Section D- Hepato Biliary and Pancreatic System

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Chapter – 1: Gall Bladder and Biliary System

1a- Introduction

• Crypts of Luschka*: mucous folds in GB.

• Common hepatic duct- 2.5 cm*
• Common bile duct- 7.5 Cm*
• CBD enters the duodenum at ampulla located posteriorly 10 cm from pylorus*
• Cystic artery*- arises from Right hepatic artery behind common hepatic duct
• Accessory cystic artery- From Gastro duodenal artery*
• Valves of Heister*- Valves present in the Neck of Gall Bladder and Cystic duct

CALOTS TRIANGLE Hepato cystic Triangle:

Formed between Formed between
• Inferior- • Inferior-
• Medial- • Medial-
• Above- • Above-

• Node seen in Calot’s Triangle- Lund Node**

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 • Right Hepatic artery taking a Tortuous
course and running in Calot’s
Triangle- is known as Caterpillar Turn
or Moynihan’s Hump**

Figure: Moynihan’s hump

Sphincter of ODDI:
• Made of 4 sphincters as a complex
• Superior and Inferior Choledochal
sphincter, Sphincter pancreaticus and
Sphincter Ampulla.
• Always closed at Resting pressure
from 12 to 120 mmHg
• The pressure in SOD is always greater
than Duodenal Pressure and this
prevents contents entering the SOD
from Duodenum.
• Only one Hormone acts here and
opens it- CCK*
Figure: Sphincter of ODDI
• CCK- Contracts Gb and Opens the
SOD.
Applied Anatomy:
• CCK is stimulated by Fatty chyme*
• If GB contracts and Ampulla not
opens is known as Sphincter of ODDI
dyskinesia.
• Characterised by Biliary colicky pain.
• Can also cause Pancreatic pain.
• Classification is known as Milkwauke
Classification ( NEET SS)
• Treatment: ERCP and Sphincterotomy
procedure

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Endoscopic Retrograde Cholangiopancreatography ( ERCP)
• Done with help of Side viewing Scopy.
• We cut the sphincter at 11’0 or 1’0 clock position- known as Sphincterotomy
• The SOD pressure falls down and SOD will be always relaxed and opened.
• The contrast is passed inside the Biliary and Pancreatic system studied.
• We will keep a stent inside the Bile duct known as Double Pig tail or DJ stent.

Figure: Normal ERCP

Indications for ERCP Complications

• Most Common – ERCP induced
Pancreatitis**
• Cholangitis
• Bleeding
• Perforation of Duodenum
• Mortality**- 0.1%

Magnetic Resonance Cholangio Pancreatography: (MRCP)

• Non invasive
• Has replaced ERCP in diagnostic purposes.
• IOC for BD stones, BD malignancy and Pancreatic duct pathologies.
• No contrast is used- Bile and pancreatic juice acts as contrast

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Figure: MRCP

Percutaneous Transhepatic Cholangiography:

• Invasive procedure
• Cannulate the intrahepatic Bile duct- and push contrast and study the Bile duct
• It’s diagnostic as well as therapeutic.
• Therapeutic to drain Bile in Obstructive Jaundice- known as PTBD ( percutaneous
Transhepatic Biliary Drainage.
• This is the IOC for studying the proximal Bile duct**

Hydroxy Imino Diacetic Acid (HIDA Scan)

• It’s a radio tracer substance injected into Blood stream- taken up by liver and excreted
into Bile duct without metabolization. On the way it gets concentrated in Gall bladder.
Applications:
• Detects physiology of Bile flow
• Detects Bile leak
• Gold Standard for Acute Cholecystitis**- Non Visualisation of Gall bladder.

Figure: HIDA scan

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Protocol for Biliary Pathology:
• 1st Investigation done- USG abdomen
• Based on pathology in USG abdomen we have so many other investigations as choices.

Findings in USG Salient Points

1. Gall stones are diagnosed • Posterior Acoustic Shadow
• 95% sensitive
• Mercedes Benz and Seagull sign are seen

Figure: Gall stone

2. Acute Cholecystitis

3. CBD stone • IOC is MRCP**

• Gold Standard is ERCP as we can remove the
stone via this procedure.

Other investigations:
1. Oral Cholecysto gram: (Graham Cole Test)
• Using Iopanoic Acid
• To diagnose the 90% radiolucent stones.

2. Xray Abdomen in Bile system:

• 10% Gall stones
• Porcelain GB- Calcified GB- Premalignant- Surgery Advised.
• Limey Bile- Tooth paste material in GB in Chronic Pancreatitis- Non premalignant
• Air in Biliary system known as Pneumobilia**

Pneumobilia Causes:
•
•
•

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 One liners from Introduction:
• Moynihan’s Hump- Caterpillar turn of RHA
• Valves of Heister- Cystic duct and neck valve
• Phrygian cap- MC anomaly of GB, Fundus of GB folded upon itself.
• Von Meyenburg Complexes
- Also Known as Biliary Hamartomas
- They are embryological remnants of Bile duct. Associated with PCKD**.
- They are premalignant and can produce Cholangio carcinoma**
- IOC to diagnose this is MRCP( MRI)
• Mercedes Benz Sign or Seagull Sign is air in Gallstones
• Meniscus sign- Feature of CBD

Figure: Merceded benz Sign

Figure: Meniscus sign in CBD stone

Benign Gall bladder diseases:

1. Cholesterosis: @ Strawberry Gall bladder:
• Contains Multiple Cholesterol Stones seen
• Inflammatory Pathology.

2. Adenomyomatosis
3. Diverticulosis
4. Polyps:
• MC type is Cholesterol Polyp**

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 • Other one is adenomatous polyp- premalignant
• Risk of malignancy in Polyp in GB:
- Age > 60 year
- Polyp associated with stone
- Size > 10 mm
- Increasing size of polyp
- Family H/o Gall bladder cancer
• Above cases must be operated as there is risk of malignancy inspite of them being
asymptomatic also.
• Surgery by Lap or Open Cholecystectomy. Informed consent obtained regarding re
opening if there is malignancy* in Biopsy

1b- Gall stones

Types of Gall stones:

Cholesterol • MC type of stone in western Composed of Cholesterol
countries Monohydrate crystals**
• Golden Yellow Color 15% of these stones are radio
• Hard stones opaque
Mixed • MC type of Stone in world Composed of
• Cholesterol Component is more • Insoluble Bilirubin
than 30% • Calcium Phosphate
• Calcium carbonate

Pigment • Black and Brown pigment Composed of

stones • Ca. Palmitate
• Brown pigment is mc type in • Ca. Stearate
Asians and Indians • Ca. Bilirubinate
• Black stone is mc type in
Children 50% of Brown stones are radio
• In pigment stone Cholesterol opaque
Component is less than 30% All black stones are radiolucent
• Black stone is also hard
• Brown stone is soft and earthy
stones**

Cholesterol Stones:
• Formed by supersaturation of Cholesterols
• Ratio of Cholesterol: Phospholipids (Bile salts)= 1:20 is ideal ratio; if the ratio becomes
1:13 i.e the cholesterol content increases and Bile salts decreases- Stone forms.

Increased Cholesterol Decreased Bile salt

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 Obesity Decreased Entero Hepatic Circulation:
Cholesterol rich diet • Short Bowel Syndrome
Clofibrate therapy • Ileal resection
Stasis of Bile: • Crohn’s disease
- Fasting
- TPN Decreased Bile salt production:
- Pregnancy • Cirrhosis of Liver
- OCP • 7 alpha hydroxylase deficiency
- Octreotide

Obese lady with Gall stone:

o Saint’s Triad- Gall stones+ Diverticulosis colon+ Hiatus hernia

BROWN PIGMENT BLACK PIGMENT

(Calcium Bilirubinate+ Calcium Palmitate+ Calcium ( Insoluble Bilirubin Pigment polymer+ Calcium
Stearate+ Cholesterol) Phosphate + Calcium Carbonate)
• M/c in hemolytic states
• • Hereditary spherocytosis, sickle cell
• disease
• • Heart valves [mechanical]
• • Liver cirrhosis
• • Gilbert’s syndrome
• • Cystic fibrosis
• • Ileal resection
•
•
•
•
•
• Patient coming with CBD stone after
cholecystectomy:
- <2 years: Retained stone
- >2 years : Recurrent stone.
- MC recurrent stone is Brown Stone

Clinical features of Gall stones:

• Mostly asymptomatic
• MC symptom- Biliary Colicky** (Pain after eating fatty foods)- Misnomer- it’s not a
typical colicky pain. The pain increased gradually after food intake and gets relieved once
the stone in cystic duct passed out or falls inside the GB. Usually pain starts after 45
minutes. Surgery advised for such cases.

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Complications of Gall stones:
1. Acute Cholecystitis- MC complication
2. Chronic Cholecystitis
3. Stone impaction at Neck of GB/ Cystic duct- Mucocele, Empyema and Perforation.
4. Stone near Hartman’s pouch or Neck and compressing CBD- Mirizzi Syndrome
5. GB can adhere to adjacent bowel and result in Cholecysto duodenal fistula- Gall stone
ileus**
6. Cancer GB- 0.5%
7. CBD entry of Stone- Cholangitis, Gall stone pancreatitis

Discussion of Each complication:

1. Acute Cholecystitis:
• C/F- Pain in right hypochondrium
• Murphy’s Sign- Tenderness in 9th Costal cartilage on Deep Breath
• Moynihan’s Method- Patient lies down and the tenderness elicited by Palpation using
Thumb.
• Boas sign- Sign of Hyperaesthesia**
• IOC- USG abdomen
• Gold standard- HIDA scan shows non visualisation of GB

Tokyo Guideline of Acute Cholecystitis

Mild Cholecystitis Moderate Cholecystitis Severe Cholecystitis
Grade 1 Grade 2 Grade 3
• Only Clinical • Clinical features+ • Signs of organ
features seen • Elevated WBC failure++
count+ ( >18000) • Renal
• Palpable Mass+ • Respiratory
• Gangrene+ • Hypotension
• Localised features • Altered sensorium
only
• Advised Lap • • Treatment is
cholecystectomy Urgent
Percutaneous
Cholecystotomy

Management:
o Nil oral
o IVF
o Ryles tube aspiration
o Higher Antibiotics
o Early or Interval Cholecystectomy

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 o Early Cholecystectomy ( Bailey says in 72 hours- Other Books say up to 7 days)-
Mostly followed. The only problem is more chances of conversion from lap to open
method.
o Interval cholecystectomy or Delayed one is done after 6 weeks

2. Mirizzi Syndrome:
o Stone in Hartman’s of Neck causing compression of CBD
o Causes Obstructive Jaundice
o Csendes Classification:
▪ Type 1- Compression only
▪ Type 2- 1/3rd circumference is eroded
▪ Type 3- 2/3rd Circumference eroded
▪ Type 4- Fistula between GB and Bile duct or adjacent fistula
( Choledocho cholecysto Duodenal fistula)
o Treatment: open cholecystectomy is best option as calot’s triangle is disturbed.
o If fistula is seen- GB wall is used as a Buttress to close the fistulous part of Bile
duct.

