Anatomy + physio

 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:

 1st line investigation

 Not easy if there is too much fat and bowel gas s
 Size of gb, whether there are stones, or polyps, wall thickness can be measured
 Inflammation in the gb, size of CBD (whether dilated or not), stone w/n the extra hepatic biliary
apparatus can be seen also seen
  In pt with obs jaundice – it can identify intra and extra hep bile duct dilatation due to stone – the
part proximal to stone will be dilated – so it may also help to identify the site of the obstruction
 Cause of obstruction may also be identified
 Other bile duct lesion such as – cholangiocarcinoma, enlargement of pancreatic head indicating
pancreatic carcinoma can be identified
 This was all about trans abdominal ultra sound (probe placed on abdominal wall)
 Endoscopic ultrasound: probe introduced by endoscopy – seen the bile duct and gb from inside
the stomach and duodenum – it can diagnose
o It can also dx pancreatic and peri ampullary carcinoma
o Here biopsy can also be taken

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:

 Less operator dependent (vs usg)

 Isn’t affected by body fat content
 Can see: liver, gallbladder, bile duct, pancreas
 Enlarged LN can be seen, metastatic disease can be identified
 Only 75% of gallstones are indetified by CT – not used as a screening method for gallstones

MRCP (magnetic resonance cholangio-pancreatography)

 Bile is used as contrast agent

 MRI is then done and the extra hepatic biliary apparatus is visualized – its patency, dilation,
stone, stricture, obstruction etc

ERCP (endoscopic retrograde cholangio-pancreatography)

 Endoscope enterted thru mouth  esophagus  stomach  duodenum  ampulla of vater 

common bile duct  see everything inside; also can go to pancreatic duct and see
 See + take substance for biopsy if needed
 Also can loosen the tight sphincter if needed (sphinterotomy)
 It can also remove small stones in bile ducts
 It can place stent in strictured bile ducts or sphincters (like angioplasty)
 Thus it has both diagnostic and therapeutic uses
 Injection of contrast in done to visualize the bile duct
 Stone, malignant stricture etc can be seen
 But ercp has side effects since it is a very invasive procedure  such as it can irritate the
pancreas and cause acute pancreatitis
Congenital abnormalities of GB and bile duct: during early fetal life, GB is entirely intra hepatic

Absent GB – this maybe a problem

The Phrygian cap:

looks like caps worn by people of phyrgia – it is a normal anatomic variant; not a pathological variant

Floating GB: it may hang on to the mesentery – it makes it vulnerable to torsion

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 biliary atresia:

 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

congenital dilation of the intrahepatic ducts: (caroli’s disease)

 multiple irregular dilation in the intrahepatic biliary ducts

 congenital hepatic fibrosis
 presentation:
o abdominal pain
o jaundice
o fever
o cholangitis
o end stage liver disease
o long standing complication: malignancy
 management:
o for cholangitis/jaundice: antibiotic
o for bile obstruction: stenting by ERCP

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

trauma to gall bladder/bile duct: rare

 rare
 may occur due to GB/bile duct trauma
 iatrogenic injury during surgery may als occur
 bile duct section is repaired by choledocho – jejunostomy

Gallstone (cholelithiasis) : most common pathology of bile duct

Gallstones are asymp. In majority of the cases (80%)

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

Clinical presentation of gallstone:

 May remain asymp

 Maybe detected upon usg/ct etc done for some other reasons
 If symptoms occur:
 RUQ pain, epigastric pain, may radiate to back
 Pain: dull and constant, may be sometimes described as colicky (biliary colic = not true colicky
pain)
o Biliary colick = severe RUQ pain that ebbs and flows
o Associated with nausea and vomiting
o May radiate to chest
o Pain severe
o Lasts for minutes, even several hours
o Pain starts during the night and wakes the pt
o Similar episodes of pain – may be felt during the day
o THIS MAY LAST over a few weeks and then no more trouble for some months
 Dyspepsia
 Flatulence
 Food intolerance – particularly fat rich foods
 Jaundice – if stone from gb comes out and obstructs the common bile duct
 Rarely. Gallstone can go to gut and cause obstruction in gut (gallstone ileus)
 If s/s continue (RUQ /epigastricpain) and associate with fever + leukocytosis = acute cholecystitis

d/d of acute cholecystitis:

 Common
o Appenditcitis
o Perforated PUD
o Acute pancreatitis
 Rare
o Acute pyelonephritis
o MI (inferior MI)
o Right

Effect and complications of gallstones:

 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:

