GENERAL SURGERY

Surgical Block
2012

Liver & Gallbladder

Dr. Gerardo R. Wenceslao

LIVER
ANATOMY & PHYSIOLOGY OF THE
Liver
Liver
th
1/50 of total body weight
CANTLIES LINE
Surgically divides liver into the PHYSIOLOGIC right and left
lobe
Imaginary line through the IVC and Gallbladder
RIGHT LOBE
Divided into anterior & posterior section by RIGHT Hepatic
Vein
LEFT LOBE
Divided into medial and lateral segments by Falciform
Ligament
LEFT LATERAL Segmentectomy
Segments II, III
Vascular Supply
Arterial Blood Supply
HEPATIC ARTERY
Branch of the Celiac Artery
Carry FULLY oxygenated blood
Supplies 25 % of the 1,500 ml of blood that enter the
liver
Couinaud Classification
COUINAUD CLASSIFICATION OF LIVER ANATOMY
Divides the liver into 8 functionally independent segments
Each segment has its own
Vascular inflow & outflow
Biliary drainage.
In the CENTER OF EACH SEGMENT is a branch of:
Portal vein
Hepatic artery
Bile duct.
In the PERIPHERY OF EACH SEGMENT is
Vascular outflow through the HEPATIC VEINS
Veins that divide the liver into different parts
Right Hepatic Vein
Divides the right lobe into anterior and posterior
segments.
Middle Hepatic Vein
Divides the liver into PHYSIOLOGIC right and left lobes
(or right and left hemiliver).
This plane runs from the inferior vena cava to the
gallbladder fossa CANTLIES LINE
Left Hepatic Vein
Divides the left lobe into a medial and lateral part
Designated Segments of the Liver
RIGHT LOBE
Segment 5 through 8
LEFT LOBE
segments 2 through 4
LEFT LATERAL SEGMENT
Segments 2 and 3
CAUDATE LOBE
Segment 1
Hepatic Resections
RIGHT Lobectomy
Segments V, VI, VII, VIII
RIGHT Trisegmentectomy
Segments IV, V, VI, VII VIII
LEFT Lobectomy
Segments II , III, IV

Schwartz

Venous Blood Supply

PORTAL VEINS
Carries PARTIALLY oxygenated blood as it drains the
entire splanchnic circulation
Comprises 75 % of the liver blood flow
Formed by the confluence of the 3 veins:
Superior Mesenteric Vein
Inferior Mesenteric Vein
Splenic With Coronary Vein

Liver Functions
Blood Circulation & Filtration
Bile Drainage
Blood Glucose Regulation
Energy metabolism
GLYCOGENESIS
GLYCOGENOLYSIS
Source of energy during fasting
GLUCONEOGENESIS
Source of energy from non-CHO source
Alanine
Lactate
Glycerol
Occurs after depletion of glycogen (48hrs)
LIPOLYSIS
Occurs during prolonged fasting
Formation of ketone from fatty acids
Synthetic function
ALBUMIN
10 gm/day
NOT a marker of acute hepatic dysfunction due to
LONG HALF-LIFE (15-20 days)
Marker of CHRONIC hepatic dysfunction
VITAMIN K DEPENDENT CLOTTING FACTORS
II, VII, IX, X
Prothrombin Time
Measures the rate of conversion of prothrombin
to thrombin
if vitamin K clotting factors are deficient
International Normalize Ratio (INR)
Ratio of Pro-time to mean control pro-time
Metabolic functions
Absorption, metabolism and storage of fat soluble
vitamins
A, D, E and K
ONLY SITE for storage of VITAMIN A
One of the sites for activation of Vitamin D
25-hydroxylation
ITO CELLS
Presinusoidal cells
Involved in Collagen and Vitamin A metabolism
Absorption & Storage of VITAMIN B12
Detoxification
PHASE 1
Cytochrome P-450-enzyme
Facilitates oxidation, reduction and hydrolysis
PHASE 2
Conjugation reaction
Addition of subgroups
Binds (glutathione) and converts toxic substance
to harmless product
Reticuloendothelial function
Clear the circulation with particulate matters and
microbes.

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KUPFFER CELLS
Fixed phagocytic cells
Clearance function
Ammonia
Converted to urea via UREA cycle
Indirect bilirubin
Taken up from the blood by the hepatocytes
Hepatocellular injury enzyme markers
AST (SGOT)
Found on
Liver
Cardiac muscle
Skeletal muscle
Kidney
ALT (SGPT)
Predominantly found on the LIVER
MORE SPECIFIC
Cholestasis
SERUM BILIRUBIN
Indirect (Unconjugated)
Increased in intrahepatic cholestasis
FAT SOLUBLE
Direct (Conjugated)
Increased in extrahepatic obstruction
WATER SOLUBLE
Can be found on the urine of patients
ALKALINE PHOSPHATASE
Found primarily in the BILIARY TRACT & BONES
Half life: 7 days
Takes several days to normalize even after resolution
of biliary obstruction
GAMMAGLUTAMYLTRANSPEPTIDASE (GGTP)
EARLY MARKER and sensitive test but NON-specific
Elevated in
MI
COPD
Renal Disease
Alcohol abuse
Formation of Bile
500-1000ml-bile produced by the liver daily.
>95% bile salts are reabsorbed in the intestine (ILEUM)
Components of bile
Water-90%
Electrolytes
Organic substances
Bile acid - 80%
Phospolipid (LECITHIN) - 15%
Cholesterol - 5%
Functions:
Aid in the digestion and absorption of lipids and lipid
soluble vitamins
Elimination of waste product (bilirubin and
cholesterol)
Bilirubin Metabolism
Bilirubin
Product of Heme Catabolism
Bound to ALBUMIN in the circulation and sent to the
liver
In the liver it is conjugated to Glucoronic Acid to form
Bilirubin Diglucoronide
Most are excreted thru the intestine some escapes into
the circulation and excreted to the urine
Enterohepatic Circulation
90-95% of bile salts are reabsorbed the TERMINAL ILEUM
PRIMARY BILE ACIDS
60-90% of bile acid pool
Synthesized in the LIVER
5-10% enters the colon and transformed into SECONDARY
BILE SALTS
Deoxycholic Acid
Lithocolic Acid
Both primary and secondary bile acid are transported back to
the liver

PATHOLOGICAL CONDITIONS OF THE

Liver
Hepatic Injuries
Clinical manifestation
Shock
Abdominal pain
Spasm
Rigidity
Diagnostic
CT scan is MOST USEFUL
May also use ultrasound or peritoneal lavage
HEPATIC INJURY GRADE