Figure: Mirizzi syndrome

3. Gall stone ileus:
o Inflammed Gb adhered with duodenum and huge stone passes from Gb to
Duodenum in the fistula . ( usual size >3cm stone)
o Can cause obstruction in Duodenum- Bouveret Syndrome
o Can cause obstruction in terminal ileum- Intestinal obstruction- Gall stone
Ileus
o Triad : Rigler’s Triad:
▪ …..
▪ Fistula between GB and Bowel
▪ Pneumobilia
o Treatment:
o Unstable patients- Enterotomy and stone removal
o Stable patients- Along with enterotomy and stone removal, we will also remove
the GB and close the fistula also.

4. Gall Bladder Cancer:

o Incidence= < 0.5%
o Risk increased - stone > 2.5 cm size, Stone + polyp, Family history
o The above cases to be operated even without symptoms.

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 Management of Gall stones

Medical Treatment:
• Useful only for cholesterol gall stones not for pigment stones*
• Mechanism is by inhibiting HMG CO –A reductase in cholesterol synthesis, thus decrease
cholesterol Super saturation or by giving Urso deoxycholic acid ( UDCA) and increasing
Bile salts.

Useful only in**

o Radiolucent
o Size <15 mm
o Functioning gall bladder
o Non acute symptoms

Surgical Treatment:
• Lap or Open Cholecystectomy ( MC done is Laparoscopic method)
• 1st Done Lap Cholecystectomy- ERIC MUHE
• 4 ports needed- Primary port at umbilicus and 3 secondary ports along Right
Hypochondrium ( Epigastrium, MCL and Anterior Axillary Line)
• Two Methods:
- Retrograde method- From calot’s triangle to fundus ( MC done method)
- Antegrade method – Fundus First Approach* when calot’s triangle is not clear.

Critical view of Strassberg:

• Prevents Being Clipped.
• On Laparoscopy we must see only 2 tubular structures entering GB- Cystic artery and
Cystic Duct

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Indications of Surgery:
• All symptomatic stones operated.
• Asymptomatic cases:

• Other indications:
- Heart or lung Transplantation – Cyclosporine therapy can cause Gallstones
- Bilio-pancreatic Bypass surgery- Prophylactic surgery done as there is more chances of
Stones.

• Rare indications:
- Typhoid carriers
- TPN on long term can cause gall stasis
- Immuno-suppressed patients- Chemotherapy cases, HIV cases
- Diabetes Mellitus with Asymptomatic Gall stones is an indication according to Bailey and
Love.

The following is not indication for asymptomatic stone-Multiple Gall stones**

Indications for open Cholecystectomy ( Contraindications for Laparoscopy)

- Cirrhosis with Portal Hypertension
- Bleeding Disorders
- Poor cardio pulmonary status ( COPD, CAD)
- Suspicious of GB cancer** ( To avoid Dissemination of Malignancy)
- Abdominal pathologies like Adhesions, Morbid Obesity, Pregnancy, Perforated GB peritonitis
are relative Contraindications.

Acalculus Cholecystitis:
• Highest mortality among all cases of Cholecystitis
• Because this is common in patients having other pathologies- sepsis, Major surgery,
Burns or TPN, Typhoid or Streptococcal infections.
• Incidence- 5%
• IOC- USG
• Gold standard- HIDA scan ( Absent filling of GB)
• Immediate cholecystectomy advised if patient is fit by open method.
• If patient is unfit percutaneous Cholecystostomy advised.

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 1c. Bile Duct Injury - Protocol

• Post cholecystectomy one patient is in your ward- C/0 Abdominal pain + Fever
• O/E- Severe tenderness in Right Hypochondrium and increased Pulse rate.
Suspect Bile duct injury:
• Incidence- 0.3- 0.8% in lap and 0.1 -0.2% in open Surgery
1. 1st Done investigation is USG abdomen. USG abdomen-Shows Collection in RIF known as
Bilioma
2. Immediately Percutaneous drainage of Bilioma done.
3. PCD draining Bile and gradually gets reduced in 2 more weeks
4. After 2 weeks we must do the IOC for Bile duct injury – ERCP**

ERCP Shows: Strassberg Classification for Bile duct injury and leak:
o Type A-
o Type B-
o Type C- Aberrant duct cut
o Type D-
o Type E- Transection of CBD

• MC type of injury- Type A, Cystic Blow out

• In whom there is no leak- Type B injury, ERCP looks normal ( NEET SS Question)
• Type A injury no need to worry , as the leak stops by itself. If the leak not stops > 2week
we will do ERCP sphincterotomy and Stenting is done.

5. After 8-12 weeks ; the injuries will heal with Strictures:

IOC for Bile duct Strictures- MRCP*

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 Classification – Bismuth Classification
• TYPE 1-
• TYPE 2- Proximal stricture. Stump< 2 cm
• TYPE 3-

• TYPE 4- Destructed confluence. Right and left ducts separated

• TYPE 5- Involvement of right aberrant sectoral duct alone or along with stricture at
CHD.

• Type 1,2,3 has confluence preserved and hence one anastomosis only needed
• Type 4- 2 anastomosis will be needed.

Gold Standard treatment of Bile duct stricture- Hepatico Jejunostomy

Bile duct injury Diagnosed during Surgery itself:

• Injured duct < 3mm- Ligate it
• Injured duct > 3mm- Important duct and hence must be repaired.
• Circumferential injury : < 50%- Keep a T tube and repair
• Circumferential injury: >50% - Hepatico jejunostomy done
• Repair done by using 4’0 Vicryl ( Polyglactic acid)

If you are inexperienced Surgeon and encountering an injury like this – What will you do?
• Keep a drain and refer to a Experienced Hepato Biliary Surgeon for immediate repair.

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 1d. CBD Stones
Types:
• Primary CBD stone- Formed in Bile duct itself
• Secondary CBD stone- Formed in GB and moves to CBD

Clinical Features:
Charcot’s Triad- Cholangitis (Inflammation of Bile duct)
• Obstructive jaundice
• Pain
• Fever with Chills
Mortality- 10%
MC organism- E.Coli and Klebsiella
• Reynauld’s Pentad- Above 3 features+ Septic shock + Mental status changes.
• Mortality is 50% in cases of Reynauld’s pentad.
• IOC is MRCP**

CBD stone with no Cholangitis CBD stone with Cholangitis

• Treatment of Choice is
1. ERCP + Sphincterotomy +removal
of stones and stenting followed by Lap
cholecystectomy (Two stage procedure)
2. Laparoscopic Removal of CBD +
Cholecystectomy (Single stage
procedure)
3. Open Cholecystectomy+ CBD
exploration and removal of stone
• Most commonly followed Procedure is
ERCP followed by Lap
cholecystectomy.
CBD Exploration:
• Opening the Bile duct Vertically and
removal of stone.
• If CBD <12 mm- T tube and closure
• If CBD >12 mm- Choledocho-
duodenostomy.
ERCP Contraindications:
• CBD stone> 1.5 cm
• Multiple Impacted stones
• Ampullary Stenosis
• More proximal stone
Immediate next treatment:
• Start Antibiotics-
PIPERACILLIN+TAZOBACTUM or
Meropenam
• IVF
• See for resolving cholangitis.
If fever Subsides and patient recovers from
Cholangitis:
- Plan elective ERCP and stone removal
- Followed by laparoscopic
Cholecystectomy
If fever doesn’t subside and persistent
cholangitis:
- Emergency ERCP, sphincterotomy and
stone removed with Stenting by Medical
Gastroenterologist.
If ERCP failed- call the interventional
radiologist to remove the infected bile by
putting a percutaneous Biliary drainage tube
transhepatically. ( PTBD)
If PTBD also failed- Call the Surgical
Gastroenterologist for CBD stone removal .

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 This surgical procedure has high mortality

CBD Exploration ( Choledochotomy) and Stone

removal:
- Vertical incision
- Desjardin forceps to remove the stone
- T Tube kept inside.
- CBD <12 mm- T tube drainage
- CBD> 12 mm- Choledocho
duodenostomy

T Tube Protocol:

Why T Tube is kept?

• For temporary diversion of Bile we keep a T tube as there will be ampullary spasm.
• To prevent leak
• To drain the bile in presence of any obstruction

As the patient is passing yellow stools means T tube is draining Bile into the Duodenum

Removal of T Tube:
• After doing T tube Cholangiogram – usually done on 7th/8th POD
• If T tube cholangiogram is normal- Remove the T tube on 10-14 days and discharge

If there is a stone in CBD on T tube cholangiogram:

• The name given is Missed or Retained stone ( Name given for stones in < 2 years)
• Step 1- Wash with Saline or Methyl Terbutyl Ether
• Step 2- Come back after 6 weeks- The tract will be well formed now and via the T Tube
tract; We go inside using Cholangioscope and remove the Missed stone ( THIS TECHNIQUE
IS KNOWN AS BURHENNE TECHNIQUE**)

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Retained or missed stone Recurrent Stones
( <2 years ) ( >2 years)- Brown Pigment stone
The recurrent stones are usually bigger ( >
2cm size) and usually not feasible for ERCP.

Choledochotomy and stone removal followed

by CHOLEDOCHO DUODENOSTOMY**

1e. Miscellaneous Lesions

Choledochal Cyst Extra Hepatic Biliary Atresia Primary Sclerosing cholangitis

Abnormal dilatation of Bile Abnormal dilatation and
duct is known as Choledochal stricture of Bile duct.
cyst.
• MC in Infants, Female • MC in Males
• MC in 40 years

Clinical features: C/F:

Triad of: • Obstructive jaundice
• Pain • Cholangitis
• Jaundice
• Mass
Complications: Complication:
• Stones • Cholangiocarcinoma
• Cirrhosis • 10% risk every year
• PV thrombosis
• Cholangitis
• Malignancy risk – in
Bile duct, Pancreas,
Liver or GB. MC on
posterior wall of Cyst

Todani or Alonso Types of PSC:

Classification:
• Type 1- Fusiform • Primary PSC-
Dilatation Unknown etiology,
HLA association,

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 • Type 2- Diverticulum Reidel’s Thyroiditis or
type Dequervain’s
• Type 3- Ampullary
level Diverticulum, • Secondary PSC: UC >
Choledochocele CD. This is most
• Type 4: common type
✓ 4a- All ducts Intra
and extra hepatic
dilated
✓ 4b- Extra hepatic
Dilatation
• Type 5: ( Caroli’s
Disease)
✓ Intrahepatic dilatation
Investigations:
IOC- MRCP IOC- ERCP
• Caroli’s Disease- Appearance is Prune tree or
Shows a sign on CECT Beaded Appearance**
abdomen: Central Dot
sign**- Portal vein
radicle appears like
that

Management: Only treatment is Liver

It’s premalignant cyst formed transplant
by Anomalous Pancreatic bile
duct Junction ( APBDJ) with
pancreatic reflux.