 Based on hx and examination

 Confirm by USG, radionuclide scan
 In acute phase: murphy’s sign
o Press on the right subcostal area and ask the patient to inspire deeply
o At the height of inspiration there is sudden cessation of inspiration due to the
gallbladder being pressed against the examining hand as it goes down due to descent of
the diaphragm
o Positive murphy sign = acute inflammation
o Assoc with leukocytosis and elevated LFT and fever
o Inflamed omentum around gallbladder may be palpated as a mass
 Do USG/CT to confirm
 In most cases, the stone that caused the inflammation slips back into the gallbladder and the
bile drainage into cystic duct is continued, and the inflammation resolves itself – self limited
 If resolution doesn’t occur – the inflmmation spreads to muscularis layer and serosa – empyema
of GB = perforation and peritonitis may occur
 Important: stone in GB usually never causes palpable gall bladder, because stone for long time
= chronic cholecystiis = shrunken small GB = GB small and should not be palpable
o If GB is palpable, it means there is distral obstruction in ampulla of vater such as due
to carcinoma head of pancreas or peri ampullary carcinoma – so palpable gall bladder
= worse prognosis
o These are called “Courvoisier’s Law/sign ”
o Exception to this law: obstruction of GB neck by stone causes “mucocele” and thethen
GB is palpable

Treatment:

 Observation only fot asymp patients

 Prophylactic cholecystectomy for symptomatic pt / those who develop complication
 Diabetic pt should undergo prophylactic cholecystectomy even if no symptom is present
 Cholecystectomy is the rx of choice
 90 percent cases: acute cholecystitis resolves with conservative/non operative rx
 Conservative rx:
o NPO + IV fluid until pain resolves
 oAnalgesics
oAntibiotics – broad spectrum ab against gram –ve aerobes: ciprofloxacin, cefuroxime,
cefazolin)
o When temperature, pulse etc indicate that the acute inflammation has subsided, oral
fluid started, then regular diet
o USG done to confirm the resolution
o If there is jaundice do MRCP to see stone in bile duct
 When to do cholecystectomy: if the pt has grade III disease, if the pt has co-morbidity etc

Grade II: elevated, WBC, palpable tender mass in RUQ, complain >72 hour, sign of local inflammation

Grade III: cvs/neurological/renal/respiratory/hepatic/hematological dysfunction present

If s/s of neither I/II: grade I = acute cholecystitis in an otherwise healthy person with no organ
dysfunction

Empyema of gallbladder: GB is distended with pus; rx is: drainage followed by cholecystectomy

Drainage of GB is called: cholecystostomy

Acalculous cholecystitis: in the absence of stone; s/s and other feature same to calculous cholecystitis

 It is seen in critically ill pt

 Also seen in pt recovering from major surgery, trauma, burns

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:

 S. typhi. S. typhimurium can infect GB

 Acute cholcecystitis can occur
 More commonly chronic can occur
 Pt becomes a chronic carrier excreting this in bile
 Not sure whether salmonella predisoposes to stone/or stone predisposes to salmonella
 Rx with ampicillin + cholecystectomy
 If ampicillin allergy: use quinolone antibiotic

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

Laparoscopic cholecystectomy (Lap chol.)

 Procedure of choice for majority of pt with GB disease

 Induction and maintenance of GA
 Pneumoperitoneum established (co2 entered into the abdomen to make it swollen)
 Three ports usually made for laparoscopy: sub umbilical, sub xiphoid, right subcostal
 Sub umbilical port usually for camera
 Other two ports for handling instruments by operator/assistant
 Pt is in reverse Trendelberg position: slightly rotated to left: this exposes fundus of GB
 See the calot’s triangle
 Define the gallblaader, cystic duct, cystic artery definitely; if any doubt, cholangiogram may be
performed
 Cystic duct and artery are clipped and divided
 Gb removed from gb bed by sharp dissection/cauterization
 Once free, GB is removed via umbilical/sub umbilical port

Open method: ---

Mirizzi syndrome: stone ulcerates thru neck of GB into the common hepatic duct

Indication for choledochotomy (resection of CBD)

 Palpable duct stones

 Jaundice+cholangitis history
 Dilated CBD
 Abnormal LFT especially raised ALP

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

Stricture of bile duct:

Causes of benign biliary stricture:

 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

Investigation for biliary stricture:

 USG
 T tube cholangiography (if T tube is inserted)
 ERCP
 MRCP
 CT scan
 Percutaneous transhepatic cholangiography

Benign tumor of bile duct:

 Papilloma
 Adenoma
 Multiple biliary papillomatosis
 Granular cell myeloblastoma
 Neural tumor
 Leiomyoma
 Endocrine tumor

Malignant tumor of GB/bile duct

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

Treatment and prognosis of GB cx:

 Most pt have advanced dss at time of dx

 Not candidate for surgical therapy
 Surgery indicated in only a very few cases
 Non resectable cases: palliative treatment: such as ERCP stent placement to ensure the bile flow