Imaging of the Liver

Used to define parenchymal lesions:
ULTRASOUND
HIGHEST YIELD in defining:
Hepatic abscesses
Cystic lesions
Most hemangiomas
INTRAOPERATIVE ULTRASOUND (IOUS)
GOLD STANDARD in detecting the number, extent
and association of tumors with intrahepatic blood
vessels
Can be done laparoscopically or during laparotomy
CT SCAN
Used To Evaluate Presence Of:
Peritoneal Lesions
Portal Lymphadenopathy
Other remote lesions
DUAL & TRIPLE PHASE BOLUS IV CONTRAST HELICAL CT
SCAN
MOST ACCURATE
Detects lesions that are 1cm in size
LESS ACCURATE
In detecting tumors in HCC than for metastasis
(40-60%-<2cm)
MRI (3-TESLA MRI)
LESS SENSITIVE than CT scan in
Spatial discrimination of lesions
Detecting liver metastasis
MORE SENSITIVE than CT scan for
Detecting early HCC
Distinguishing HCC from macroregenerative nodules
Detecting cystic lesions
ANGIOGRAPHY
Determine the arterial supply
Detect large parenchymal lesion
ANGIOPORTOGRAPHY
Combines CT scan with contrast infusion through a
catheter placed in the Superior Mesenteric Artery
NEEDLE BIOPSY
Provides liver tissue for histologic studies

Schwartz

Grade 1
Subcapsular hematoma
NON-EXPANDING
<10cm
Capsular tear, NON-BLEEDING,
Intraparenchymal Hematoma
<1cm parenchymal depth

Grade 2
Subcapsular hematoma
NON-EXPANDING
10-50% surface area
Intraparenchymal hematoma
NON-EXPANDING
<10cm
Capsular tear, ACTIVE BLEEDING:
1-3cm depth
<10cm in length

Grade 3
Subcaspular hematoma
>50% surface area or
EXPANDING
Ruptured subcapsular hematoma
BLEEDING
Intraparenchymal hematoma
>10cm or
EXPANDING > 3cm depth

w/

ACTIVE

Grade 4
RUPTURED intraparencymal hematoma w/ ACTIVE
BLEEDING.
Parenchymal disruption
25-75% of hepatic lobe
1-3 Coiunaud segment in single lobe

Grade 5
Parenchymal disruption
>75% of hepatic lobe
> 3 Couinauds segment in a lobe.
Juxtahepatic venous injuries
Grade 6
Hepatic AVULSION
TREATMENT
Non-operative Management:

Schwartz

Hemodynamicaly stable
Absence of peritoneal signs
Precise delineation and grading of injuries
No associated peritoneal or retroperitoneal injuries
Operative Management:
Grade 3-6
Bimanual compression w/ resuscitation
PRINGLE MANEUVER
A large haemostat is used to clamp the
hepatoduodenal ligament interrupting the
flow of blood through the hepatic artery
and the portal vein
Helps to control bleeding from the liver.
Finger fracture w/ repair or ligation
Debridement of non-viable parenchyma
Omental pack
Closed suction drains
If + for bleeding after compression or Pringles
Manuever PACK THE WOUND
Re-explored after 18-36 hrs, packs are removed
If still + for bleeding like in retrohepatic VC, hepatic
venous injury
VASCULAR ISOLATION AND INTRAVAL SHUNT
HEPATIC RESECTION:
High mortality rate
Considered for those w/total destruction of liver
parenchyma
Extent of injury precludes perihepatic packing
COMPLICATIONS of Surgery
Recurrent bleeding
Inadequate hemostasis or loss of coagulation
factors secondary to massive transfusions
Intra-abdominal sepsis/ abscess formation
Hemobilia
Free communication between blood vessels and
biliary tree
TRIAD
Abdominal Pain
GI Bleeding And Previous Trauma
Jaundice

Acute Liver Failure

ETIOLOGY:
Cellular death exceeds the regenerative capability of the
liver
Western countries:
Drugs and toxin
Acetaminophen (PARACETAMOL)
MOST COMMON etiologic agent in
USA
UK
Europe
Eastern and developing countries
Viral infections
Hepatitis A, B, C
CLINICAL PRESENTATION:
Cerebral edema
Hemodynamic instability
Susceptibility to bacterial and fungal infections
Renal failure
coagulopathy
MOST COMMON CAUSE OF DEATH:
Intracranial Hypertension d/t cerebral edema
OTHER CAUSES
Sepsis
Multiorgan Failure
TREATMENT:

For Acetaminophen Overdose

Activated charcoal
N-acetylcysteine (NAC)
an antidote
stabilizes gluthathione
Liver transplant
DEFINITVE THERAPY

Hepatic Abscess
PYOGENIC ABSCESS
Etiology:
Ascending biliary infection
Cholangitis 2 to Calculi or CA
MOST FREQUENT CAUSE
Hematogenous spread
Generalized septicemia
SECOND MOST FREQUENT CAUSE
Direct extension from intraperitoneal infection

AMOEBIC ABSCESS
MOST COMMON abscess WORLDWIDE
ETIOLOGY
d/t infection of E. histolytica
Reach the liver by way of portal venous system from a
focus in the bowel wall
Usually a large single abscess affecting the RIGHT lobe of
the liver (dome or inferior surface)
Contains REDDISH BROWN fluid
anchovy paste appearance
Outer zone:
Where amoebas can usually be seen

MOST COMMON ORGANISMS ISOLATED

E. coli
Klebsiella
Streptococcus
They can be solitary, multiple and multilocular
40%-monomicrobial
40%-polymicrobial
Single and multiple abcesess
occur in equal frequency
SINGLE ABSCESS
usually located in the RIGHT Lobe
CLINICAL MANIFESTATIONS
Fever (picket fence)
MOST COMMON
Pain
LATE symptom
Hepatomegaly - 30 - 60 %
Hepatic tenderness 5 %
DIAGNOSTIC STUDIES
Laboratory Findings
Leucocytosis
Anemia: 5 %
alkaline phosphatase
Radiographic Findings
Elevation and immobility of the right leaf of the
diaphragm
Obliteration of the cardiophrenic angle and
costophrenic angle
Air fluid level
Abscess
formed
by
gas
forming
microorganism
CT scan
MOST ACCURATE: 90 %
TREATMENT
Correction of underlying cause
Aspiration and IV antibiotics
Effective in 80-90% of patients
Surgery
laparotomy or open drainage
Surgical resection
for recalcitrant abscess

Schwartz

CLINICAL MANIFESTATIONS
Fever and pain right lower intercostal space
MOST FREQUENT COMPLAINT
Painful epigastric swelling
LEFT lobe abscess
Diarrhea is uncommon ( 1/3)
DIAGNOSTIC STUDIES
Stool exam:
+ for amoeba in only 15%
X-ray:
similar to those with Pyogenic abscess
Elevation and immobility of the right leaf of the
diaphragm
Obliteration of the cardiophrenic angle and
costophrenic angle
Air fluid level
Rupture of the amoebic abscess
FLUORESCENT ANTIBODY TEST (FAT)
+ most of the time
Aspiration of the abscess cavity:
Anchovy paste
Considered PATHOGNONOMIC
Frequently ESTABLISHES THE DIAGNOSIS
COMPLICATIONS
Secondary bacterial Infection
MOST COMMON
Rupture of the amoebic abscess
NEXT MOST COMMON
PLEUROPULMONARY
MOST COMMON root of rupture
Rupture to the pericardial cavity
MOST SERIOUS
TREATMENT
Metronidazole
750mg 3x day for 7-10 days
Aspiration of amoebic abscess is done if:
Does not respond to medical tx
Superinfection w/ bacteria
If the abscess is large and adjacent to important
structure
BENIGN TUMORS OF THE
Liver