It needs to be resected as
there is malignancy risk

• Type 1 and 2- Resect

the cyst and do
Hepatico jejunostomy
• Type 3- Trans
duodenal
sphincteroplasty
• Type 4 and 5- Liver
transplantation

Lilly Procedure: if posterior

wall is very adherent to

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 Portal vein – we remove the
anterior wall and remove the
mucosa of posterior wall
leaving the muscular part
behind itself. ( Not Done now)

• Liver transplantation is the final resort in all patients

• MC indication in New born – EHBA**

Images:

Figure: Todani Classification

Figure: Central Dot sign in caroli disease

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Figure : Kasai Procedure ( porto enterostomy)

1f. Cancer Gb and Bileduct

• MC site of malignancy in Biliary system- Gall bladder
• In Bile duct cancer common at bifurcation- Klatskin Tumor**

Clinical features:
• GB malignancy is associated with stones in 90% cases and mimics symptoms of Gall stones.
• Pain, Jaundice and weight loss.

Obstructive Jaundice: is MC due to Stones and Cancer.

Clinical examination method- Courvoisier’s law to find the etiology by Examination in Obstructive
jaundice patients:

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Courvoisier’s law states:
• When Gallbladder is enlarged- its due to cancer
• When Gall bladder is not enlarged- its due to stones in CBD, because the stone would
have already caused fibrosis and won’t enlarge anymore.

Exceptions to Courvoisier’s Law:

• Cancer case but no Gb enlarged – Hilar cholangiocarcinoma ( Klatskin tumor)
• Stone case but GB enlarged- Double Impacted stone ( One at CBD and one at Cystic
Duct)

Gallbladder Cancers:
Predisposing factors:
• MC – Gall stones
▪ 0.5% of Gall stones leads to cancer
▪ 95% of Cancer GB will have stones**
▪ Incidence is 10% if stone size 3cm or more.
• Polyps > 10 mm
• Typhoid carriers
• Oestrogen
• Clonorchis sinensis
• Ulcerative colitis
• Choledochal cyst, APBDJ
• Primary sclerosing cholangitis
• Carcinogens- Nitrosamines, Rubber and Dyes and chemicals

Investigation:
• USG usually shows Gallstones or Gallstones with Polyps or a mass lesion is usually the 1 st
done investigation
• IOC – CECT abdomen with Triple Phase contrast
• Tumor Marker- CEA

For Bile duct Cancer:

IOC for staging- MRCP+ MRA
Tumor marker- CA 19-9 and CEA

Management and Staging:

TNM Staging Procedure
T1a- Tumor into Lamina Propria

T1b- Tumor into Muscle layer

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T2- Tumor into peri muscular
connective tissue
▪ T2a- Invade the
perimuscular connective
tissue on peritoneal side
with no extension to serosa
▪ T2b- Invade the Radical Cholecystectomy:
perimuscular connective • Remove segments – 4b +5
tissue on the hepatic side • Remove all nodes mentioned already.
with no extension into liver.

T3- Serosal Perforation and/or

Direct invasion of the Liver or any
other single extra hepatic organ

Options:
• Radical Cholecystectomy- 4b+5
• Extended Right hepatectomy- 4a+4b+
5,6,7,8
• 3. Central (Taj mahal) hepatectomy-
4b+5+8
T4- Invades main PV or HA or two Inoperable cancer
or more extrahepatic organs.
• N1- Metastasis in 1-3 regional nodes – Pericholedochal nodes ( CD, CBD, HA
and PV)
• N2- Metastasis in 4 or more regional nodes- Distant nodes ( Periaortic,
pericaval, SMA and Coeliac nodes)
• M1- Distant mets

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Recent advances:
• No need to remove the port sites in present scenario on resection cases after
biopsy report.
• If already diagnosed as GB cancer and planning a radical surgery- one
investigation that must be done now is D.Lap. In around 30% cases there are
small peritoneal deposits or liver mets. D.Lap is a staging investigation

Scenario 1: Incidental GB cancer in specimen:

• Lap cholecystectomy done for Multiple GB stones.
• Pathologist is telling there is a cancer in the specimen.
What next?
• The further management depends on staging:
T1a- Already done Lap cholecystectomy is enough
T1b- if everything is negative ( PNI, LN,Margins)- Lap cholecystectomy is enough
T1b- if any of the above positive- Reopen and do Extended Cholecystectomy
T2- Reopen and do Radical Cholecystectomy

T3 and T4 will not seen in Incidental as we can see the growth on putting the
laparoscopy itself.

Scenario 2: On Lap cholecystectomy 1st port you are seeing a cancer in GB:
• Unexperienced surgeon- Remove the port and refer to Hepato Biliary surgery
• Hepatobiliary surgeon- Convert to open and proceed with radical surgery

Adjuvant therapy:
• Gemcitabine therapy is given

Bile duct cancers:

Predisposing factors:
• Inflammatory causes- PSC, UC and Hepatitis C and Oriental Cholangiohepatitis
• Parasites- Clonorchis sinensis, Opisthorcis Vivernii**
• Chemicals- Thorium, Asbestos, Vinyl Chloride
• Congenital- Caroli disease and Choledochal cysts
• Post op causes- Bilio enteric anastomosis

MC type is Adenocarcinoma
Types:
• Sclerosing type has worst prognosis
• Papillary type has best prognosis
• Nodular types

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Bismuth Corelette Classification:
• TYPE 1- At common hepatic duct only.
• TYPE 2- Involving confluence without involvement of secondary ducts
• Type 3-a- Involving right secondary intra hepatic ducts
• Type 3 b- involving left secondary intra hepatic ducts
• TYPE 4 – Involves secondary ducts on both sides

Fig. Bismuth Corelette classification of Hilar cancers

Treatment:
o For 1 and 2- Bile duct resection done radically and Hepatico jejunostomy done
o For 3a- we do extended Right Hepatectomy( Right trisectionectomy)- 4a+4b+
5,6,7,8
o For 3b- we do extended Left Hepatectomy ( Left trisectionectomy)- 2,3,4a,4b+ 5
and 8
o Type 4- inoperable

Criteria for Unresectability of Hilar Cholangiocarcinomas:

o Bilateral hepatic ducts upto secondary radicles involved (Type 4)
o Main PV Involvement
o Atrophy of one lobe (One Hepatic artery involved) with Contralateral PV
o Atrophy of One lobe (One Hepatic artery involved) with Contralateral
Secondary Radicles involvement
o Distant Mets, Ascites

RRM’S SURGERY SIXER APP BASED WORKBOOK 25

 Chapter 2: Pancreas

Basics of Pancreas:
Embryology:
• Pancreas derived from Dorsal and ventral bud
• Ventral bud rotates and fuses with dorsal bud by 6 weeks.
• If the ventral bud not rotates- Annular pancreas
• If the ventral and dorsal bud not fuses with each other- Pancreas Divisum

Annular Pancreas Pancreas divisum

• Ventral and dorsal bud encircles the • Minor duct is draining the major part
pancreas like a ring** of pancreas.
• C/F- Gastric outlet obstruction • Hence there will be recurrent
• Associated with Down’s Syndrome, pancreatitis.
Duodenal atresia • IOC- ERCP> MRCP
• IOC – CECT abdomen • Treatment- Minor duct
• ERCP will show absence of ventral sphinterotomy**
bud.
• Treatment:
Duodeno Duodenostomy ( Bailey) or
Duodeno jejunostomy**
Resection not needed.

Anatomy of Pancreas:

• Tunnel of Love- in neck of pancreas. SMV enters and comes out as portal vein.
• Major duct of Wirsung drains- Tail, Body, part of head And uncinate process.
• Minor duct of Santorini drains small part of Head.
• Wirsung Duct is formed by Distal part of Dorsal bud and full ventral bud**
• Santorini Duct is formed by Proximal part of Dorsal Bud.

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Ectopic Pancreas:
• MC in Duodenum > Stomach > Meckel’s Diverticulum
Acute Pancreatitis

ETIOLOGY OF PANCREATITIS; ( GET- SMASHED- I)

• G- ( MC cause in adults)
• E-
• T- ( MC cause in Children)
• S-steroids
• M-mumps
• A-autoimmune(PAN,SLE etc.,)
• S-scorpion venom
• H-Hyper lipidaemia, Hyper calcaemia, Hyperparathyroidism
• E-ERCP ,Emboli
• D-Drugs (Azathioprine, Thiazides, Furosemide, Tetracyclines, 6- Mercaptopurine etc)
• I- Infections (Cox-Sackie, CMV, Echovirus, Ascaris Lumbricoides and clonorchis sinensis
etc)

Drugs that cause Acute pancreatitis are:

• Corticosteroids
• Azathioprine
• Asparaginase
• Valproic Acid
• Thiazide diuretics
• Estrogens

Clinical features:
• Mohammed Prayer Sign: Pain radiating to back from Epigastric region making patient sit
like a Muslim Praying appearance.
• Hemorrhagic pancreatitis:
- Cullen’s Sign:
- Grey Turner’s Sign:
- Fox Sign:

• Differential Diagnosis: Perforation

RRM’S SURGERY SIXER APP BASED WORKBOOK 27

 • X ray Abdomen erect findings:
▪ Gasless abdomen**
▪ Colon Cut off sign**
▪ Ground Glass appearance
▪ Sentinel Loop Sign
▪ Renal Halo Sign

Investigations:
• Serum Amylase: 4 times increased than normal , Not specific. It can be elevated in other
GI pathologies – Perforation, Obstruction, Diverticulitis, mesenteric ischemia
• Serum amylase usually becomes normal after 3 days after attack
• Most Sensitive test-
• Most specific test- Serum trypsinogen > Serum Lipase**
• CRP: >150 implies severe AP
• Radiological IOC- CECT abdomen with oral and IV contrast (usually advised after 72
hours)- Balthazar Score or CTSI ( CT severity Index)

Scoring Systems in Acute pancreatitis

• Ranson’s scoring – Most widely used- 3 is severe
• Apache 2- Uses 12 factors: >8 is severe
• Modified Glassgow score > 3
• CT severity index/ Balthazar et al scoring- Best Scoring **
• C –reactive protein- more than 150 mg/dl is severe
• BISAP score – Bed side Index of Severity of Acute Pancreatitis**
• Revised Atlanta Scoring System(RAS)*
• Modified Marshall Score
• q SOFA score used in Sepsis

BISAP Score:
• B- Blood urea Nitrogen
• Impaired Mental status
• S- SIRS
• A- Age > 60 years
• P- Pleural effusion

Ranson Score: ( Mnemonic – LAGAW BUCHOW)

On admission Within 48 hrs
o L- LDH >350 u/l o B-
o A- AST >250 sigma frankel units % o U-
o G- Glucose >200 mg/dl or > 1.1 o C-
mmol/l o H-
o A- Age>55 yrs o O-
o W- WBC Count >16000/mm3

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 o W-
• Ranson’s score > 3 is said to be severe AP.

