↑ ALP & bilirubin  further investigation
- CBD stones detected preoperatively, but endoscopic clearance was either
Diagnostics
not available or unsuccessful cholecystectomy
- Small stones in the duct  saline irrigation via the cholangiography
- UTZ: Dx TOC

catheter after the sphincter of Oddi has been relaxed with glucagon.  Demonstrates distended GB with thickened wall
 Biliary sludge
- If irrigation is unsuccessful  balloon catheter via the cystic duct and down
the CBD to retrieve the stones.  Pericholecystic fluid
 Abscess formation
- Choledochotomy - an incision into CBD itself - Abdominal CT: to rule out other Dx
- flexible choledochoscope - passed into the duct for visualization and
- HIDA scan: nonvisualization of GB, high false (+) in px who are fasting, on
TPN, have liver dse
clearance of stones
Mgnt
- Urgent intervention!
Choledochal Drainage Procedures
- when the stones cannot be cleared - PERCUTANEOUS UTZ OR CT GUIDED CHOLECYSTOSTOMY: TOC
- duct is very dilated (>1.5cm in diameter) Since these px usually unfit for surgery.
- Dx & therapeutic
- 90% of px improve
- Open cholecystostomy or cholecystectomy – if px did not improve

BILIARY CYSTS
- CHOLEDOCHAL CYSTS: congenital cystic dilatations in biliary tree
- rare
- females affected 3-8x more
- frequently diagnosed in infancy or childhood
- 15% risk for cholangioCA
Etiology
- unknown cause
- required for biliary cyst formation:
 Weakness of bile duct wall
 ↑ pressure 2⁰ to partial biliary obstruction

- >90% have anomalous pancreatobilary duct junction (pancreatic ducts


joins CBD >1cm proximal to ampulla) long common channel that allows
free reflux of pancreatic secretions into biliary tract  inflammatory
changes, ↑ biliary pressure, cyst formation (cysts lined by cubiodal
epithelium, 2cm to giant cysts)
S/S
- jaundice or cholangitis in adults
- <1/2 present with classic triad (abd pain, jaundice, mass)
Type Mgnt
fusiform cystic dilations of >50% Excision of extrahepatic
I the extrahepatic biliary tree most common biliary tree (cholecystectomy
w/ a Roux-en Y
saccular diverticulum of an <5%
II extrahepatic bile duct Rare
hepatocojejunostomy) –
mobilizing the 2nd part of the duodenum (Kocher also used in type IV
Choledochoduodenostomy maneuver) & anastomosing it side to side with the CBD bile duct dilatation w/
bringing up a 45-cm Roux-en-Y limb of jejunum & III duodenal wall 5% Sphincterotomy
Choledochojejunostomy anastomosing it end to side to the CBD (choledochoceles)
Choledochojejunostomy repair CBD strictures or as a palliative procedure for IV multiple cyst 5-10%
malignant obstruction in the periampullary region
IVa affects extrahepatic & Additional segmental - Asso with
intrahepatic bile ducts resection of liver esp if (+)  Inflammation
intrahepatic stones, strictures,  Fibrosis
IVb extrahepatic bile ducts only abscess) or if dilatation  Muscular hypertrophy
confined to 1 lobe
- possible RF:
1%
V intrahepatic biliary cysts
Very rare  Trauma from passage of stones
 Sphinter motility d/o
 Congenital anomalies
 Recurrent jaundice
 Pancreatitis
S/S
- Episodic pain of biliary type w/ AbN liver fxn tests
Diagnostics
- impt Dx feature: Dilated CBD that is diff to cannulate with delayed
emptyting of contrast
 Ampullary manometry
 Special provocation tests
Diagnostics Mgnt
- UTZ or CT confirms Dx - ENDOSCOPIC OR OPERATIVE SPHINCTEROTOMY