Hepatic Cysts
CONGENITAL CYSTS
Most common BENIGN CYSTIC lesion
More common among FEMALES
4:1

They are excluded hyperplastic bile rest

SMALL CYSTS
Most are asymptomatic
LARGE CYSTS
Abdominal pain
Epigastric fullness
Early satiety
Diagnosis:
Hepatic imaging
Thin walled homogenous fluid filled structures
with few to no septations
Treatment:
Asymptomatic
Conservative
Symptomatic
Ultrasound or CT-scan guided aspiration
followed by sclerotherapy
Lap or open cysts fenestrartion
Excised wall sent for path analysis
POLYCYSTIC LIVER DISEASE
AUTOSOMAL DOMINANT
Common among FEMALES
Usually presents in the third decade of life
Increases with advancing age and severity of renal cysts
and renal dysfunction
Few and small cysts (<2)
asymptomatic
LARGE AND NUMEROUS CYST
cyst parenchymal ratio: >1
Symptoms
Abdominal pain
Shortness of breath
Early satiety
Renal failure
For progressive disease
COMPLICATIONS:
Intracystic hemorrhage
Infection
Post-traumatic rupture
Diagnosis:
CT scan
Biochemical test
Gamma-glutamyltransferase
Treatment:
Lap or open cyst fenestration
50% recurrence rate
Liver transplant
DEFINITIVE TREATMENT
Cavernous Hemangiomas
Most common BENIGN SOLID tumor
More common in WOMEN
Most of the time they are asymptomatic
Spontaneous rupture is RARE
MOST COMMON symptom
PAIN
Often felt with lesions > 5-6cm
Most common indication for surgical intervention
DIAGNOSTIC STUDIES
Usually identified by US or CT scan
Subglissonian Hematoma
Dx for small lesions not seen by US or CTscan
Percutaneous biopsy
CONTRAINDICATED because of high risk of bleeding
Focal Nodular Hyperplasia
Common in women of CHILDBEARING AGE
Possible link w/ oral contraceptive
Most are diagnosed incidentally on operation
DO NOT RUPTURE spontaneously
NO SIGNIFICANT RISK for malignant transformation
PAIN
usual indication for resection
Use oral contraceptive or estrogen must be stopped
Diagnosis:
BI-PHASIC CT SCAN
demonstrate central stellate scar

Schwartz

Tc99 LABELED SULFUR COLLOID

Can be used to differentiate from Hepatic Adenoma
(HA)

Hepatic Adenoma
> 50% used oral contraceptive > 5 years
Lesions persist even after discontinuation of the drugs
They may also develop during pregnancy, DM and Glycogen
Storage Disease.
They are bigger and higher rates of intramural or
intraperitoneal bleeding
for contraceptive users
May transform to HEPATOCELLULAR CARCINOMA
More frequently with adenomatosis
> 10 adenomas
80% are symptomatic with pain or mass effect
Percutaneous biopsy
Not advisable due to risk of hemorrhage
30%-SPONTANEOUS rupture
TREATMENT
Resection
Embolization
For inoperable HA

METASTATIC TUMORS OF THE

Liver
Metastatic Neoplasm
MOST common CA of the liver
CAUSES
METASTATIC COLORECTAL CANCER
MOST COMMON CAUSE
50% will eventually have liver metastasis

FOUR ROUTES in which neoplasm may reach the liver:

Portal venous
Lymphatic spread
Hepatic arterial
Direct extension
The growth pattern of metastatic tumor is more rapid than the
original lesion
CLINICAL MANIFESTATION
Hepatic pain
Jaundice
Ascites
Anorexia
Hepatic nodularity
Apparent physically in 50 % of cases
DIAGNOSTIC STUDIES
Laboratory studies

 Alkaline phosphatase in 80 %
SGPT 2/3
AFP is negative
CEA is in metastatic colonic CA
Imaging Studies
Intraoperative Ultrasound
MOST ACCURATE method in identifying hepatic
metastasis
CT-scan (Helical CT-scan)
Can detect tumor < 2cm
Can miss tumors that are < 1cm
Transabdominal ulrasound
As accurate as CT-scan for tumors that are >2cm
TREATMENT
Hepatic resection
ABSOLUTE INDICATION
Can be tolerated by the patient
Volume of liver remnant
Health of the remnant liver parenchyma
RELATIVE INDICATION
No systemic metastases
Control of the primary tumor is anticipated
Fewer than 4 METS
Chemotherapy
Radiation
POORLY TOLERATED by the liver
May be palliative for painful liver metastasis
Hepatic artery ligation
May cause shrinkage in tumor size but ONLY
TRANSIENT
Cryoablation
May palliate the symptoms and slow the progression
of the lesion in unresectable tumors

PRIMARY MALIGNANT TUMORS OF THE

Liver
Primary Malignant Tumors
TH
5 most common malignant neoplasm world wide
HEPATOBLASTOMA
< 2 years old
More common in MALES
FIBROLAMELLAR CA
Variant of HCC
M=F
Common in adolescent &
young adults
Hepatocellular Carcinoma
Aka: Hepatoma
INCIDENCE
Endemic in
Africa
Southeast Asia
30-65 per 100,000/year
Japan
70-90% with cirrhosis
3-6% annual conversion rate of cirrhosis to HCC
Men are affected twice as often as women
M>F, 2:1
Average age affected is 50 years
Can occur at any age
RISK FACTORS
Chronic liver disease
Alcohol abuse
Schistosomiasis
Hemochromatosis
Cirrhosis
Chronic infection
Hepatitis B and C
Hepatotoxins
Aflatoxins
Anabolic steroids
CLINICAL PRESENTATION
Weight loss & weakness-80%
Dull aching pain in RUQ
Fever
Jaundice

Schwartz

PHYSICAL EXAMINATION
Hepatomegaly (88 %)
Weight loss (85 %)
Tender abdominal mass (50%)
Findings associated with cirrhosis (60 %)
10 15 % present with acute hemorrhage into the
peritoneal cavity with resultant shock
Paraneoplastic syndromes in which tumor cells secrete
hormone like substance that
Cause unusual syndrome (cushings syndrome) also may
occur
DIAGNOSIS
Alkaline phosphatase
Most consistently altered
Alpha-fetoprotein
Elevated in 70 90 % of cases
Elevated also in:
TeratoCA
Yolk sac tumors
Imaging studies:
CT scan
MRI
Arteriography
Ultrasound
Percutaneous needle biopsy
TREATMENT
Resection
GOLD STANDARD
Criteria
HCC w/ out cirrhosis
Cirrhosis w/ preserved liver function
(- )Portal Hypertension
still controversial
Liver Transplant
GOLD STANDARD IN END-STAGE LIVER DISEASE
Poor liver function
Milan criteria
Early stage HCC-1 nodule<5cm
2-3 nodules <3cm
No gross vascular invasion or extrahepatic
spread
Regional liver therapies
Transarterial Chemoembolization (TACE) and
Hepatic Pump Chemoperfusion
MOST COMMON treatment of UNRESECTABLE
HCC
A percutaneous transfemoral approach of
injecting chemotherapeutic drugs combined with
embolic particles into the hepatic artery that
supplies the liver tumor
Transarterial Chemoebolization (TACE)
Improved survival rate
1 year-57%
2years-26%
Control grp.-1 and 3 year survival of
32% and3%
TACE related mortality-0.5%
Complications
Liver failure
Hepatic abcess
Hepatic artery thrombosis
Selective Internal Radiation Therapy ( SIRT )
A selective internal radioembolization (Ytrium
90) using transfemoral percutaneous approach
Main indications
Multiple involvement of both lobes
Inoperable HCC
Failed chemotx for metastatic colon CA
Ablation techniques:
Radiofrequency Ablation ( RFA )
Probe delivers extreme heat or radiofrequency
energy that destroys cancer cells
Percutaneous Ethanol injection
Cryosurgery
Portal Hypertension
Abnormal elevation in portal venous pressure
> 5mmHg 8mmHg