CT Severity Index ( old Name Balthazar )

Pancreas inflammation Necrosis
• Normal- 0 • <30% necrosis: 2
• Focal/ Diffuse Enlargement- 1 • 30-50% necrosis: 4
• Intrinsic changes – 2 • > 50% necrosis: 6
• Single fluid collection- 3
• Multiple fluid collection- 4
• Total score= 10
• Severe AP= 7-10 ( mortality – 17%)

Revised Atlanta Classification:

Organ failure Local Complications Systemic Complications
• Shock- SBP<90 mmHg • Necrosis • DIC
• ARDS- PaO2< 60 mmHg • Pseudocyst • Metabolic disturbances
• ARF- Se. creatinine >2mg • Abscess • Fibrinogen level
• GI bleed> 500 ml/day decreasing
RAC Classification takes into account all the above:
• Mild: No Local Complication or organ failure ( only amylase Increased)
• Moderate: Organ Failure +, but it’s transient and it resolves in 48 hours**+ Local/
Systemic Complications but no persistent organ failure ( in 48 hours patient recovers.
• Severe: > 48 hours: there is persistent organ failure+ Local or systemic complications

Complications of Acute Pancreatitis:

• Release of Trypsinogen which will activate all the enzymes from pancreas and does
Autodigestion and results in list of complications:

Local Complications Systemic Complications

caused by IL-1,6 and TNF
alpha
• < 4 weeks: Acute Pancreatic fluid collection ( APFC) • Shock
• > 4 weeks: Pseudocyst • ARDS
• < 4 weeks: Acute Necrotic fluid collection ( Necrotic • ARF
material also seen) • GI Bleed
• > 4 weeks- Walled Off Pancreatic necrosis ( WOPN) • MODS ( MC cause of
• MC complication – Infection ( Pancreatic abscess)- MC death in AP overall)
cause of late death and MC local complication causing
death.
• Pancreatic ascites
• Pancreatico pleural fistula
• Pleural effusion

RRM’S SURGERY SIXER APP BASED WORKBOOK 29

 • Splenic vein thrombosis
• Splenic artery Aneurysm ( False aneurysm caused by
Elastase enzyme)
• Colonic gangrene or perforation

Pseudo Cysts:
• Follows Acute or chronic pancreatitis
• MC site is lesser sac. ( But can happen anywhere inside Abdomen)
• MC near Body and tail of Pancreas**
• D’egidio Classification:
o Type 1- Follows Acute Pancreatitis; Duct is normal
o Type 2- Follows Acute on Chronic Pancreatitis. Duct is abnormal with no
stricture*
o Type 3- Follows Chronic Pancreatitis; Communication seen with Duct and duct
has strictures**

Figure: Pseudocyst in Tail of pancreas.

• C/F- Presents after 4 weeks with persistent pain and epigastric fullness and vomiting
and early satiety**
• Persistent elevation of Serum Amylase
• IOC – CECT abdomen;
• EUS guided Fluid analysis shows – Increased amylase and Normal CEA ( To
differentiate from Cystic Neoplasm)

Management:
• Surgery Advised for Symptomatic pseudocysts only and for complications.
• Old Rule : Rule of 6 : Surgery done if cyst > 6 weeks, > 6 cm diameter or thickness 6
mm wall.

Complications in Pseudocyst:
• Mc complication- Infection ( Pancreatic abscess)
• Rupture into abdominal cavity causes pancreatic ascites
• Rupture into Thoracic cavity – Pancreatico pleural fistula
• Bleeding ( Known as Haemosuccus Pancreaticus**)

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Surgical treatment:
• Internal Drainage : Cysto jejunostomy > Cystogastrostomy or Cysto duodenostomy.
• Cysto gastrostomy done by open method , Endoscopic method or laparoscopic method
• Infected Pseudocyst – External drainage done

Pancreatic ascites:
• Communication seen with pancreatic duct
• Increased amylase seen
• High Protein Ascites ( Low SAAG < 1.1)
• Treatment : Paracentesis + Injection Octreotide
• 2nd Line : Endoscopic Therapy – ERCP and Pancreatic stenting done through the duct
disruption.
• Last option – Surgeon called only if there is no resolution on ERCP. Procedure done is
Lateral Pancreatico jejunostomy of Puestow**

Pancreatic necrosis:
• CTSI: < 30 % necrosis= 2 points, 30-50% =4 points; > 50% necrosis= 6 points
• Mostly the necrosis is sterile.
• If it gets infected – there will be air, Increased WBC count and temperature.
• Infected necrosis cases we start antibiotics.
• Under antibiotic coverage – we must remove the necrosis.

Figure: Pancreatic necrosis

• Step up approach- From minimally invasive to maximally invasive procedure. USG
guided PCD done 1st, Later as patient improves , Minimally invasive method by
Laparoscopic Necrosectomy or Video assisted Retroperitoneal debridement ( VARD)-
via a nephroscope introduced into the PCD tract.

• Step Down approach: Open laparotomy and keep wide drains for regular lavage.

RRM’S SURGERY SIXER APP BASED WORKBOOK 31

Management of Acute pancreatitis:
• Key step in management- Fluid replacement enormously expecting good urine
output**
• Octreotide has a doubtful role and hence advised and given for pancreatitis cases.

Mild Acute pancreatitis Severe Acute Pancreatitis

In General ward In SICU
Single Surgeon can treat Multidisciplinary management needed
No antibiotics needed Only in infective necrosis- antibiotics needed.
Analgesics advised- opioids are used DOC- Metamizole and Tramadol are given
( don’t give NSAIDS)
Nutrition: Nutrition:
• Patient is in shock we have to go
for TPN.

Intervention:
• Gall stone Pancreatitis +
Cholangitis - ERCP and
sphincterotomy and stenting can
be done in < 72 hours
• Mostly no intervention needed
Intervention:
• Necrosectomy Management
• Pseudo cyst management
• Pancreatic ascites management

Chronic pancreatitis

It is a triad made of
• Endocrine Loss- > 90% lost results in Diabetes
• Exocrine loss- > 90% lost Steatorrhea
• Strictures and stones- Severe Pain Epigastric region radiating to Back: pain is not due
to Enzymes; it is due to Ductal Hypertension.

TIGAR- O Classification of Aetiology:

• T- Toxic ( Alcohol )- MC causes
• I- Idiopathic/ Tropical– Unknown cause; Eating Casava Root fibres in kerala
• G- Genetic-PRSS gene mutation, SPINK -1 gene mutation, CFTR gene mutation
• A- Autoimmune
• R- Recurrent Acute Pancreatitis ( like in Pancreas Divisum)
• O- Obstructive

RRM’S SURGERY SIXER APP BASED WORKBOOK 32

Clinical features:
• Pain abdomen; severe recurrent pain; addicted to Opioids
• Diabetes- responds only to Insulin
• Steatorrhea

Investigations:
• Old Tests not done now- Lundh meal test, Pancreaolauryl test
• Latest for steatorrhea:
o Fecal measurement of Elastase:
o Fecal fat excretion ( on 100 gm fat given):
• IOC to diagnose Established Chronic Pancreatitis: CECT abdomen- Stricture, Stones and
atrophy
• Gold standard to diagnose Early Cases of Chronic Pancreatitis: ERCP- Chain of lakes
appearance seen**
• Recent Gold standard to diagnose Early cases of Chronic Pancreatitis: EUS
• ERCP Criteria- Known as
• EUS criteria- Known as

Management:
Pain management:
• Analgesics is given initially
• Coeliac plexus Block using Absolute Alcohol**- Laparoscopic or CECT guided method
• Thoracoscopic Sphlanchinectomy also available

Steatorrhea and weight loss:

• Pancreatic enzyme supplements- Creon, Pancrealipase
• The enzyme supplements must be given along with food**
• Acid reduction with PPI is needed while giving Pancreatic enzyme tablets.

Diabetes Mellitus:
• Best is by giving Inj. Insulin**

Surgical Management:
Drainage Procedures
• Dilated duct: > 7mm
diameter:- Modified
Puestow procedure-
Lateral Pancreatico
jejunostomy procedure.
Resection+ Drainage Procedures
(Hybrid Proecdures)
• Frey’s Procedure- Head
coring along with Lateral
Pancreatico Jejunostomy
Resection procedure
Distal Pancreatectomy and
splenectomy for problems
in Body and Tail- Child
Duval Procedure
Presence of head mass
Duodenum Preserving
Pancreatic head resection

RRM’S SURGERY SIXER APP BASED WORKBOOK 33

 • For Undilated duct:- (DPPHR)
Izbicki Procedure in which - Beger’s Procedure
V’ Shaped excision of the - Bern’s Modification
duct done.
If suspicious of malignancy:
Whipple’s procedure

2b- Tumors in pancreas

Types:
• Mc are adenocancers
• Endocrine tumors of Pancreas
• Cystic neoplasms of pancreas

Adenocarcinoma of Pancreas:
• Tumor within 2cm of ampulla is known as Periampullary cancers
• Head of pancreas- Most common site
• Body and tail.
Periampullary Cancers Pancreatic head cancers Body and tail
• C/F- Painless • C/F- Pain abdomen+ • Worst prognosis
intermittent jaundice Jaundice • Presents with Mets in
due to sloughing out • Late diagnosis 100% cases
of tumor. • Only 10% operable
• Early presentation • 90% are inoperable
and hence has good
prognosis
• 60% are operable

Genetic factors associated with Cancer pancreas:

• MC mutation- k- ras**
• Others- P16, P53,
• PRSS gene- Trypsinogen gene mutation
• SPINK- 1 mutation
• CFTR mutation
• Peutz jeugher syndrome ( STK-11)- 100 fold risk** ( NEET SS)
• Familial adenomatous polyposis
• Familial atypical melanoma syndrome
• BRCA-2
• Lynch 2- HNPCC**

Clinical features:
• Pain abdomen – Head tumors
• Painless intermittent Jaundice- Periampullary cancers

RRM’S SURGERY SIXER APP BASED WORKBOOK 34

 • Vomiting- MC cause is due to external compression of Duodenum by Tumor**
• Courvoisier’s Law- Gall bladder is enlarged in Pancreatic cancers.
TNM classification:
T1- <2cm
T2- 2-4 cm
T3- > 4cm
T4- Involvement of SMA, Common Hepatic artery and Coeliac artery
• Infiltration into SMV or Portal vein doesn’t change the staging

Resectable tumors Borderline resectable Unresectable

• Not infiltrating into
SMV/ Portal vein or
infiltration < 180
degree
• No mets
• SMV / PV infiltrated • Involvement of SMA,
even if more than Coeliac, Coeliac artery
180 degree > 180 degree
• SMA/ CHA or coeliac • Mets seen
artery involved < 180
degree**

Investigations:
• CECT abdomen is the IOC for staging- Pancreatic protocol CT is taken in which the cuts
are made at every 2-3 mm to look for small lesions and infiltration.
• Tumor Marker- CA- 19-9 **
• ERCP/ MRCP - Double duct sign seen*
• Barium meal shows- Frost berg sign or Reverse 3 sign** ( Epsilon sign)
• Biopsy is not mandatory for operable pancreatic cancers**. We advise Biopsy only for
inoperable cases.

