Professional Documents
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Underside of liver
Pear shaped
7.5-12 cm long
Capacity: 25-30 mL
Fundus, body, neck
Cystic duct: 3 cm in length
Muscle in wall of GB: arranged in criss cross manner
Well developed in neck
Mucosa have indentation that sink upto muscle coat: crypts of Luschka
Cystic duct: 3 cm in length
Lumen: 1-3 mm in dM
Mucosa of cystic duct: arranged in spiral fold: valves of Heister; wall surrounded by sphinchter
of Lutkens
Common hepatic duct: less than 2.5 cm
Cbd: 7.5 cm: 4 PARTS
o Supraduodenal: free edge of lesser omentum: 2.5 cm
o Retroduodenal
o Infraduodenal: posterior to pancreas
o Intraduodenal: surrounded by sphincter of oddi – terminates in ampulla of vater
Calot’s triang;e/hepatobiliary triangle:
o Superiorly: inferior surface of liver
o Laterally: cystic duct + medial border of GB
o Medially: common hepatic duct
Importance of callot’s triangle: the cystic artery (artery to GB) can be found here
Congenital anomaly in the hepatic artery or cystic artery: difficulty during cholecystectomy
Lymphatics: cystic LN (LN of Lund) – this is the sentinel LN - lies in the angle between cystic duct and
common hepatic duct – they go LN in hilum of liver – then celiac group of para aortic LN
Physiology: bile produced in liver – stored in GB – and it is released in duodenum – bile in duodenum –
then upto terminal ileum – there 95 percent is reabsorbed – back to liver again by portal vein (this
whole thing is called enterohepatic circulation)
Functions of GB:
Reservoir of bile
o During fasting: sphincter of oddi is closed (the sphincter that guards opening of CBD in
2nd part of duodenum ampulla of vater) – then the bile from liver is diverted to GB
o After meal – sphincter open – then gb also contracts due to cholecystokinin and bile
goes to dueodenum
Concentration of bile by reabsorption of water, NaCl, Hco3 – increase in concentration of bile
salt, bile pigment, calcium, cholesterol
Secretion of mucus (20 ml per day) (complete obstruction of cystic duct/neck of GB – this mucus
accumulates – mucocele of GB)
Investigations in GB:
Plain x ray/Plain CT
Gall stone 2 types: radiopaque (only 10 percent), radioluscent (not seen in x ray) – center of
gallstone may have radioluscent gas – Mercedes benz sign
Plain x ray also shows: porcelain GB (whole GB is calcified in cases of prolonged and chronic
cholecystitis)
If porcelain gb develops – cholecystectomy indicated – it has a high chance of GB carcinoma
USG:
Cholescintography:
Tc99 – injected – taken up by liver – excreted into bile – this allows visualization of biliary tree
and GB
If GB cannot be seen” acute cholecystitis
Contracted GB: chronic cholecystisis
Gallbladder ejection fraction low: gb dyskinesis
CT scan:
looks like caps worn by people of phyrgia – it is a normal anatomic variant; not a pathological variant
Absence of cystic duct: not an anatomical variant, but it is a pathological problem. Occurs proximal to
the stone in common bile duct
Extra hepatic bile ducts are gradually destroyed by inflammatory process that starts around
birth
Cause unclear
Intra hepatic change also occurs
Sometimes, portal htn develops
If untreated,death occurs due to liver failure
Clinical feature:
o Jaundiced at birth
o Jaundice deepens progressively
o Feature like obstructive jaundice – elevated ALP, elevated bilirubin (elevated ALP
indicated bile duct pathology)
o Pale stool and dark urine
o Prolonged steatorrea osteomalacia (no D abs maybe?) biliary rickets
o Severe pruritus
o Raised serum cholesterol clubbing and skin xanthoma
d/d: any cause of obs jaundice in children may be the d/d
o alpha 1 antitrypsin deficiency
o cholestasis/liver failure due to IV feeding (iv feeding includes glucose, amino acid, fat
which causes such biochemical changes that is injurious to the liver)
o choledochal cyst
o inspissated bile syndrome
rx:
o hepaticojejunostomy: the part of the bile duct proximal to the obstruction is
anatomosed to a portion of jejunum
choledochal cyst:
congenital dilation of intra/extra hepatic biliary ducts: but not associated with hepatic fibrosis
presentation: abd pain, fever, jaundice, RUQ pain
there is also abnormal communication between bile duct and pancreatic duct at the ampulla of
vater – so pancreatitis is also a complication
increased risk of developing cholangiocarcinoma
dc with usg/mri/ct
rx:
o excision of the cyst
rare
may occur due to GB/bile duct trauma
iatrogenic injury during surgery may als occur
bile duct section is repaired by choledocho – jejunostomy
Cause of gallstone:
gallstone 3 types
o cholesterol stone
o pigment stone (brown/black)
o mixed
usa and Europe: 80 percent cholesterol and 20 percent pigment
asia: 80 percent pigment stones
stone content: cholesterol, calcium salt, bile acid, bile pigment, phospholipid
bile is a solution: cholesterol is the solute, phospholipid and bile acid is the solvent
if solute is more than solvent, then the solute precipitates and becomes stone
so if cholesterol concentration in bile increases and bile acid/phospholipid concetration
decreases in proportion, then there is cholesterol precipitation and stone formation
this may be the pathogenesis of formation of cholesterol gall stone
increase concentration of cholesterol due to
o high calorie diet
o fatty and obese people
o OCP and some drugs
Decreased concentration of bile acid/phospholipid due to
o Decreased enterohepatic circulation of bile (normally liver makes bile, goes to bile duct,
then duodenum, then ileum, then reabsorbed and then sent to liver, liver gets back 95%
of the bile it made byt his way, if this recirculation is hampered, liver gets back less bile,
so liver has to make more and more bile, bile acid, phospholipid, if this goes on, liver
capacity to re-synthesis bile decreases and concetration of bile acid and phospholipid
deceases). Enterohepatic circulation of bile is hampered due to
Resection of gut such as terminal ileum due to some cancer or ohr causes
Crohn’s disease where there is malabsorption in the terminal ileum
Other causes of malabsorption
Pigment stone: gallstone with <30 percent cholesterol
o Black pigment stone: insoluble bilirubin polymer + Ca phosphate + Ca bicarbonate
Associated with hemolysis – such as sickle cell disease, spherocytosis
Cirrhosis pt also have higher incidence of these
o Brown pigment stone – contain calcium calcium bilirubinate, ca palmitate, ca stearate,
cholesterol
Brown stones USUALLY form in bile duct, not in gall bladder
Related to bile stasis and infected bile
Infected bile = bacteria in bile causes de-conjugation of conjugated bilirubin and
thus causes stone formation (Bacteria has beta glucuronidase that degrades
conjugated bilirubin/bilirubin glucuronide) – this unconjugated bilirubin is
insoluble in bile and then it precipitates
Brown stones also associaiited with presence of foreign body in bile duct such as
stent/ or organism such as Ascaris lumbricoides or clonorchis sinenesis within
the bile duct lumen
Common
o Appenditcitis
o Perforated PUD
o Acute pancreatitis
Rare
o Acute pyelonephritis
o MI (inferior MI)
o Right
Biliary colic
Acute cholecystitis
Chronic cholecystitis
Empyema of the gallbladder
Mucocele (if stone obstructs the neck of the GB and mucus secreted and accumulates in the GB)
Perforation
Biliary obstruction
Acute cholangitis
Acute pancreatitis (stone goes in pancreatic duct)
Fistula of gallbladder with ascending/transverse colon/intestine
Stone in gut – int obstruction – gallstone ileus
Diagnosis:
Treatment:
Grade II: elevated, WBC, palpable tender mass in RUQ, complain >72 hour, sign of local inflammation
If s/s of neither I/II: grade I = acute cholecystitis in an otherwise healthy person with no organ
dysfunction
Acalculous cholecystitis: in the absence of stone; s/s and other feature same to calculous cholecystitis
Cholesterosis (Strawberry GB): interior of GB looks like strawberry: yellow speck are the submucous
aggregations of cholesterol
Diverticulosis of the GB: black pigmented stones impacted in the outpouchings of the lacunae