 In pressure stimulates the development of venous collaterals,

which attempt to decompress the portal system into the
systemic system
Collateral veins are very fragile
When portal pressure exceeds >12 mm hg
Dilated veins or varices are likely to develop and
subsequently bleed
COLLATERAL VESSELS
Hepatopetal Flow
Intrahepatic vasculature is normal
Only the portal vein is obstructed
Hepatofugal Flow
MOST COMMON PATHWAY of collateral circulation.
VEINS affected
CORONARY VEINS
AKA:
Coronaria Ventricul
Gastric Vein
Derives tributaries from both surfaces of
the stomach
Runs from right to left along the lesser
curvature of the stomach, between the two
layers of the lesser omentum, to the
esophageal opening of the stomach, where
it receives some esophageal veins. It then
turns backward and passes from left to right
behind the omental bursa and ends in the
portal vein
(+) Esophageal Varices
SUPERIOR HEMORRHOIDAL VEINS
UMBILICAL & PARAUMBILICAL VEINS
(+) Caput Medusa
VEINS OF RETZIUS
Connect the intestinal veins with the
inferior vena cava and its retroperitoneal
branches
ETIOLOGY
INTRAHEPATIC CAUSES
MOST COMMON cause of Portal Htn
COMMON CAUSES
CIRRHOSIS
Causes 85 % of portal hypertension
TYPES
Nutritional Cirrhosis Secondary To
Alcohol Abuse
MOST COMMON.
Alcoholic Hepatitis
AST: ALT ratio 2:1
Postnecrotic Cirrhosis
Viral hepatitis.
AST: ALT Ratio: 1:1
Biliary Cirrhosis

Pathologically produces:
Progressive narrowing of sinusoidal
and postsinusoidal vessels due to
centrilobular collagen deposition
Distortion of the sinusoidal anatomy
by cirrhotic regenerative nodules
sinusoidal block increases resistance to
portal blood flow through the liver and
portal pressure Portal Htn

Schwartz

SCHISTOSOMIASIS
Portal HPN develops when parasitic ova in
small portal venules cause a PREsinusoidal
block
No impairment of hepatic function until late
in the course of the dse.
OCCASIONAL causes of portal HPN
Wilsons disease
Hepatic fibrosis
Hemochromatosis
PREHEPATIC CAUSES
Rare but are more common in CHILDREN
CAUSES
PORTAL VEIN OBSTRUCTION
Due to either thrombosis, congenital
atresia
STENOSIS
Caused by extrinsic compression (tumors)
POSTHEPATIC CAUSES
RARE
CAUSES
BUDD-CHIARI SYNDROME
Characterized by hepatic venous outflow
which causes a postsinusoidal block with
resultant hepatomegaly and ascites
PRIMARY OBSTRUCTION
Due to endoluminal vein thrombosis
Inferior Vena Caval Webs
MOST COMMON cause of hepatic
vein obstruction in ASIA
SECONDARY OBSTRUCTION
Due to compression by lesions outside
the vein
CONSTRICTIVE PERICARDITIS
Produces a markedly elevated inferior vena
cava pressure resistance to venous
outflow
Suspected when CALCIFICATION of the
pericardium is present
CLINICAL MANIFESTATIONS
Hepatic Encephalopathy
Malnutrition
Skin Spider Angiomas
Esophageal Varices

Splenomegaly
Periumbilical Caput Medusa
Hemorrhoids
Testicular Atrophy

ESOPHAGEAL VARICES
Leading cause of mortality and morbidity in patients with
portal Hypertension
1/3 of all pts with varices will experience bleeding.
Each episode: 20-30% risk of mortality
70% of those who survive the initial bleed will
experience recurrent bleeding within 1 year if
untreated
Prevention of bleeding:
Improvement of liver function
Avoid:
Alcohol
Aspirin
NSAIDs
Administration of PROPANOLOL
Prophylactic EVL for medium to large varices
Every 1-2 weeks until obliteration
Followed by EGD 3 mos later and every 6 mos
EVL
FIRST LINE OF TREATMENT for acutely bleeding
varices
TREATMENT
Esophageal Banding
Management of acute bleeding
Blood resuscitation to achieve a Hgb of 8g/dL
Pharmacologic tx:
Ceftriaxone 1gm/day IV
Somatostatin
Octreotide
50ug IV bolus then 50ug/h
Cause splanchnic vasoconstriction
Can be given 5 days or longer
TREATMENT OF CHOICE for initial
management of variceal bleeding

Vasopressin:
Potent vasoconstrictor
Lowers portal pressure by splanchnic
vasoconstriction mesenteric
blood flow
Useful only for short term hemorrhage
control

MANAGEMENT OF ACUTELY BLEEDING VARICES

INJECTION SCLEROTHERAPY
FIRST LINE TREATMENT
Controls bleeding in 80-90% of patients
Re-bleeding rate of 30-50% of cases
Complication rate-20-40%
Perforation
Fever
Chest pain
Pleural effusion
BALLOON TAMPONADE
Sengstaken-Blakemore tube
Is a nasogastric tube with
esophageal and gastric balloons
for tamponade of varices
Tubes control bleeding in up 80 %
Bleeding
may
resume
in
approximately 20 50 % when
balloon is deflated

Schwartz

COMPLICATIONS
Pneumonia
d/t inability to clear salivary
secretions
Common unless proximal
suction tube is placed above
the esophageal balloon
Esophageal Rupture
d/t mechanical disruption or
ischemia of the esophagus
To minimize complications

Tube should be used for a limited

time (<24 hours)
PORTO-SYSTEMIC SHUNT THERAPY
Used to control refractory bleeding
CHILD-TURCOTTE-PUGH
Class
CLASS A: 5-6 points
CLASS B: 7-9 points
CLASS C: 10-15 points

Operative
Mortality
Rate

2%

10 %

50 %

TYPES OF PORTOSYSTEMIC SHUNTS

Transjugular Intrahepatic Portasystemic Shunt
(TIPS)
For those with decompensated liver
CTP B or C
Metallic stent is inserted between the
intrahepatic branch of portal vein and a hepatic
vein radicle
Needle tract is dilated until portal venous
pressure is reduced (< 12mm Hg)
90% success rate
25% incidence of encephalopaty