Figure: Shows Double Duct sign

Management of Pancreatic cancer:

• Resectable cancer- in Head of pancreas / Periampullary cancer is Pylorus preserving
Pancreatico duodenectomy ( best answer) or Whipple’s operation is done.
• Distal pancreatic cancers- Distal pancreatectomy+ Splenectomy
• Inoperable patients: Palliative procedures
o Pain- Ceoliac plexus Blockade using Absolute alcohol

RRM’S SURGERY SIXER APP BASED WORKBOOK 35

 o GOO- Duodenal stenting by Endoscopy or Bypass procedures
o Jaundice- SEMS into biliary system or Bypass procedures
o Triple Bypass procedure is the one done for inoperable pancreatic cancer with
jaundice and GOO- Gastro jejunostomy+ Cholecysto jejunostomy+ Jejuno
jejunostomy

Operable cancers: Whipple’s Procedure

• The most important step in this operation- Pancreatico jejunostomy**

Complications of Whipple’s operation:

• Delayed Gastric emptying- increased Ryles tube aspirate or Vomiting- Incidence 18%
• MC cause of death- PJ anastomosis leak**; the active pancreatic enzymes leaking will
damage all the anastomosis and patient dies.
(Suture material for PJ anastomosis- Prolene or PDS- Don’t use Vicryl)
• Pancreatic Fistula: Drain kept after Whipple’s operation shows fluids which is having
increased amylase content:
- Rule of 3: 3rd POD, DT fluid amylase is 3 times higher than serum amylase**
• Bleeding

Pylorus preserving Pancreatico Duodenectomy ( Longmire and Traverso operation)

• This modification is done only to prevent Delayed Gastric emptying** - < 1% as nerve of
Laterjet is preserved.
• This is the procedure of choice for pancreatic cancer now.

Figure Shows – PPPD

RRM’S SURGERY SIXER APP BASED WORKBOOK 36

Endocrine tumors of pancreas

• MC NET of pancreas- Pancreatic Polypeptidomas ( PPomas)- Non functional

• MC Functional NET – Insulinoma in sporadic**; Gastrinoma in MEN-1 Syndrome**

Insulinoma Gastrinoma
MC NET in MEN-1 Syndrome

MC in Passaro triangle
• Junction of CD/ CBD
• Neck of Pancreas
• 2/3rd Part Duodenum

MC site – Duodenum> Pancreas

Mostly Malignant
Clinical features: Zollinger Ellison Syndrome
• Unusual peptic ulcer disease
• Diarrhoea

IOC to diagnose:
• Serum Gastrin >1000 pg/ml
• In border line elevated cases we must
do- Secretin Stimulation test**
• On SSI- the value increases from
baseline to 200 pg /ml above in 15
minutes.

Localisation : ( No Somatostatin receptor) Localisation:

• Intra op USG ( Best ) • Somatostatin Receptor Scinitigraphy**
• Endo USG
• Selective Arteriography venous
sampling of blood

RRM’S SURGERY SIXER APP BASED WORKBOOK 37

 Management: Management:
• Enucleation is enough as this is a Malignancy and hence radical resection
Benign tumor** needed.
• Whipple’s is TOC ( PPPD is
contraindicated ) for Head tumors
• Distal Pancreatectomy for Tail and
body cases
Adjuvant therapy/ Inoperable/ metastatic: Inoperable cases/ Metastatic cases:
• Streptozocin • Octreotide
• Diazoxide • Triple dose PPI
• Total Gastrectomy may also be done

Other NET:
1. Glucagonoma:
• Presents with Diabetes+ Dermatitis
• Dermatitis- Necrolytic migratory erythema**
• MC in Head*
• Mostly Malignant

2. VIPoma:
• Also known as Verner Morrison Syndrome/ WDHA syndrome/ Pancreatic cholera
• WDHA syndrome- Watery Diarrhea+ Hypokalemia+ Achlorrhydria
• MC site is Tail**

Cystic neoplasms of Pancreas

RRM’S SURGERY SIXER APP BASED WORKBOOK 38

Salient Points:
• IOC for Cystic Neoplasms- EUS guided Biopsy and Fluid analysis
• Fluid analysis shows elevated CEA level** in IPMN and Mucinous neoplasm
• CECT- SCN- Sun burst calcification
• CECT- MCN- Egg Shell Calcification
• ERCP for IPMN shows- Fish Mouth Appearance in Ampulla ( NEET SS)
• Solid Papillary Mucinous Neoplasm (SPMN)- Frantz tumor

RRM’S SURGERY SIXER APP BASED WORKBOOK 39

 Chapter 3: Liver and Portal Hypertension

3a- Introduction

Anatomy of liver:
Portal triad structures:
• Posterior – Portal Vein
• Anterior to right- CBD
• Anterior to left- Hepatic artery

Hepatic artery:
• Aberrant/ Abnormal/ Accessory Right Hepatic artery arises from Superior mesenteric
artery and runs posterior to portal vein.
• Aberrant/ Abnormal/Accessory Left Hepatic artery arises from Left gastric artery
• Abnormal cystic artery from GDA*

• Bile Duct : Blood supply arises from Right Hepatic artery at 3’0 and 9’0 Clock position**
from above downwards and from GDA from below upwards.
• Major Blood supply to liver- 70-80% by Portal vein, 20% by Hepatic artery.
• Major oxygenated blood to liver is by Hepatic artery
• 100% blood supply to a tumor is from Hepatic artery only
• The venous drainage is via- right, left and middle hepatic vein into IVC and systemic
circulation.

Coiunaud’s Surgical Segments of Liver:

• Total segments in liver= 8 segments

RRM’S SURGERY SIXER APP BASED WORKBOOK 40

 • The Middle Hepatic vein corresponds to an imaginary line CANTLE’S Line- runs from Gall
bladder fossa to right of IVC. ( Cantle’s line- Cholecysto caval line)
• Left and Right Hepatic veins further divides the liver and runs along Left and Right main
fissures*
• Portal veins also divides the liver by running on the Right and left scissura**

Figure: Liver segments

• Segment 1 is located on Posterior surface of liver

• Segment 2 and 3 are seen medial to falciparum ligament- Left lateral segments
• Segment 4a and 4b are seen lateral to Falciparum ligament- Left medial segments
• Segment 6 and 7 are known as Right posterior segments
• Segment 5 and 8 are known as Right anterior segments
• Each segment is a separate functional unit and contains HA, BD, PV and HV branches.
• Because of this concept- We can now do segmental resection of Liver and Live Donor
transplant**
• Segment 1- Caudate lobe; Directly drains into IVC**
• Caudate lobe is further divided into- Segment 9 and Spiegel lobe.
• Caudate lobe is enlarged in Budd Chiari Syndrome*

Brisbane 2000 is the latest naming for hepatectomy:

• Left hemihepatectomy=
• Right hemihepatectomy=
• Left lateral hepatectomy= ( lateral to Falciparum ligament)
• Right Posterior hepatectomy=
• Radical Cholecystectomy=
• Central hepatectomy= (Tajmahal Hepatectomy)
• Right Trisectionectomy= Extended Right hepatectomy= 5-8+ 4a and 4b
- Done for Type 3a Hilar Cholangiocarcinoma
• Left Trisectionectomy= Extended Left hepatectomy= 2,3,4,5 and 8
- Done for Type 3b Hilar Cholangiocarcinoma

RRM’S SURGERY SIXER APP BASED WORKBOOK 41

 • Paediatric liver transplant donated Segments 2 and 3 are used
• Adult Liver Transplant Donated segments-5,6,7,8

Scans in Liver:
Liver parenchyma is made up of two types of cells
• Hepatocytes – Perform excretory and synthetic functions.
• Kupffer cells- They have Reticulo endothelial function
• Both of these cells can be investigated with Radionuclide scanning.
• ITO cells ( Stellate cells)- used for Vitamin A storage

Two types of radio nuclide imaging procedure are used in liver

HIDA Scan Sulphur Colloid Scan
• This Scan is based on • This is based on the functioning RES
Functioning Hepatocytes. cells (Kupffer cells) of liver

IDA compound are taken up by the
functioning hepatocytes, excreted
unchanged in bile ducts and gallbladder.
Clinical Uses:
• Assess regional liver function
• Bile leaks in liver trauma
• Investigation of biliary
obstruction
• Choledochal cyst
• Acute cholecystitis (Gold
standard)
• Differentiate hepatocellular
tumors
Hot spots- mass lesions which contain
functioning RES cells ( kupffer cells)
Non-functioning areas- mass lesions which
do not contain kupffer cells.
Clinical Uses:
• FNH- only tumour which consistently
contains functioning RES cells and
therefore shows uptake of colloids.
• Hepatic adenoma- nonfunctioning
kupffer cells, hence do not uptake

HCC will not take up colloid or HIDA scan**

Liver Function tests:

• AST/ ALT- Liver specific is ALT** ( AST is not specific)
• Alkaline Phosphatase- Obstruction of Bile duct
• GGT- Alcohol induced liver damage**
• Chronic Liver disease:
o Albumin is a marker of Chronic liver disease.
o PT/INR will be elevated

RRM’S SURGERY SIXER APP BASED WORKBOOK 42

 Scoring Systems in liver

Modified Child Pugh Score ( Mnemonic- BAAPE)