Typhoid in GB:
Cholecystectomy:
Preparation:
Cbc and LFT and coagulation profile should be done – to see anemia, coagulation abnormalities
and liver function
Renal function test – for excretion of anesthetic drugs
Administer prophylactic antibiotics: 2nd generation cephalosporin
Subcutaneous heparin to prevent thromboembolism
Consent from the patient about the operation should be taken
Lap chol/open chol: the preparation and indications are the same; in both cases identification and safe
dissection of Calot’s triangle is extremely necessary
Mirizzi syndrome: stone ulcerates thru neck of GB into the common hepatic duct
Complications of cholecystectomy
Recovery after lap chole – less pain and faster return to normal activity than open method
Post operative fever, chills, abdominal pain etc if they occur require immediate investigation
Post operative mortality increases with: advanced age, comorbidity and acute presentation
Complications occur in 10-15 percent cases
Operative mortality is only 1 percent
Complication: 2 types
o Access complication
o Bile duct injuries – rare
Occurs due to poor dissection
Occurs due to failure to define the surgical anatomy
Deepening obstructive jaundice if there is a distal obstruction
Jaundice + fever may occur due to cholangitis ( needs immediate investigation)
Bile leakage may result in bile peritonitis
In case of incomplete obstruction, the bile duct will be fibrosed and then
jaundice will develop delayed
Management of complication
o USG – to see intra or extra hepatic duct dilatation
o MRCP/ERCP/HIDA scan to see the anatomy and place of the leak
o ERCP will help to remove stone/insert stent
o Small biliary leaks will resolve spontaneously if there is no obstruction
o If the cbd is damaged, it should be reconstructed
o In case of damaged cbd, an external drain should be placed percutaneously (such as T
tube) – this will allow the distal part of bile duct to heal unhampered by bile
o When the injury has healed, a definitive reconstruction surgery can be undertaken
o Treatment for bile duct stricture is: roux-en-Y choledochojejunostomy
o If the stricture is recent, ballon dilation with stent insertion (like angioplasty of heart
coronary arteries) can be done
Late symptoms after cholecystectomy
o Post cholecystectomty syndrome: if cholecystectomy fails to relieve the s/s for which
the operation was performed
o Cause:
Presence of stone in bile duct
Stone in stump of cystic duct
Operative damage to biliary tree
o Management
Full investigation to see the defect
MRCP/ERCP
ERCP also can be used to remove the obsturciton/stone or place a stent if
needed
Cholelithiasis after cholecystectomy:
o May occur due to infection of biliary tree
o May occur due to infestation by Ascaris lumbricoides or Chonorchis
o Any obstruction to bile flow can give rise to stasis + formation stone inside the duct s
o Consequence of duct stone: obstruction to bile flow and infection
o Symptoms of choledocholithiasis
Bouts of pain, jaundice, fever: charcot’s triad
This triad if present indicates cholangitis
o Sign
Tenderness in epigastrium and RUQ
If there is distension of the GB floow the Courvoisier’s law : obstruction from
stone usually doesn’t result in palpable GB, but obstruction from other causes
esp malignancy will make the GB palpable
o Pus may be present in biliary tree or liver abscess may develop
o Management
Determine the causew of jaundice by all invsestigartions necessary
USG, MRI, MRCP, ERCP, LFT – to identify the cause, nature and site of
obstruction
Rehydration, clotting mamagnement, diabetes exlusion
Administer broad spectrum antibiotics
After resuscitation has been done, relief the biliary obstruction
Treatment measures (minimally invasive)
Endoscopic papillotomy (cutting/loosening the ampulla of vater)
Stent placement
Removal of stones if present
Open laparotomy, followed by choledochotomy is done if these are not effective
Cbd is drained
Longitudinal inscision along the cbd and the sotnes are removed