- Endocoscopic, transhepatic or MRC  assess biliary anatomy and plan BILE DUCT STRICTURES
surgical tmx Etiology
SCLEROSING CHOLANGITIS - OPERATIVE INJURY most common cause, esp laparoscopic
- rare cholecystectomy
- INFLAMMATORY STRICTURES involving transhepatic and extrahepatic - Other causes:
biliary tree  fibrosis d/t chronic pancreatitis
 CBD stones
- progressive dse  2⁰ biliary chirrhosis  acute cholangitis
- 30-45yo  biliary obstruction d/t cholecystolithiasis (Mirizzi’s Syndrome)
- men 2x more affected


sclerosing cholangitis
cholangiohepatitis
- 10-20% risk for cholangioCA
-
 strictures of a biliary-enteric anastomosis
if improperly managed, leads to:
o CA presents anytime, does not correlate with extent of disease or  recurrent cholangitis
devt of liver failure  secondary biliary cirrhosis
o aggressive  portal HPN
Etiology S/S
- Primary Sclerosing Cholangitis: (PSC) - present with episodes of cholangitis
 No attributing cause - less common: jaundice without evidence of infxn
 Asso with UC in 2/3 of px Diagnostics
- Secondary Sclerosing Cholangitis: (SSC) - UTZ or CT scan: dilated bile ducts proximal to the stricture, level of
 Bile duct stones stenosis
 Acute cholangitis - MRC - location & degree of dilatation
 Previous biliary surgery - PTC:
 Toxic agents
- Other dses asso w/ sclerosing cholangitis:  outlines proximal biliary tree
 Riedel’s thyroiditis  define stricture and location
 Retroperitoneal fibrosis  decompression of biliary tree with transhepatic catheters or stents
- Other factors: - endoscopic cholangiogram - outlines distal bile duct
 Autoimmune rxn
Mgnt:
 Chronic low grade bacterial or viral infxn - Depends on location & cause of stricture
 Toxic rxn
 Genetic - Percutaneous or endoscopic dilatation and/or stent placement in more than
 HLA B8, DR3, DQ2, DrW52A half of px
S/S
- intermittent jaundice, fatigue, wt loss, pruritus, abd pain
- ROUX-EN Y CHOLEDOJEJUNOSTOMY or HEPATICOJEJUNOSTOMY –
- sx of acute cholangitis rare std of care (80-90% excellent results)
- cyclic remissions & exacerbations - CHOLEDOCHODUODENOSTOMY - For strictures in distal most part of
duct
- some are asymptomatic for yrs, other rapidly progress to obliterative
inflamm changes  secondary biliary cirrhosis  liver failure INJURY TO THE BILIARY TRACT
- px with UC:
 abn liver fxn test
 colectomy for colitis make no difference to the course of PSC
GALLBLADDER
- median survival of PSC: 10-12 yrs, most die from HEPATIC FAILURE - Uncommon
Diagnostics 1. Penetrating injury – usually caused by GSW or stab wounds
- ERC – confirmatory. Reveals multiple dilatations and strictures (BEADING) 2. Nonpenetrating trauma – rare
of both intra and extrahepatic biliary tree. o Includes:
- HEPATIC DUCT BIFURCATION ofen most severely affected a. Contusion
b. Avulsion
- Liver biopsy - not Dx, but impt to determine degree of hepatic fibrosis and c. Laceration
presence of cirrhosis d. Rupture
Mgnt e. Traumatic cholecystitis
o Cholecystectomy – TOC
- strictures can be dilated & stented endoscopically or percutaneously 
long term improvements in only half of px
- Px with extrahepatic and bifurcation strictures without cirrhosis or fibrosis – EXTRAHEPATIC BILE DUCT
RESECTION OF EXTRAHEPATIC BILIARY TREE & o Penetrating trauma – rare; asso w/ trauma to other viscera
HEPATICOJEJUNOSTOMY o Usually iatrogenic in the course of cholecystectomy
- Px with sclerosing cholangitis and advanced liver disease  LIVER o Less common cause:
TRANSPLANT 1. CBD exploration
 85% 5 yr survival 2. Division or mobilization of the duodenum during gastrectomy
 10-20% recurrence of PSC retransplantation!
o
3. Dissection of hepatic hilum during liver resections
Incidence of bile duct injury:
STENOSIS OF SPHINCTER OF ODDI 1. Open cholecystectomy – 0.1-0.2%
Etiology 2. Laparoscopic cholecystectomy
o Major injury - 0.1-0.55% Major injuries s/a variable biliary enteric anastomosis w/ jejuna loop ( end-to-side
o Minor injury - 0.3% length of duct removed Roux-en-Y choledochojejunostomy or Roux-en-Y
hepaticojejunostomy); transhepatic biliary catheters
o Causes of ↑ bile duct injury in laparoscopic cholecystectomy: placed thru the anastomosis
1. Surgical technique w/ inadequate exposure & failure to ID Injury to the distal CBD choledochoduodenostomy
duct-to-duct repair done over a T tube
No or minimal loss of
structures before ligating  most common cause ductal length
a. Bile ducts narrow  mistaken for cystic duct Cystic duct leaks percutaneous drainage ffd by endoscopic biliary stenting
b. Cystic duct may run alongside the CBD before joining it Major injury dx postop transhepatic biliary catheter placement (for biliary
c. Cystic duct may enter RHD & RHD may enter CBD decompression) & percutaneous drainage
2. Limited view, difficult orientation & assessment of depth on a 2D Acute inflammation has operative repair
image resolved 6-8wks later
3. Lack of tactile sensation & unusual manual skills Bile duct stricture from
injury or as a sequel of
a. transhepatic biliary drainage catheter placement
o Factors asso w/ bile duct injury during laparoscopic cholecystectomy:
previous repair present w/
 for decompression
1. Acute/chronic inflammation  defining anatomy & location & extent of damage
↑ liver fxn test or  aids during subsequent biliary enteric anastomosis
2. Obesity
3. Anatomic variation cholangitis b. anastomosis between duct proximal to injury & Roux
4. Bleeding loop of jejunum
o Intra-operative technical factors of biliary duct injury: c. Self-expanding metal or plastic stents placed
Error Result percutaneously or endoscopically across the stricture –
Excessive cephalad retractive of GB  aligns CBD is mistaken for cystic duct provide temporary or permanent (in high risk px)
cystic & CBD Mgnt: angle laparoscope drainage
o visualize anatomic structures &
triangle of Calot OUTCOME
o aid in proper placement of clips
Careless use of electrocautery thermal injury - 70-90% good results
Dissection deep into liver parenchyma injury to intrahepatic ducts - Operative mortality rate 0-30% but commonly 5-8%
Poor clip placement close to hilar area or to clip across bile duct - Common complications of duct repairs:
structures not well visualized  Cholangitis
o routine use of intraop cholangiography to prevent bile duct injury  