CLINICAL** 1 2 3
Encephalopathy None 1 or 2 3 or 4
Ascites None Mild moderate
Bilirubin (mg/dL) 1-2 mg/dl 2.1- 3 mg/dl ≥ 3.1 mg/dl
Albumin (gm/dL) ≥3.5 gm/dl 2.8- 3.4 gm/dl ≤ 2.7 gm/dl
Prothrombin time 1-4 4.1 - 6 ≥ 6
(increase in seconds)
 Grade A: 5-6
 Grade B: 7-9
 Grade C: 10-15 points

MELD: Modified End Liver Disease Scoring:

Based on: “CBI”
• Creatinine
• Bilirubin
• INR
o Recently Waiting list for transplant is made on the basis of MELD score*
o Initially MELD score was used to predict mortality after TIPSS
o Values vary from 6-40*
o Liver transplant is allowed only for MELD > 15** ( ref. Sabiston Page 658)
Paediatric End Stage Liver Score: (Mnemonic “BANIA”)
• B- Bilirubin
• A- Albumin
• N- Nutritional status
• I- INR
• A-Age
King’s College Selection Criteria for Liver Transplant in Acute Liver Failure:
Paracetamol Induced Non Paracetamol Induced
• pH <7.30 (Irrespective of grade of • PT > 100 Seconds (Irrespective of
encephalopathy) grade of Encephalopathy)
(or) (Or)
• Prothrombin Time( PT ) > 100 Any three of the Following :** NEET PG 2020
Seconds + Serum Creatinine > 300 • Age <10 years or >40 years
Micro mol/litre + Encephalopathy of • Etiology being Non A , Non B,
Grade 3 or 4 ( all three together) Halothane or Drug reaction
• More than 7 days Jaundice before
Encephalopathy
• PT> 50 seconds
• Bilirubin > 300 Micromol/ Litre

RRM’S SURGERY SIXER APP BASED WORKBOOK 43

 Chapter 3b- Cirrhosis with portal hypertension

Explanation for image given above:

• Portal vein formed by SMV+ SV joining
• Portal vein = 5-8 cm length
• PV divides into Right and left and divides into multiple sinusoids in liver.
• Three hepatic veins drains from sinusoids into IVC
• Normal PV pressure= 5-8 mmHg

Causes of Portal Hypertension:

Presinusoidal Sinusoidal ( MC)
• Intrahepatic-
Schistosomiasis (MC ),
NCPF
• Extra hepatic-
EHPVO
• Left sided Portal
Hypertension (
Sinistral portal
hypertension)
Post sinusoidal
• Cirrhosis causing • Intrahepatic- Veno
fibrosis ( MC) occlusive disease- Sub
lobular venules
obstructed
• Extra hepatic- Budd
Chiari Syndrome- HV
or IVC occlusion

Pathophysiology:
• Due to high portal pressure- the collaterals will open..
• Collaterals between Systemic and Portal venous system:

RRM’S SURGERY SIXER APP BASED WORKBOOK 44

 o Left gastric vein with Hemi azygous vein- Esophageal varices
o Inferior mesenteric vein ( Superior rectal vein) with Middle and inferior rectal
vein- Hemorrhoids develop
o Left Umbilical ( Paraumbilical vein) opens up- Caput medusae
o Bare area
o Retroperitoneum
• Ascites due to increased SMV pressure
• Splenomegaly

Complications:
• MC cause of death- liver failure ( only option is Liver transplant)
• 2nd MC cause of death- Bleeding**
▪ Esophageal variceal bleed ( MC)
▪ Portal Hypertensive gastropathy

Hepato-pulmonary syndrome Porto Pulmonary Hypertension

There is pulmonary vasodilatation There is Vasoconstriction of the vessels
resulting in Hypoxia, Platypnea resulting in Pulmonary artery pressure
increases > 25 mmHg

IOC- Echo IOC- Wedge Pressure of Pulmonary Artery

Treatment- Liver transplant
( PCWP)
Treatment- Liver transplant
Bad prognosis and more serious
• If Pulmonary pressure > 50
mmHg- Liver transplant will be
contraindicated**

Protocol in Oesophageal variceal Bleeding:

• Among upper GI bleed- 20% is due to Portal hypertension.
• Causes of Bleeding – Variceal bleed in Esophagus or Stomach and PHTG
• Varices formed at PP> 10 mmHg
• Varices Bleeding occurs at PP >12 mmHg

1st Step: Massive hematemesis:

• IVF, Ryles Tube aspiration, Foley’s catheter
• DOC for variceal Bleeding- Injection Octreotide** infusion ( Please don’t forget the first
drug given in Upper GI Bleed= PPI)
• Other drugs- Vasopressin or Terlipressin along with GTN to avoid Coronary ischemia*

2nd Step: Ryles tube shows continuous Bleed:

• Modified Sengstaken Blakemore Tube:
o Kept in freezer

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 o Two Balloons
o 4 lumens
o Made up of rubber
o 1st Inflate Gastric Balloon using 300 ml of Air ; followed by Esophageal
Balloon upto 40 mmHg
o Inserted via Mouth or nose.
o Lumens are used to Inflate and aspirate the contents.
o Tamponade effect is produced on Varices
o Tamponade effect can be used only for Varices and not for Dieulafoy’s lesion,
Mallory Weiss tear as they are arterial bleeding** ( NEET SS)
o Maximum Time to retain the Balloon- 12 hours
o Extended pressure results in Esophageal necrosis and perforation.

Figure: Modified Sengstaken Blakemore Tube

3rd Step: Patient lands up in MGE unit:

• Treatment of Choice for EV is Endoscopic Banding > Endoscopic Sclerotherapy
• Sclerosants used are- Sodium Tetra decayl.
• Gastric varices are treated by Endoscopic Glue injection- Cyano acrylate Glue**

4th Step : Failed Endoscopy by MGE – Call the Interventional radiologist:

Transjugular Intrahepatic Shunt ( TIPS)
• Intra hepatically a stent kept between HV and PV by trans jugular Route**
• The stent will now reduce the Portal pressure immediately and Varices bleed stops.
• Stent is made up of Polytetra floroethylene ( PTFE)

Complications of TIPS:
• Early Complication**- Capsule Rupture ( NEET SS/PG) with intra peritoneal
haemorrhage.
• Within 1 month- Encephalopathy can happen**
• Shunt thrombosis also develops in 1 month
• Shunt stenosis occurs in 1 year ( Most common)

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 Contraindications for TIPS:
Absolute Contraindications
Added Advantage of TIPS – Ascites also resolves**
5th Step : if TIPS not possible or feasible:
Surgical Shunt operations:
Non Selective shunts
Entire Portal Blood is diverted into systemic
circulation and hence Encephalopathy
develops*
Types :
Contraindications of Shunt Operations:
• Splenic vein thrombosis
• SMV thrombosis
• Splanchnic vein thrombosis
RRM’S SURGERY SIXER APP BASED WORKBOOK
Relative Contraindications
• Portal vein thrombosis
• Encephalopathy
• Liver tumors
Selective Shunts
Only Splenic blood diverted ; Portal Blood is
flowing into liver and metabolised and hence
no Encephalopathy; But there is ASCITES
formed
Types :
• Warren’s= Distal Spleno renal shunt:
the distal splenic vein is anastomosed
to left renal vein. Increased pressure in
SMV causes Ascites**
• Inokuchi shunt: Left gastric vein (
Coronary vein) anastomosed to IVC*
47
6th Step : if Shunt operations not possible: Devascularisation operations:
Sugiura operation:
• Ligation of veins near
Esophagus.
• Vagotomy
• Pyloroplasty
• Esophageal transection and
anastomosis
• Splenectomy

Final resort in all cases of PHT= Liver transplant

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 Various causes of portal hypertension

Sinistral / Left PORTAL hypertension

• There is a splenic vein thrombosis due to Chronic pancreatitis
• Hence Short Gastric vessels dilate and develop only left side PHT with Isolated Gastric
Varices+ Splenomegaly**
• Treatment of Choice- Splenectomy.

Non Cirrhotic Portal fibrosis ( NCPF) EHPVO ( Extra Hepatic PV obstruction)

2nd and 3rd order of PV branches are fibrosed Main or 1st order Portal vein obstructed
MC in age 20-40 years MC in < 10 years
Hence stunted growth seen
Common Features:
• Esophago gastric varices rypture and hematemesis ( MC presentation)
• Splenomegaly ( More bigger in NCPF)
• Liver histology is normal
• LFT is normal
• No ascites**
Treatment:
• Splenectomy + Proximal Splenorenal shunt ( LINTON)
• They don’t develop encephalopathy as their liver is normal
• REX shunt- most physiological shunt done for EHPVO between SMV to Left portal vein
using IJV of the baby.

Figure : REX shunt for EHPVO

Post sinusoidal causes of Portal Hypertension- VOD Vs BCS

Veno occlusive disease:
• Sublobular venules gets thrombosis
• MC etiology: Follows Bonemarrow transplant
• Others- Pyrazolidone alkaloids, Azathioprine
• DOC – Defibrotide
• Venography shows HV and IVC normal ; Wedge HV pressure is increased.

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Budd Chiari Syndrome:
• 2 causes- HV thrombosis and IVC occlusion by Congenital membranous webs
• BCS- MC cause in western is HV thrombosis**- The thrombosis mc due to Polycythemia
Rubra vera**
• BCS – MC cause in Asians/ Indians is IVC webs
• IOC to diagnose- Hepatic Venography is gold standard- SPIDER WEB appearance**
• CECT abdomen- shows Enlarged Caudate Lobe – HOT SPOT of caudate lobe seen
Management:
• No role of Thrombolytic agents as it is a well formed thrombus.
• Liver is normal – Shunt operations are planned as shown below:
• Liver failure cases- Liver transplant is TOC

Figure: Shunt operations in BCS

Shunt operations:
• HV thrombosis- Side to side Porto caval shunt ( SSPCS)done
• IVC webs- Double shunt operation done ( SSPCS+ cavoatrial shunt ) or SSPCS with IVC
stenting

Clinical method to find – HV thrombosis alone or IVC web?

• Yes we can find out seeing the Multiple collaterals running from Below upwards in IVC
obstruction cases.