10

Schwartz

TIPS INDICATIONS
Initial treatment for bleeding refractory to
endoscopic and medical management
Refractory ascites
Budd-Chiari syndrome
Hepatopulmonary syndrome
Surgical shunts
For those with preserved liver function
70% long term survival in Child-Turcotte-Pugh
class A &B
Best used in Child class A & B who are not
candidate for liver transplant
Patients who may require liver transplant in the
future ( >1 year )
BEST TREATMENT for Recurrent Variceal
Bleeding
Non-selective Shunts
High risk of encephalopathy especially for
patients with marginal liver function
Used in patients with bleeding and ascites
refractory to medical treatment with
preserved liver function
PORTACAVAL SHUNT
Joins the portal vein to the IVC
Stops bleeding in 95%
High incidence of encephalopathy and
decreased liver function
Rarely done today
End to side
completely disrupts portal
vein flow to the liver
Side to side
MESOCAVAL SHUNT
Uses DACRON GRAFT in connecting the
superior mesenteric vein to the IVC
Technically easier than portacaval
shunt
Higher incidence of
Thrombosis
Rebleeding
Selective shunts
Decompress the gastrosophageal region
while preserving portal flow to the liver
Low incidence of encephalopathy
WARREN SHUNT
AKA: Distal Splenorenal Shunt

MOST DIFFICULT to perform

End to side splenic vein to left renal
vein anastomosis
Shunt used MOST OFTEN
Lowest rate of encephalophaty and
decompensation
INOKUCHI SHUNT
AKA: Coronary-caval shunt

ASCITES
MOST COMMON complication of cirrhosis
2 year survival of 50%
Sign of advanced disease
Transudation of fluid from the liver and intestine
Hypoalbuminemia
Salt and water retention
Antidiuretic hormone
Secondary Hyperaldosteronism
The following examinations must be done on the ascitic
fluid:
Culture and leucocytes count
WBC count 250/L INFECTIOUS
LDH level
Ratio of > 0.6 LDH in the ascitic fluid to serum
Suggestive of INFECTIOUS or CA
Serum amylase
Albumin
Ratio of serum to ascitic
> 1.1 gm/dl Portal Hpn
< 1.1 gm/dl malignant ascites
Medical tx:
Controls 90% of patients
Aim is loss wt. (0.5kg-0.75kg/day) by
Sodium restriction (2000mg/day)
Diuretics
Spironolactone and Furosemide
Fluid restriction
Not necessary unless w/ pronounced
hyponatremia (< 120mmol/L)
REFRACTORY ASCITES
Serial therapeutic paracentesis w/ or w/o
administration of albumin
Peritoneo-venous shunt
AKA: Le Veen shunt
INDICATIONS
Those who cannot undergo repeated
paracentesis
Not candidates for liver transplant
CONTRAINDICATIONS
History of variceal bleeding
Uncorrectable coagulopathy
Bacterial peritonitis
Cardiac failure
Transjugular Intrahepatic Portosystemic Shunt
Liver transplant
ultimate treatment
ENCEPHALOPATHY & COMA
Due to
Hyperammonemia
Ammonia intoxication
Protein from the intestine are converted to ammonia by
bacteria
Ammonia are brought to the liver and converted to urea
via Krebs-Henseleit Cycle
Precipitating factors
GI bleeding
Dehydration
Sedatives
Hypokalemia
Treatment:
Identify precipitating factors
Lactulose
Cathartic
Eliminates toxic substances
Acidify the colon
Decrease ammonia absorption
Inhibits the growth of bacteria

11

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Protein restriction (Minimum 40gm/day)

Antibiotics
NEOMYCIN
Active against urease producing bacteria
S/E: Ototoxic/nephrotoxic
CLINICAL MANIFESTATION
Asterexis or Liver Flap
Altered LOC

GALLBLADDER
ANATOMY & PHYSIOLOGYOF THE
Gallbladder
Gallbladder
Parts
Neck
Body
Fundus

WALL OF THE GALLBLADDER

Composed of smooth muscle and fibrous tissue
Lumen is lined with high columnar epithelium

Process is predominantly under HUMORAL control

(via Cholecystokinin), vagal and splanchnic nerves
also play a role
Stimulus
for
gallbladder
emptying
is
Cholecystokinin (CCK-PZ)
HUMORAL control
Truncal vagotomy promotes stasis
NEURAL control affected
PATHOLOGICAL CONDITIONS OF THE
Gallbladder

VASCULATURE
Arterial supply
Supplied by Cystic Artery
Usually a branch of the Right Hepatic Artery
(95 % of the time)
Venous return
Via Cystic Veins to the portal vein and small veins that
drain directly into the liver
Lymphatic drainage
From the gallbladder goes both to the liver and to
hilar nodes
PHYSIOLOGY
BILE is produced by the LIVER and transported via
EXTRAHEPATIC DUCTS to the GB, where it is concentrated
and released in response to humoral and neural control
Hepatic Production of Bile
Under NEURAL and HUMORAL control
FACTORS that Bile Flow
Vagal and splanchnic stimulation
Secretin
Theophylline
Phenobarbital
Steroids
~ 600 ml of bile are produced daily
Normal range 250 1000 ml/day
Composition of Bile
Electrolyte concentration of bile approximates
that of plasma
Lactated Ringers Solution
Good replacement fluid for biliary
losses
COMPOSED OF
Electrolytes and water
Bile pigments
Protein
Lipids
Phospholipids
Primarily Lecithin
Cholesterol
Bile acids (bile salts)
Chenodeoxycholic Acid & Cholic
Acid
Conjugated with Taurine &
Glycine
FUNCTION
Storage of bile
Concentration of bile
Absorption of water and electrolytes by the GB
mucosa
Results in a 10 fold increased concentration of
lipids, bile salts, and bile pigments compared
with hepatic bile
Secretion of MUCUS
Protects the GB mucosa from the irritant effects
of bile
Facilitates the passage of bile through the cystic
duct.
Mucus secretion represents the white bile
seen with Hydrops of the GB
Results from cystic duct obstruction
Release of bile
The coordinated release of bile requires simultaneous
contraction of the GB and relaxation of Sphincter of
Oddi

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Cholelithiasis
AKA: Gallstones
Types & Mode Of Formation
Gallstones form as a result of biliary solids precipitating
out of the solution
70 % are made up of:
Cholesterol
MAJOR component
Bilirubin
Calcium

PATHOGENESIS OF CHOLESTEROL STONE

Clinical conditions associated with bile malabsorption

Ileal disease
Ileal resection
Small bowel obstruction
Blind-loop syndrome
TYPES OF GALLSTONES

CHOLESTEROL STONES
Large and smooth
Solubility of cholesterol in bile depends on the
concentration of:
Bile salts
Lecithin
Cholesterol
Lecithin and Cholesterol
INSOLUBLE in aqueous solution
Dissolve in bile salt lecithin micelles
Failure of the liver to maintain a micellar liquid can be
caused by:
Increase in the concentration of cholesterol
CHOLESTEROL stone formation
Decrease in the concentration of bile salts or
lecithin CHOLESTEROL stone formation