External biliary fistula
Bile leak
controversial: may limit extent of injury not prevent it  Subhepatic and subphrenic abscesses
o bile duct injury during cholecystectomy  do cholangiogram to detect &  Hemobilia
- 2/3 of recurrent strictures become symptomatic w/in 2yrs after repair
ID anatomic features - Proximal strictures are asso w/ lower success rates
o check whole biliary system w/ contrast & make sure there are no leaks
DIAGNOSIS - Worst results: many operative revision & evidence of liver failure & portal
o 25% of major bile duct injury recognized at time of operation HPN
o Dx of bile duct injury: - Deteriorating liver fxn  liver transplant
1. Intraop bile leakage
2. Recognition of correct anatomy GB CARCINOMA BILE DUCT CA
3. AbN cholangiogram 0.4% occurrence in random autopsies 0.3% occurrence in random autopsies
o >1/2 present w/ bile duct injury present w/in the 1 st postop month 7th decade- peak incidence 50-70yo: average age of presentation
♀ 2-3x more common ♂:♀- 1.3:1
o Remainder present mos or yrs later w/ recurrent cholangitis or cirrhosis
aggressive, with poor prognosis except when advanced dse at time of dx
o Early postop – ↑ liver fxn test d/t occluded or stenosed bile duct or w/ bile dx early after cholecystectomy
80 & 90% adenoCA >95% adenocarcinomas
leak from an injured duct Histologic subtypes of gallbladder Morphologically divided into
o Source of Bile leak: adenocarcinomas:  nodular (most common type)
1. Cystic duct stump
2. Transected aberrant RHD - Papillary
 scirrhous
 diffusely infiltrating
3. Lateral injury to main bile duct o < 10%  papillary
o Bile leak presents w/ pain, fever & mild ↑ liver fxn test o better outcome
o most commonly diagnosed
while localized to the
Dx studies Indications gallbladder
o collection (biloma) in the GB area or free fluid 