Figure shows- IVC web causing BCS and Liver failure**

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 Chapter 3c. Surgical infections in Liver
• Pyogenic liver Abscess
• Amoebic Liver Abscess
• Hydatid Cyst

Routes of Infection to liver:

Biliary Route Hematogenous Portal Vein route Direct spread from
(Hepatic Artery ) adjacent organs or
trauma
• MC route of • • Infection from
infection Colon like
• Follows Appendicitis,
Ascending Diverticulitis,
Cholangitis. Amoebic
• MC organism infections are
associated – carried to liver.
E.Coli ( World) • Amoeba
Klebsiella ( transferred only
Asians) by this route
• Abscess will be • • Abscess will be
multiple Macro solitary and
abscess** Large in
• Multi organisms Amoebic abscess
are isolated

Figure: Route of Infection

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Pyogenic abscess Amoebic liver abscess
Sick patient with Fever, Chills and Rigors with
Hepatomegaly.
Severe Right Hypochondrial tenderness++

M:F= 1.5:1
Predisposing Factors:
• MC in immunocompromised cases
• Diabetes mellitus
Lab Values:
• Increased AST,ALT, Alk.po4, Bilirubin

Serology: Negative for Amoeba

Blood Culture is positive

CECT abdomen: CECT Abdomen:

• Clustered Abscess seen with Peripheral
rim Enhancement**
• They may be 50: 50 Single or
multiple
• Well defined abscess with no
peripheral enhancement but there
may be peripheral wall edema++
• Trophozoites are present in the wall.
• Mostly they are solitary**
• MC in segment 7**

Complications : Complications:
• Sepsis Color of pus- Anchovy sauce color
• Endogenous Endopthalmitis ( MC in Odourless.
Diabetes- 3% of patients will develop • MC complication is reactive pleural
due to Klebsiella) effusion in Right side.** ( Not rupture)
• Osteomyelitis • MC site of Rupture into Peritoneal
• Infective Endocarditis** cavity**
• Rupture into Pleura- Put an ICD**
• Rupture in Bronchus ( Broncho Pleural
fistula)- Cough shows Anchovy sauce
sputum. Treated by Lying in Prone
position and Bronchodilators+ Chest

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 Physiotherapy. Pus drained via
sputum.
• Rupture into Mediastinum

Treatment:
• Immediate Treatment of choice is
aspiration of abscess
• Based on Pus C/S and Blood C/S-
Higher antibiotics are given.
Treatment:
1/3rd of patients has H/o Amoebic dysentery
2/3rd develops from Subclinical infection
• TOC – Injection Metronidazole 750
mg TDS for 2 weeks and convert to
oral
• Luminal Amoebicides- Diloxanide
furoate, Emetine etc X 10 days
• Aspiration- Indications:
- Doubtful diagnosis
- > 5 cm sized abscess
- Located on Left lobe
- Superficial located abscess
- Not responding for >3 days.

Surgical treatment:
• DP stent under USG guidance . Stent
left for 2 weeks to 1 month.
• Even after complete drainage of
abscess- the residual cavity remains
upto 6 months – 9 months

Hydatid Cyst Liver

• Caused by Echinococcus granulosus, Echinococcus Multilocularis
• E. Multilocularis is very rare and dangerous ( Malignant Hydatid Cyst) . Always need liver
resection.
• E. Granulosus- Dog Tape worm.
• Definitive host- Dogs
• Intermediate hosts- Sheep and Goats
• Accidental Host- Human (End host – Will not spread from one man to other)

Pathophysiology:
• The MC site of hydatid cyst- Segment 6 and 7**
• The cyst wall is formed by: 3 layers
o Outer Ectocyst/ Pericyst/ Adventitial Layer- Derived from Host Tissue
o Middle Laminated membrane- Thin membrane allows some essential
substances
o Inner Germinal Layer- Living layer producing Daughter cysts**

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 • MC site- Liver
• Other sites- Lungs, Brain, Kidney
• Ectocyst is derived from Host tissues and is absent in Lung and Brain Hydatid cyst**
• Ectocyst is seen in Liver and kidney only

Clinical features:
• MC feature- Hepatomegaly ( No pain)
• Jaundice- Hydatid rupture into Biliary tree causes jaundice
• Passing of grape like membranes in motion

Investigations:
• IOC to Diagnose- Immunoblast assay**
• Others- ELISA , Immune Electrophoresis, Casoni’s Intradermal test
• Radiological IOC- CECT Abdomen

Gharbi et al Classification of Hydatid Cysts is old classification ,

Latest classification is WHO classification:
o CE 1-
o CE 2- ( Honey comb/Rosette like)
o CE 3-
o CE 4-
o CE 5-

Type 1,2,3 are active cysts

Type 4,5 are Inactive and dead cysts

Figure; CE1,2,3 Hydatid cysts in USG

Figure: CECT shows Hydatid cyst

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Complications:
• MC is biliary rupture- 30%**
• Secondary infections

Extra Mile
Risk of biliary-cyst communication. ( For NEET SS from Blumgart repeat)
• Male patients
• Abnormal preoperative serum alkaline phosphatase and γ-glutamyltransferase (GGT);
• Multiple cysts, multilocular and degenerated cysts
• Cysts near the biliary bifurcation,
• Presence of bile-stained or purulent cyst
• Cyst diameter greater than 10 cm was an independent clinical predictor for the
presence of intrabiliary rupture.

Management:
• T. Albendazole started.
• Under cover of T. Albendazole after 2 weeks we plan for Surgery / PAIR

Surgical treatment options:

• Partial pericystectomy ( Leaving part of pericyst thereitself)- Surgical best option**
• Hepatic resection
• After partial pericystectomy look for Biliary leak inside the cavity ( Communication)- we
must suture the leak site. Some surgeons also advise T tube insertion in CBD also.

Percutaneous Aspiration , Infusion of scolicidal agents and Reaspiraion ( PAIR)

 Given with prophylactic cover of albendazole.
 Scolicidal agents- 20% hypertonic saline ( Best) , 0.5% silver nitrate, 95% ethanol,
absolute alcohol, Mebendazole 2.4 microgram/ ml, 10% povidone Iodine**

Contraindications for PAIR:

Also Know:
• PAIR: < 6 cm cyst ( < 100 ml)
• PAIR- Catheter: > 6 cm cyst ( > 100 ml)
• PEVAC ( percutaneous Evacuation of Cyst Content)

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Chapter 3d- Tumors in Liver
• IOC for SOL liver- CECT abdomen
• IOC for hemangioma-MRI **

BENIGN LIVER TUMOUR

Characters Hemangioma Focal nodular Liver cell adenoma
hyperplasia
Incidence m/c Incidentaloma Rare
m/c benign tumour
Age group/sex About 45 years Young women
m/c in females 20-40 years
Associated ------- OCP and steroids
factors
Complications Rupture / Rupture and malignant
hemorrhage transformation**

Giant
Hemangioma- > 5
cm
Kassabach merit
syndrome- Huge
hemangioma
consuming platelets
and causing
Thrombocytopenia+
CCF
Histology Small capillary type Benign histocytes
and large cavernous containing glycogen or
types are there fat

Imaging studies Slow contrast CT- heterogenous mass

CECT abdomen- enhancement from with early enhancement
Triple phase periphery to centre
due to small vessel
uptake . Typical
nodular peripheral
enhancement

MRI – T2 weighted
image shows –
Light Bulb sign”

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 Treatment No treatment Laparotomy and
needed resection**

Extra edge points in Liver cell adenoma:

• MC they are single**
• Such single adenomas are MC in females
• 20% cases are multiple- these are not associated with OCP and no female
preponderance**- These cases need liver transplant**
• Beta Catenin Mutation+ ve cases- High risk of malignancy is seen- Early surgery needed

Malignant Tumors in liver

MC malignant tumor is Secondary
MC primary malignant tumor is HCC**

Hepatocellular cancers:
Etiological factors:
Infections Cirrhosis Environmental Metabolic diseases
HBV Alcohol Aflatoxins Hemochromatosis
HCV Autoimmune Pyrrozolidone Alpha 1 AT
Primary biliary alkaloids deficiency
Thorotrast Wilsons
Nitrosamines Glycogen storage
diseases
EHBA
• HCC usually arises from Cirrhotic liver background only except in HBV induced HCC**

Clinical Features:
• K/C/O Cirrhosis sudden decompensation of Liver with Pain, Mass and weight loss all
suggest malignancy**
• Paraneoplastic syndromes:
o MC is Hypercholesterolemia > Hypoglycemia**
o Hypercalcemia
o Polycythemia( Erythrocytosis)

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 ( MC PNS in RCC- increased ESR**)
Types of HCC:

• Hanging type- Best prognosis

• Infiltrative type- Bad prognosis

Investigations:
Tumor markers:
• AFP > 20 ng/ml- 70% have elevation
• AFP > 400 ng/ml- Conclusive of HCC
• Glypical-3
• PIVKA- protein induced Vitamin K absence** - Descarboxy prothrombin**
• AFP-L3 Lectin 3 fraction

CECT abdomen with triple Phase is Gold standard:

• Rapid contrast enhancement of Tumor in arterial phase**
• Rapid wash out in Portal venous phase**
• Phases in Liver on CECT:
o Early arterial
o Late arterial
o Portal venous phase
o Delayed

Figure: See the phases of HCC in CECT

NCCN Diagnostic criteria

• > 2cm lesion: With Typical Finding in CECT explained – Diagnosis is confirmed
• 1-2 cm lesion: we need 2 imaging techniques needed like CECT+ MRI

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 • No biopsy in operable cases. Inoperable cases Biopsy may be taken

Various Staging systems in HCC:

OKUDA staging CLIP- Cancer of Liver Italian Chinese University Prognostic
Program index ( CUPI)
T- Tumor size
A- Albumin
A- Ascites
B- Bilirubin

Latest Staging system which helps in Diagnosis and treatment- Barcelona Clinic Liver Staging (
BCLC Staging )
• Very early stage- < 2cm size, Single lesion- Best treatment is Resection**
• Early stage- < 3 lesions , < 3cm size all lesion- Resection or Transplant advised.
• Intermediate stage
• Advanced Stage
• Terminal Stage

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Modalities of treatment:
• Best is Surgical resection:
o In a cirrhotic liver – Future Liver remnant ( FLR ) must be atleast 40%
o In a normal liver- FLR must be atleast 25%
o If above FLR is not possible- Liver resection in contraindicated
• Liver transplantation: Milan Criteria** of Liver transplant in Cirrhotic liver
o < 5 cm single lesion
o < 3 lesions all 1-3 cm each
o No Extra hepatic spread seen

Ablative therapies:
• Percutaneous ethanol Injection ( PEI)
• Percutaneous Acetic acid injection
• Percutaneous Thermal Ablations- RFA, Cryoablation**
• Heat sink effect- is seen in patients who have tumors very close to blood vessels will have
the thermal effect dissolved by running blood and less effective*

Interventional Procedures:
• TACE – Transarterial chemo embolization: Into hepatic artery we can inject
Chemotherapy – Loaded with Lipoidal sodium, which carries chemotherapy to tumor
• TARE- Transarterial Radio embolization

Properties of HCC:
• Tumor can grow into HA or PV
• PV invasion is bad prognosis
• Only 10-15% cases are operable
• Inoperable cases- Latest therapy- SORAFENIB- Multikinase inhibitor** - Increases 6-9
months survival:
▪ Serine threonine inhibitor
▪ VEGF inhibitor
▪ Tyrosine Kinase inhibitor
▪ Platelet Derived Growth Factor inhibitor

Fibrolamellar HCC
• M:F= Equal
• MC in young age
• Liver is normal here, NO cirrhosis
• HBV and HCV are negative
• AFP is not elevated
• Tumor marker- Neurotensin B**
• CECT abdomen: Important DD- FNH as they both have central scar**
• Good prognosis

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 • Mostly resectable tumors

Metastasis to liver
• MC primary for Liver mets- Colorectal cancer
• MC primary from Extra abdominal- Breast
• Mets with good prognosis- NET mets**> CRC mets
• Resection is approved for CRC and NET mets only so far.