PIGMENT STONES
AKA: Bilirubin Stones
Contains <10% cholesterol
Calcium Bilirubinate
gives the dark color
Types of pigment stone

13

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Black Pigment Stone

Small, black, brittle, SPICULATED
Formed by supersatruration of
Calcium bilirubinate
Carbonate
Phosphate
Secondary to:
Hemolytic disorders
conjugated bilirubin
deconjugated bilirubin
Cirrhosis
secretion of deconjugated
bilirubin
Brown Stones
Brownish-yellow, soft, often MUSHY
Formed either in the gallbladder or bile duct
Secondary to
Bacterial infection caused by bile stasis
E.Coli
Secretes B-glucorunidase
Cleaves
bilirubin
glucorunide

unconjugated bil.
Major Part of the Stone:
Precipitated Calcium Bilirubinate
Bacterial Cell Bodies
LOCATION
ASIANS
Typically found in the biliary tree
Stones d/t stasis secondary to
parasite infection
WESTERNERS
Occurs as primary bile duct
stones in patients with strictures
or other CBD stones that cause
stasis and bacterial contamination
CLINICAL PRESENTATION
ASYMPTOMATIC CHOLELITHIASIS
Few patients developed symptoms (1-4%)
2/3 of patients w/ silent gallstones remains
asymptomatic.(20 year study)
ABSOLUTE
indication
for
Prophylactic
Cholecystectomy
Porcelain GB
RELATIVE indications
Elderly patient w/ DM
Isolation from medical care for extended
period
TPN-induced gallstones
CHOLECYSTITIS
Inflammation of the gallbladder
CAUSES
MAJOR: 85 90 % of cholecystitis
Calculi
Bile stasis
Bacteria
MINOR
Pancreatic juice irritation
Play a lesser role
2 TYPES
Chronic Cholecystitis
Clinical presentation:
Abrupt and severe epigastric or RUQ
pain radiating to the RIGHT Upper back
PAIN Typically during night and after a
fatty meal
Pain typically last to 1-5 hours
IF Pain > 24 hrs
Impacted stone in the cystic
duct Hydrops Of The GB
Accumulation of mucoid
material within the gallbladder
ACUTE cholecystitis
HISTOLOGY
There are areas of FIBROSIS and
MONONUCLEAR cell infiltration

Outpouchings
of
the
mucosal
epithelium
through
the
wall
(Rokitansky-Aschoff sinuses) are also
noted
DIAGNOSIS
Abdominal Ultrasound
Standard DIAGNOSTIC test
TREATMENT
Cholecystectomy
While waiting for surgery or if
surgery must be postponed
Low fat diet
Avoid large meals
DIABETIC w/ symptomatic GB
stones
Surgery must be done
promptly
PREGNANT women that cant be
managed by diet modification
Cholecystectomy after the
nd
2 trimester
Acute Cholecystitis
Secondary to stones in 95% of cases
CLINICAL MANIFESTATION
Biliary colic
Pain does not subside
Unremiting
May last for several days
Fever, anorexia nausea and vomiting
(+) Murphys sign
Palpable mass
d/t gallbladder w/ matted
omentum
DIAGNOSIS
Laboratory Findings:
Mild to moderate leukocytosis
12,000-15,000
Liver transaminases
Usually NORMAL
MILD elevation of bilirubin
(<4mg/ml)
and
alkaline
phosphatase
MARKEDLY elevated bilirubin seen
in:
CBD stone
Mirrizis syndrome
Extrinsic compression of
the common hepatic
duct by stones impacted
in the cystic duct or
gallbladder neck

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Ultrasonography
MOST USEFUL RADIOLOGIC TEST
Documents:
+ or of stones
Thickening of the GB wall
Pericholecystic fluid
Murphys sign
Biliary Radionuclide Scanning (HIDA
scan)
Noninvasive evaluation of:
Liver
GB

bile ducts
IV
Technitium 99 labeled
dimethyl
iminodiacetic
acid
(HIDA)
NONFILLING OF THE GB after 60
minutes Acute Cholecystitis
Cholescintigraphy
CT scan
Performed in patients with acute
abdomen
Less sensitive than ultrasound in
dx gallstones
TREATMENT
Antibiotics
Third gen cephalosporin or
Second gen. cephalosporin +
metronidazole
Aminoglycoside + metronidazole
if allergic to cephalosporin
Cholecystectomy
Early cholecystectomy
2-3 days of the illness
If unfit for surgery or patient
present late (3-4 days of illness)
Antibiotics
Then cholecystectomy 2
months later
Acalculous Cholecystitis
Typically seen in
Critically ill patients
Patients on parenteral nutrition
Patients with extensive burns
Sepsis
Multiple organ failure
Actual cause is UNKNOWN
CLINICAL PRESENTATION
GB distention
Bile stasis and ischemia
DIAGNOSIS
Ultrasound
DIAGNOSTIC TEST OF CHOICE
Abdominal CT scan
To rule out other sources of
infection
HIDA scan
TREATMENT:
Percutaneous Ultrasound Or CTGuided Cholecystostomy
Diagnostic and therapeutic
90% success rate
Open Cholecystostomy
Cholecystectomy
Alternative procedure for those
that dont improve w/ the above
treatment
Complications Of BLADDER STONE
EMPYEMA of the Gallbladder
Intraluminal abscess of the gallbladder
CLINICAL PRESENTATION
Patients appears toxic
Fever
Leukocytosis
TREATMENT
Emergency Cholecystectomy
EMPHYSEMATOUS CHOLECYSTITIS
Gas within the gallbladder wall with
ischemic necrosis
AGENTS
Clostridium welchii
E. coli
Klebsiella
Seen primarily in DIABETICS
TREATMENT
Emergency Cholecystectomy
CT scan shows gas within a thickened
gallbladder wall (arrows) containing a large
gallstone (arrowhead)

Perichole
cystic dissection of the gas (G)
GANGRENOUS CHOLECYSTITIS
Results when extensive inflammation
causes thrombosis of the cystic artery
Necrosis of the gallbladder
MORPHOLOGY
Marked purulent inflammation and
necrosis
Numerous gallstones are surrounded
by thick pus
MANAGEMENT: Essentials
Bile cultures
Appropriate antibiotics
PERFORATED CHOLECYSTITIS
Results from necrosis of the gallbladder wall
and leakage of bile into the peritoneal
cavity
COMPLICATIONS
Peritonitis
Subhepatic abscess: MC
BILIARYENTERIC FISTULA & GALLSTONES
ILEUS
Complications of:
Cholelithiasis
Cystic duct obstruction
Recurrent cholecystitis
Adhesions to the surrounding viscera
Perforation
Fistula formation
Passage of the stone into the bowel
SITE OF FISTULA with the GB
Duodenum most common
Colon and other intra-abdominal
viscera may be involved
GALLSTONE ILEUS
Site of bowel obstruction
Terminal ileum
MOST COMMON
Narrowest portion of the
small bowel
Stones smaller than 2 3
mm usually passed per
rectum
If stone is passed free into the
peritoneal cavity
Extra luminal
obstruction
secondary to inflammation and
adhesions can occur anywhere
DIAGNOSIS
Correct diagnosis is made preoperatively In fewer than 25 % of
cases
Diagnosis is suggested by
History
Plain films of the abdomen
May show small bowel
obstruction
accompanied by air in
the biliary tree
May show radiopaque
stone in the RLQ (seen
in 15 % of cases)
CHOLECYSTOENTERIC FISTULA
Detection of cholecystoenteric fistula
radiologically.
ERCP