Nodular
tubular
CT or UTZ (bile) in the peritoneum abdominal discomfort, RUQ pain, N/V PAINLESS JAUNDICE - most common
o demonstrate the dilated part of the biliary tree presentation
proximal to the stenosis or obstruction Jaundice, wt loss, anorexia, ascites, & Pruritus, mild RUQ pain, anorexia, fatigue,
HIDA scan confirm site of bile leak noninvasively abdominal mass are less common. and wt loss
Injection of water-soluble define the site of leakage & anatomy of the biliary UTZ: thickened, irregular gallbladder wall or UTZ: establish the level of obstruction and
contrast media thru the tree a mass replacing the gallbladder. rule out the presence of bile duct stones as
drainage tract sonogram
o outline the anatomy & the proximal extent of the
- may visualize tumor invasion of the liver,
the cause of the obstructive jaundice

lymphadenopathy, and a dilated biliary


injury
Percutaneous cholangiogram o allow decompression of the biliary tree w/
tree
- 70-100% sensitivity in detecting
catheter or stent placements
gallbladder cancer
endoscopic cholangiogram o demonstrates the anatomy distal to the injury CT scan: staging Initial tests: UTZ or CT
o allow placement of stent placements
noninvasive delineation of the biliary anatomy both
- ID a GB mass or local invasion into
MRI cholangiography proximal & distal to the injury
adjacent organs.
- Poor method for ID nodal spread
spiral CT scan - demonstrate vascular Either UTZ or spiral CT - portal vein patency
MANAGEMENT invasion
- depends on the type, extent, & level of injury & the time of its Dx If unresectable  CT scan or UTZ-guided Difficult to visualize the tumor itself on UTZ
biopsy of the tumor to provide a pathologic or CT scan.
Injury Mgnt Dx
Major injury w/o biliary external drain, transhepatic biliary catheters are placed, In jaundiced px, a percutaneous Cholangiography – defines biliary anatomy
surgeon transferred to a referral center transhepatic or endoscopic
ligate cholangiogram to delineate the extent of
Transected bile ducts <3
biliary tree involvement, & shows a long
mm or those draining a stricture of the CBD
single hepatic segment MRCP: single noninvasive imaging method that allows complete assessment of biliary,
Injured duct >4mm reimplant vascular, nodal, hepatic, and adjacent organ involvement
Lateral injury to CBD or T-tube placement Surgery – only curative option
common hepatic duct Pathologic stage determines the operative For curative resection, the location & local
T-tube placed thru incision as if it were a formal tmx. extension of the tumor dictates the extent of
Injury is a small incision
choledochotomy the resection.
T-tube placed thru a separate choledochotomy & the Px without evidence of distant metastasis  Surgical exploration:
More extensive lateral
injury closed over the T-tube end exploration for tissue Dx, pathologic o no signs of metastasis
injuries staging, and possible curative resection.
o resectable disease Layer affected Operation Survival
rate
Recurrence  PALLIATIVE CARE NOT surgery!
T1 muscular layer of the GB Simple cholecystectomy 85-100%
perimuscular CT without
CARCINOMA OF THE GALLBLADDER T2 extension beyond the
Extended cholecystectomy +
>70%
Regional lymphadenectomy
- Rare serosa or into the liver
- Elderly beyond the serosa or
Complete tumor excision with
T3 invade the liver or other
- 5% overall survival rate an extended right hepatectomy
& organs  high likelihood of 20-50%
INCIDENCE intraperitoneal and distant
(segments 4-8) if no peritoneal