Hypodense/ Hypovascular mets Hyperdense/ Hypervascular mets

They are detected on Late Portal Venous They are detected on Late Arterial Phase after
Phase** 35 Seconds of contrast injection.

• Git primaries • Renal cancer

• Lung cancer • Insulinomas
• Breast Cancer • Carcinoids
• Head and Neck cancer • Sarcomas
• Melanoma
• Also Breast cancer

CECT- Hypodense mets

CECT- Hyperdense mets

Fong Score of Outcome for Colorectal Cancer Metastasis in Liver: ( NEET SS)
• 5 Predictive factors for outcome of CRC mets liver: all the below are bad points*
1. Size > 5cm
2. Disease free interval < 1 year
3. More than 1 tumour
4. Lymph node positive primary
5. CEA > 200 ng/ml
Each given 1 point and scoring made as shown below:
Based on these points Survival rate is mentioned.
• If score is 1- Median survival is 51 months
• If score is 5- Median survival is 22 months**

RRM’S SURGERY SIXER APP BASED WORKBOOK 61

Other liver lesions- Images may be asked in exams

Simple cyst liver:

• Symptomatic cases are treated by
Laparoscopic Fenestration (
Deroofing)
• No risk of malignancy

Biliary cystadenoma:
• Septal wall enhancement seen on
CECT
• Can go for malignancy
• Resection of entire cyst advised.

Polycystic liver disease:

• Liver failure never happens inspite of
so many cysts
• Treatment is only for Symptomatic
reasons
• They will develop PCKD and renal
failure**

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 Chapter 4: Spleen

Anatomy of Spleen:
• Ligaments attached with Spleen:
- Gastrosplenic Ligament
- Spleno colic Ligament
- Spleno phrenic Ligament
- Lieno renal Ligament

• The ligament containing the Splenic Vessels – Lienorenal ligament**. Hence this is the
ligament which must be Ligated and cut in emergency Splenectomy of Trauma.
• Gastrosplenic ligament has short gastric vessels. We must cut the Gastrosplenic Ligament
1st in elective surgeries.
• The ligaments which are avascular- Spleno colic and spleno phrenic ligament**

Dimensions:
• 150 gm
• 12X7X3 cm size
• Lying along 10th Rib it lies.
• Notch seen in Anterior border of Spleen.

Splenic artery Is the largest artery from Coeliac trunk:

- Divides near Hilum known as Magistral type- 30%
- Divides very proximal into multiple branches – 70%

• Splenic artery runs on the superior border of pancreas

• Splenic Vein runs inferiorly on the posterior part of Pancreas.

Functions of Spleen:
• Immune Function: IgM produced*
• Filtering Function: Culling – removal of iron from RBC and bringing into
circulation**, Removal of senescent RBCs.
• Pitting- Removal of Particulate inclusions in RBC.
• Reservoir function- Stores 8% of RBC**- 2% Blood volume is inside spleen

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 • Haematopoiesis.

Peripheral smear after splenectomy:

• Howel Jolly Bodies- Non Functional nucleus
• Heinz Bodies- Denatured Haemoglobin
• Pappenheimer Bodies- Iron Particles in RBC
• Target Cells

Indications for Splenectomy:

Emergency Splenectomy Elective Splenectomy
MC indication for splenectomy- Blunt trauma Idiopathic Thrombocytopenic purpura is the
MC Elective indication
During Some other Surgery:
- D2 Lymphadenectomy
- Gastric cancer + Spleen infiltration
- Pancreatic Tail neoplasm
Haemolytic Anemias
- Sickle cell
- Auto immune
- Hereditary spherocytosis
Multiple Abscess in Spleen
Tumors in Spleen

Methods:
• Open method
• HALS- Hand Assisted Laparoscopic Surgery. Hand port used to remove the specimen
finally

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 • Laparoscopic method- Spleen Removed via a Plastic pouch with maceration. It can be
used in Tumors as there will be spillage.

Complications of Splenectomy:
Immediate complications
o Haemorrhage
o Gastric distension
o Hematemesis
Intermediate Complications Delayed Complications
o Thromboembolic
manifests
o OPSI
o PV thrombosis

Opportunistic Post Splenectomy Infections:

o MC after splenectomy for Haematological causes > trauma causes
o Bacterial infection**-Inability to remove capsulated Bacterias- Streptococcal Pneumonia,
H.Influenza and meningococcal
o Parasitic Infection- Babesia and malaria
o Viral Infection- Not increased

Haematological Effects:
o Increased Platelet Counts- Can cause Thrombotic manifests ( if count > 8 Lakhs ;Anti
platelet drugs started)
o Increased WBC counts.

Prevention of OPSI:

RRM’S SURGERY SIXER APP BASED WORKBOOK 65

On discharge: Post op antibiotics:
o Method 1: Children are advised for next 2 years after splenectomy
o Method 2: Some advocate for life-long Prophylaxis
o Method 3: Rational approach: To have antibiotics in hand and take when there is onset of
febrile illness and rigors by patient himself and later come to hospital**- MC followed.

Idiopathic Thrombocytopenic Purpura

o Autoimmune disease
o IgG Antibodies are produced from Spleen against the Platelets** and destroy the platelets.
o Hence platelet count falls, Mega thrombocytes seen.
o Bone marrow study is normal and all causes of Thrombocytopenia ruled out before
branding a patient as ITP
o Clinical Features:
▪ MC in Young women
▪ In children M=F
▪ C/B- Mucocutaneous Bleeding, Epistaxis, petechiae and Purpura**
▪ Massive Bleed or GI bleed or Hematuria or Intracerebral bleed are very
rare.
o Management depends on Platelet Counts:
▪ > 50000:
▪ 30000-50000:
▪ < 20000 + Mucous bleeding :
▪ < 10000:
o Treatment of ITP:
▪ < 50000 with Mucous bleeding only treatment started.
▪ Above 50000 with no symptoms no treatment needed.
▪ DOC: Prednisolone 1mg/ kg Body weight**
▪ Infusion of platelets: Only in significant haemorrhage
▪ Infusion of immunoglobin: Pregnancy or planning a major surgery/
Splenectomy
▪ Refractory ITP : Rituximab IV or Thromboplastin receptor antagonists like
Romiplastin or Eltrombag**

Indications for Splenectomy in ITP

• >6 weeks*
• Refractory to steroids
• Requirement of toxic doses of steroids
• Incomplete response to steroids
• Pregnant women in 2nd trimester
• Engagement in High risk activities.

During Splenectomy:
• Platelets are given only after ligating the splenic pedicle**

RRM’S SURGERY SIXER APP BASED WORKBOOK 66

 Post op response:
• 72% Complete response
• Preop Indium 111 Scan shows Splenic Sequestration- Excellent
response, Liver sequestration will have bad response( NEETSS)
• 15% cases relapses. MC cause of relapse is missed out Ectopic spleen

Tumors in Spleen:
• Most common neoplasm of Spleen-
• Most common primary benign tumor of spleen –
• Most common primary malignant tumor of spleen – Hemangiosarcoma
Mets in spleen are very rare:
• “Types- Multi visceral (MC) and Isolated”
o Most common primary for Multi-visceral- Lung > Breast> Malignant melanoma**
o Most common primary for Isolated- Ovary> Colorectal**
o Most common primary with highest percentage (No of cases of splenic metastasis/
100 Primaries) – Malignant Melanoma**

Ectopic Spleen: (Splenenculi= Accessory Spleen)

• MC reason is due to embryological non fusion or incomplete fusion during 5th Week of IUL
• Incidence= 10-30%
• It is seen along the Dorsal Mesogastrium:
▪ Splenic Hilum ( MC)
▪ Tail of Pancreas ( 2nd MC)
▪ Splenocolic ligament
▪ Presacral
▪ Renal
▪ Left side scrotum
• Properties of Ectopic spleen:
▪ Multiple usually
▪ Always have capsule
▪ Contains Red and white pulp like normal spleen.
▪ MC to go for Torsion**
Splenosis:
• Rupture of Spleen and its distribution all along the abdominal cavities
• Seen anywhere in abdominal cavity ( DD- Ectopic spleen in Dorsal mesogastrium only)

Splenic artery Aneurysm:

• Incidence < 1%
• Old age : MC in females
• Solitary
• MC cause- Arteriosclerosis

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 • Other aetiology: Sepsis and pancreatitis**
• Usually asymptomatic, May rupture suddenly**
• Rupture risk is increased in:
▪ Young
▪ Pregnancy ( 2nd and 3rd Trimester)
▪ Absence of Calcification
▪ Hypertension
▪ Size > 1.5cm
• Management:
- Upto 2cm (Asymptomatic cases)- Observation
- Indications for Splenectomy with aneurysm:
• Symptomatic
• > 2cm
• Pregnancy
• Young age
- Angioembolisation can be done for unfit cases.

Splenic Abscess:
• MC in immunocompromised, Polycythemia, IV drug abusers, Trauma.
• 70% due to Hematogenous route
• MC is
• Immunocompromised fellows may develop Fungal abscess- Candida
• Sickle cell anemia- Salmonella causes abscess
• IOC for Diagnosis: Hypodense lesion
• Unilocular abscess- Percutaneous drainage
• Multiple abscess- Splenectomy

Figure: Splenic abscess

Splenic Cyst:
• MC cyst in spleen-
• MC non parasitic cyst-
• MC cause of true cyst- Congenital Epidermoid Cyst; Rare < 10% ( Lined by Squamous
epithelium). Fluid analysis shows CEA, CA 19-9 +ve. But they are benign**. Partial
splenectomy done and leave 25% of spleen to prevent OPSI.

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RRM’S SURGERY SIXER APP BASED WORKBOOK 69