15

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Showing
appearance
of
pneumobilia with common bile
duct stone and a fistula between
collapsed
gallbladder
and
transverse colon
TREATMENT
Patients are often extremely ill
Emergency
laparotomy
may
permit only:
Localization of the stone
Proximal enterotomy
Stone extraction
Closure of the enterotomy
Whole small bowel, CBD and GB
Must be palpated for stones
Recurrent gallstones ileus (due to
other stones) develops in 5 9 %
of patients
Cholecystectomy and closure of the
biliary fistula
Can
be
performed
either
concomitantly or after an
interval, depending on the
patients condition
GALLBLADDER
NEOPLASMS OF THE
Gallbladder

Gallbladder Carcinoma
th
5 most common GI malignancy
AGGRESSIVE tumor
Most are unresectable at time of diagnosis
PROGNOSIS
5year survival rate: <5%
Median survival of 6 months
INCIDENCE
1% for those underwent cholecystectomy
Risk factors
CHOLELITHIASIS
MOST IMPORTANT risk factor
95% of patients have gallstones
Gen population with gallstone- < 0.5% risk
1.5% for high risk group
Large stones (>3cm)
10 fold risk of GB CA
Risk is higher in symptomatic pt
CALCIFIED GB (Porcelain GB)
Mandatory cholecystectomy

Cholecystectomy performed as soon after

diagnosis as possible because of HIGH
INCIDENCE OF MALIGNANCY
Presents w/ extensive, yellowish intramural
calcification and stones
POLYPS
>10mm risk
CHOLEDOCHAL CYST
SCLEROSING CHOLANGITIS
EXPOSURE TO CARCINOGENS
Nitrosamines
MORPHOLOGY
Gallbladder wall is infiltrated by firm, greyish-white tumor
Lumen contains gallstones
TREATMENT
T1- limited to the muscular layer
Cholecystectomy
T2- invasion of the perimuscular connective tissue w/o
extension to the serosa or to the liver
Extended Cholecystectomy

Segments 4 and 5 + lymphadectomy

T3 and T4- beyond the serosa, invade the liver or other
organs
Extended (Rt) Hepatectomy
Segments 4-8
BILIARY TRACT
DISORDERS OF THE
Biliary Duct

Choledocholithiasis
Stones in the common bile duct
Can be single or multiple
Found in 10 20 % of patients who undergo cholecystectomy
6-12% of patients with GB stones
Incidence increases with age
Most stones are formed in the GB and pass into the duct
Primary common bile duct stones can form in the absence of a
gallbladder
POSITIONS where GALLSTONES may get stuck

RETAINED OR RECURRENT STONES

Stones that remain after surgery complicate up to 5 10 %
of CBD explorations
No treatment is necessary for small stones
Usually pass spontaneously
Treatment options for large stones
CHEMICAL DISSOLUTION
Intraductal administration of methyl-tertbutyl
ether or mono-octanoin
MECHANICAL EXTRACTION
Endoscopic removal
BEST TREATMENT
Sphincterotomy
Removal via a T-tube tract using Dormia basket
under fluoroscopic guidance
For patients who underwent open CBD
exploration
PRIMARY OR RECURRENT CBD STONES
Can be treated surgically with a biliary-enteric connection
to allow stones to pass out of the biliary
tree
2 most common methods are:
Choledochoduodenostomy
Choledochojejunostomy
OTHER options
Transduodenal Sphincteroplasty
Endoscopic Sphincterotomy
TYPES
Primary CBD stone
Usually brown pigment stones
Associated with stasis and infection
More common in Asian countries
Secondary CBD stone
MORE COMMON
Mostly cholesterol
Formed in the GB
CLINICAL PRESENTATION
Some patients are asymptomatic
Most patients present with RUQ pain that radiates to the
back and right shoulder

16

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Intermittent obstructive jaundice

Acholic stools
Bilirubinuria
Pain, nausea and vomiting
Cholangitis
Symptoms maybe intermittent (ball valve)
DIAGNOSIS
GB is not palpable in contrast to neoplastic obstruction of
the CBD
Diagnostic studies include
Ultrasonography
GB stone
Dilated CBD (>8mm)
ERCP
Transhepatic Cholangiography
Radionuclide Scan
Magnetic Resonance Cholangiography (MRC)
Can dx CBD stone in a >5mm diameter CBD
Endoscopic Cholangiogrphy
GOLD STANDARD
Liver function test
Consistent With Obstructive Jaundice
Includes Elevations In Bilirubin And Alkaline
Phosphatase
TREATMENT
Endoscopic cholangiogram followed by sphincterotomy
LAP CBD exploration
Open CBD exploration
T-tube inserted
Cholecoduodenostomy/ Roux en-Y Choledocho
Jejunostomy
For stones impacted in the ampulla
Cholangitis
Infection of the bile ducts
Potentially life-threatening disease that results from concurrent
biliary infection and obstruction
E. coli
most common offending organism
ETIOLOGY:
Benign postoperative strictures & CBD stones
MC cause, 60 %
Other causes:
Neoplasms
Sclerosing cholangitis
Plugged biliary drainage tubes
Biliary contrast studies
CLINICAL PRESENTATION:
Charcots triad (70%)
Fever
Jaundice
RUQ pain
Reynolds pentad
Present in severe cases Ascending Cholangitis
Combinations of Charcots Triad plus
Shock
Altered mental status
TREATMENT:
Antibiotics
Resuscitation with fluids and electrolytes
Relief of obstruction
PROGNOSIS:
Depends on the cause of the obstruction
Best prognosis to worst
Stones
Benign stricture
Sclerosing cholangitis
Neoplasm
SCLEROSING CHOLANGITIS
Characterized by inflammatory strictures involving both
the extrahepatic and intrahepatic biliary system
Primary Sclerosisng Cholangitis
NO KNOWN CAUSE
Associated with ulcerative colitis in 2/3
More common on MALES
Hepatic duct bifurcation
MOST COMMONLY AFFECTED