T4 or nodal involvement is found
- 5th most common GI malignancy in the west spread
*Extended cholecystectomy – resection of liver segments IVB & V, & lymphadenectomy of
- 2-4% of all malignant GI tumors the cystic duct, & pericholedochal, portal, right celiac, & post pancreatoduodenal LN
- 1% undergoing cholecystectomy for gallstone dse have GB CA
- High prevalence in native americans (75/100,000) Mexico, Chile PROGNOSIS
- Poor prognosis
ETIOLOGY
- Most are unresectable at time of dx
- Risk Factors:
- Median survival of 6mos
1. CHOLITHIASIS  most impt risk factor - Median survival for pxs w/ distant metz – 1-3mos
95% have gallstones
o
o 20-year risk for developing gallstones:
- Recurrence after resection of GB CA – most commonly in the liver or celiac
 <0.5% - overall population or retropancreatic nodes
 1.5% - high risk - Death d/t biliary sepsis or liver failure
2. Probably r/t chronic inflamm - Most common problems: pruritus & cholangitis asso w/ obstructive
jaundice, bowel obstruction 2⁰ to carcinomatosis & pain
3. Large stones (>3mm)  10x ↑ CA risk
4. Symptomatic px
BILE DUCT CA
5. Polypoid lesions of the GB  polyps >10 mm - Rare
6. calcified "porcelain" GB  >20% incidence of GB carcinoma. - arise from biliary epithelium, anywhere along the biliary tree
- Mgnt: GB removed even if asymp - 2/3 located at hepatic duct bifurcation
- palliative measure - to provide biliary drainage to prevent liver failure and
7. choledochal cysts  ↑ risk of cancer anywhere in the biliary tree,
cholangitis
highest in the GB - Unresectable disease – die within 1 year
8. Sclerosing cholangitis
ETIOLOGY
9. anomalous pancreaticobiliary duct junction
- Features common to most risk factors:
10. carcinogens (azotoluene, nitrosamines)
o biliary stasis
PATHOLOGY
- SPREADS through the lymphatics, with venous drainage, and with direct
o bile duct stones
o infxn
invasion into the liver parenchyma.
- Risk Factors:
o Lymphatic flow from the GB  cystic duct node (Calot's)  pericholedochal & 1. PSC
hilar nodes  peripancreatic, duodenal, periportal, celiac, & SMA nodes. 2. choledochal cysts
o GB veins  directly into the adjacent liver (segments IV & V) where tumor 3. UC
invasion is common 4. Hepatolithiasis
5. biliary-enteric anastomosis
o Lymphatics are present in the subserosal layer only  CA invading but not
growing through the muscular layer have minimal risk of nodal disease. 6. biliary tract infxns with Clonorchis or in chronic typhoid carriers
- when diagnosed: 7. liver flukes
GB Ca metastasis 8. dietary nitrosamines
25% localized to the gallbladder wall 9. Thorotrast
35% regional nodal involvement or extension into adjacent liver 10. exposure to dioxin
40% distant metastasis PATHOLOGY
CLINICAL MANIFESTATIONS & Dx - Anatomically, they are divided into
- indistinguishable from cholecystitis & cholelithiasis. 1. distal
- >1/2 of GB Ca are not dx before surgery. 2. proximal
- Common misdiagnoses:
o chronic cholecystitis
3. perihilar tumors (Klatskin tumors): 2/3 of cholangioCA
o acute cholecystitis - Perihilar tumors further classified based on anatomic location by:
o choledocholithiasis Type BISMUTH-CORLETTE CLASSIFICATION
o hydrops of the gallbladder I confined to the CHD
II bifurcation without involvement of the secondary intrahepatic ducts
o pancreatic cancer
IIIa right secondary intrahepatic duct
- Lab findings  not Dx but, if AbN, are most often consistent with biliary IIIb left secondary intrahepatic ducts
IV right & left secondary intrahepatic ducts
obstruction