Insert a T tube and close the duct around that (T tube is a tube, one part
is inside the bile duct, the other end comes outside the body through
skin outside the RUQ, this allows drainage of bile outside the body while
the bile duct is healing)
Place T tube until the bile has become clear and pt has recovered
Perfrom a cholangiogram to see if there are any more stone
If stones are found, the T tube is not removed but kept for a time of 6
weeks – after this time the stone can be removed from inside the bile
duct out through the T tube
Then the T tube is taken out
Congenital
o Biliary atresia
Iatrogenic during surgery
o Cholecystectomy
o Choledochotomy
o Gastrectomy
o Hepatic resection
o Liver Transplantation
Inflammatory
o Stones
o Inflammation (cholangitis)
o Parasitic
o Pancreatitis s
o Primary sclersoing cholangitis
o Radiotherapy
Trauma
Idiopathic
USG
T tube cholangiography (if T tube is inserted)
ERCP
MRCP
CT scan
Percutaneous transhepatic cholangiography
Papilloma
Adenoma
Multiple biliary papillomatosis
Granular cell myeloblastoma
Neural tumor
Leiomyoma
Endocrine tumor
Cholangiocarcinoma
Rare malignancy
Risk factor:
o PSC (primary sclerosing cholangitis) – long standing
o PSC with IBD
o It occurs in an earlier age if pt has PSC
o Hepatitis C infection
o Parastitic infection of bile duct/gb: (in Thailand, Vietnam, Laos)
Clonorchis sinensis
Opisthorchis viverrini
o Congenital conditions:
Caroli’s disease
Choledochal cyst
o Chemical insult
Vinyl chloride
Asbestos
o Post surgical
Clinical feature:
o Early s/s non specific: abd pain, early satiety, anorexia, wt loss
o In some: s/s of biliary obstruction: pruritus and jaundice
o If there is distal obstruction in bile duct, according to Courvoisier’s law there may be
palpable gall bladder
Investigation
o Elevated bilirubin
o Raised ALP
o Raisef GGT
o Ca 19-9 may be elevated
o MRI, MRCP, USG, CT – to see extent and location of the disease
o Ercp can be done and also place stents: good for distal lesions in CBD
o PTC: percutaneous cholangiography: for proximal lesion in CBD: those which are nearer
to abdominal wall and far for ERCP probe to reach
o PET scan: detect LN, distant metastasis
Treatment:
o Depends of site and extent of the tumor
o Only 10-15 percent suitable for surgical management
o Resectability depends on
Patient factors – comorbidities, presence absence of cld
Tumor factors – extent of disease, vascular involvement , presence or absence
of metastatic disease
o Surgical options
Standard hepatic resection
Extended heaptic resection
With en bloc lymphadenectomy
Distal cbd tumor: requires pancreaticoduodenectomy (whipple procedure)
If locally unresectable without distant metastasis: liver transplantation
Transplantation may be combined with neoadjuvant chemo
Unresectable disease: palliative therapy:
Aim: relief symptom + improve quality of life
Prevent liver failure due to bile obstruction
Relief the obstruction by ERCP/PTC
Ca of Gallbladder:
Rare
Highest in chile, American india, northern india
Etiology:
o Association with pre existing gallstone disease
o Stone chronic inflammation
o Chronic cholecystitis leading to calcification porcelain gall bladder is also
related to development of gb carcinoma
o Carriers of typhoid in gall bladder also may develop
Gallbladder polyps may also be found – in USG
Pathology of GB carcinoma:
o Mostly – 90 percent – adenocarcinoma
o Some: chronic irritation of the mucosa by stone: squamous metaplasia leading to
squamous cell carcinoma
o TUMOR spreads by direct extension to the liver, seeds the peritoneal cavity
o May also involve the perihilar lymphatics
S.s
o May be asymp at time of dx
o S.s – same as biliary colic/cholecystitis/ gallstones
o In old pt – jaundice and anorexia
o Late sign: palpable mass
o Most pt present with advanced disease
Inv:
o Consistent with biliaty obstruction – raised bilirubin, raised ALP, raised GGT
o Anemia, leukocytosis
o Raised ESR, CRP
o USG, CT, MRI to see extent and distal metastasis
o Pet scan may alos bw done