17

Risk for development of CHOLANGIOCARCINOMA

CAUSE OF DEATH
Most die from Hepatic Failure
Clinical presentation:
Symptoms and signs includes
RUQ pain
Painless jaundice
Usually without fever or chills
Pruritus
Fatigue
Nausea
Symptoms of hepatic failure
Other inflammatory conditions, particularly
ulcerative colitis may be present
Diagnosis:
Usually made by ERCP or a transhepatic
cholangiogram
Occasionally
made
by
intraoperative
cholangiography
CRITERIA NEEDED TO FULFILL THE DIAGNOSIS
Thickening and stenosis of a major portion
of the biliary ductal system
Absence
of
prior
surgery,
choledocholithiasis,
malignancy
or
congenital biliary anomalies
No evidence of primary liver disease,
particularly primary biliary cirrhosis
ERCP
Multiple dilatations and strictures (beading)
Hepatic Duct Bifurcation
MOST COMMONLY affected
Cholangiography (PTC)
Treatment:
Operative management is dependent on the
level of bile duct involvement and the amount of
fibrosis present
GOAL OF OPERATIVE MANAGEMENT
Restoration of adequate and permanent
biliary
APPROACHES
Internal Biliary Drainage
Hepatico-Enteric
or
CholedochoEnteric Anastomosis
PREFERRED
METHOD
of
management
Successful only when the major
area of involvement is the
extrahepatic bile ducts
External biliary drainage
T tube or other Percutaneous stent
Establishes adequate drainage
Cholestectomy
Performed only when GB disease
requires it
Postoperative treatment:
Strongly dependent upon the presence of
preoperative
sepsis and the adequacy of
drainage
Steroids
NOT BENEFICIAL
Could
potentially
complicate
the
postoperative course
Prognosis
Poorly defined at present
If the liver parenchyma has been damaged or if
the intrahepatic ducts are significantly involved
HEPATIC TRANSPLANTATION
Offers a real chance of longevity

Schwartz

Only possible when the patient is free

of sepsis
Secondary Sclerosing Cholangitis
CAUSES
Bile duct stones
Previous biliary surgery
Toxic agents
GALLBLADDER
NEOPLASMS OF THE
Bile Duct

Cholangiosarcoma
Tumor that arises from the bile duct epithelium
Represents 5 30 % of all primary hepatic malignancies
Clinical presentation:
Right upper quadrant pain
Jaundice
Hepatomegaly
Occasionally a palpable mass
Patients are usually 60 70 years of age
Cholangiocarcinoma
CBD tumor
RARE and difficult to cure
Clinical presentation:
Pruritus
Anorexia
Weight loss
Aching RUQ pain
Jaundice is usually severe
Diseases a/w this MALIGNANCY
Sclerosing cholangitis
Chronic parasitic infection of the bile ducts
Gallstones (18 65 % of cases)
Prior exposure to Thorotrast
DIAGNOSIS
Percutaneous Transhepatic Cholangiography (PTHC) or
ERCP
Both procedures are capable of biopsy for pathologic
examination

PTHC
GOLD STANDARD
Defines the extent of the tumor
Contrast material administered through a Chiba
needle (Arrows) completely fills the intrahepatic bile
ducts w/c are extremely dilated because of an
obstruction of the common bile duct
Ultrasound or CT scan
Dilated intrahepatic biliary tree but normal GB and
extrahepatic bile ducts
ERCP
Asses the distal bile ducts
CA 19-9
Sensitivity 79%, Specificity 98%
>129 U/ml
Can be seen also in:
Cholangitis
Other GIT and GYNE neoplasm
LOCATION of tumor
Distal CBD
1/3 of cases
Common hepatic duct or cystic duct
1/3 of cases
Right or left hepatic duct when the confluence of the
hepatic ducts is involved

 May improve the life expectancy

ADVANCED & UNRESECTABLE TUMORS
Surgical Bypass for biliary decompression
Non-operative biliary decompression
Percutaneous Placement Of Metal Stents
For PROXIMAL tumors
Endoscopic Placement Of Metal Stents
For DISTAL tumors
Should have
RIGID stents placed to provide
palliation of the biliary obstructive symptoms
PROGNOSIS
Laparotomy with no bypass
Average survival time of < 6 months
Laparotomy with stenting
Average time 19 months
PROGNOSIS
Resectable:
5 year survival: 30-50%
Median survival: 32-38 months
Unresectable:
Median survival: 5-8 months
MOST COMMON cause of death
Hepatic failure
Cholangitis

Klatskin tumor
AKA: Hilar Cholangiocarcinoma
TUMOR SPREAD
Metastasizes to the regional lymph nodes (16 %)
Direct extension into the liver (14 %)
Metastasizes to the liver (10 %)
RISK FACTORS
Primary sclerosing cholangitis
Choledochal cyst
Biliaryenteric anastomosis
Hepatolithiasis
Ulcerative colitis
Thorotrast dye
Biliary tract infections
Clonorchis Sinensis infection
Typhoid carriers
TYPES
Type 1
Confined to the common hepatic duct
Type 2
Involves the bifurcation (Klatskin Tumor)
Type 3a / Type 3b
Right intrahepatic duct / left intrahepatic duct
Type 4
Both right and left secondary intrahepatic ducts
CLINICAL MANIFESTATIONS
Painless jaundice
MOST COMMON presentation
Pruritus
Mild RUQ
Cholangitis
Weight loss
TREATMENT
GENERAL
Generally surgical
< 10 % are resectable at the time of the initial
diagnosis
RESECTABLE TUMORS
Distal Bile Duct Tumor
Resected
by
Pancreaticoduodenectomy
(Whipple Procedure) with biliary and
gastrointestinal reconstruction
More Proximal Lesions
Can sometimes be locally resected with biliary
reconstruction

18

Bifurcation
Bilateral Roux Y hepaticojejenostomy
Right Or Left Hepatic Ducts
Right or left hepatic lobectomy
PROGNOSIS
Average length of survival after resection is 23
months
Postoperative radiation

Schwartz

Choledochal Cysts
Congenital cystic dilatation of the EXTRAHEPATIC and/or
INTRAHEPATIC biliary tree
More common in FEMALES
Frequently dx in infancy or childhood
Cause is UNKNOWN
90% have anomalous pancreatico-biliary duct junction
Allow reflux of pancreatic secretion into the biliary
passages leading to:
Inflammation increased pressure
Cyst formation
Classification
Type I:
Fusiform dilatation of the CBD
MC type
Type II:
Diverticulum of the CBD
Type III:
Choledochocele involving the INTRADUODENAL
PORTION of the CBD
Type IV:
Cystic involvement of both INTRAHEPATIC &
EXTRAHEPATIC bile ducts
Type V:
Cystic dse of the INTRAHEPATIC ducts
Carolis disease

CLINICAL PRESENTATION
INTERMITTENT jaundice
Cholangitis
CLASSIC TRIAD (< 50%)
Abdominal Pain
Jaundice
Mass
DIAGNOSIS
UZ or CT scan
Usual initial exam

 Will CONFIRM the diagnosis

Endoscopic Transhepatic or MRC
Needed to assess the biliary tree and to plan the
appropriate surgical treatment
TREATMENT
Types I, II, IV
Excision of the extrahepatic biliary tree,
cholecystectomy, Roux-en-Y Hepatico jejenostomy
In type IV- additional hepatic resection maybe
needed

Type III
Excision of the Cyst, Choledocoduodenotomy
Sphincterotomy
Type V (Carolis disease)
Biliary drainage (PTC or ERCP)
First line therapeutic modalitiy
Hepatic resection
If limited to a single lobe
Unresponsive recurrent cholangitis
Small T1 or T2 cholangio CA

19

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