- Intrahepatic cholangiocarcinomas occur, but they are treated like HCC, with
hepatectomy when possible
CLINICAL MANIFESTATIONS AND DIAGNOSIS
TREATMENT
- Occasionally, asymptomatic px are found to have CA while being evaluated
- palliative procedures for px with unresectable cancer and jaundice or for ↑ ALP & GGT levels.
duodenal obstruction - most frequently performed surgery for gallbladder
cancers. - CA 125 & CEA ↑ but nonspecific
- obstructive jaundice  endoscopic or percutaneously placed biliary stents. - CA 19-9: most commonly used to aid the Dx of cholangiocarcinoma
- No proven effective options for adjuvant radiation or chemotherapy o sensitivity of 79% & specificity of 98% if serum value is >129 U/mL
- Mild ↑ in CA 19-9:
Distal bile duct tumors resectable
Mgnt
pylorus-preserving pancreatoduodenectomy
o Cholangitis
(Whipple procedure)
o GI & gynecologic neoplasms
Distal bile duct tumors unresectable on Roux-en-Y hepaticojejunostomy, cholecystectomy,
o lack the Lewis blood type Ag
surgical exploration and gastrojejunostomy to prevent gastric outlet
- A perihilar tumor causes dilatation of the intrahepatic biliary tree, but normal
Unresectable dse on Dx evaluation
obstruction.
Nonoperative biliary decompression
or collapsed gallbladder & extrahepatic bile ducts distal to the tumor
- Distal bile duct cancer  dilatation of the extra- and the intrahepatic bile a. Proximal Percutaneous placement of expandable metal
stents or drainage catheters
ducts, & GB b. Distal Endoscopic placement
- PTC - defines the proximal extent of the tumor, which is the most
important factor in determining resectability.
- ERC - evaluation of distal bile duct tumors.
- Risk of cholangitis with internal and external drainage d/t stent occlusion 
operative intervention is not warranted in px with metastatic dse
- Celiac Angiography – evaluate vascular involvement although surgical bypass offers improved patency and fewer episodes of
TREATMENT cholangitis
- Despite UTZ, CT, & MRI, >1/2 who are explored are found to have - Unresectable dse
peritoneal implants, nodal or hepatic metastasis, or locally advanced dse o 5-fluorouracil alone (<10%) or in combination w/ mitomycin C and
that precludes resection.  do Surgical bypass for biliary doxorubicin (<30% response)
decompression & cholecystectomy to prevent the occurrence of acute o Radiation + chemo is better but no data from trials are available
cholecystitis PROGNOSIS
- unresectable perihilar cholangiocarcinoma  Roux-en-Y Perihilar cholangioCA Distal cholangioCA
cholangiojejunostomy to either segment II or III bile ducts or to the RHD Advanced, unresectable Resectable
Median survival 5-8mos Median survival 32-38mos
- 5-yr survival: 10-30% 5-yr survival: 30-50%
BISMUTH-CORLETTE CLASSIFICATION
Type Tumor Involved Mgt - for px w/ (-) margins  40%
Perihilar tumors involving the Local tumor excision with portal Death d/t hepatic failure & cholangitis
I or II
bifurcation or proximal CHD with lymphadenectomy, cholecystectomy, CBD - PRESENCE OF (+) MARGINS & LN (+) TUMORS – greatest r/f for
no signs of vascular involvement excision, and bilateral Roux-en-Y recurrence after resection
hepaticojejunostomies.
IIIa or right or left hepatic duct right or left hepatic lobectomy respectively.
Frequently, resection of the adjacent caudate
IIIb lobe is required because of direct extension
into caudate biliary radicals or parenchyma.

Helpful Laboratory Studies in Acute Abdomen


Hemoglobin
White blood cell count with differential
Electrolytes, blood urea nitrogen, creatinine
Urinalysis
Urine human chorionic gonadotropin
Amylase, lipase
Total and direct bilirubin
Alkaline phosphatase
Serum aminotransferase
Serum lactate levels
Stool for ova and parasites
Clostridium difficile culture and toxin assay

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