DEPARTMENT OF SURGERY

JONELTA FOUNDATION SCHOOL OF MEDICINE

Written report - by Group 4 (BLOCK 4)
Module 15- Liver

BLOCK MEMBERS- GROUP 4 (BLOCK4)

 ELAMATHIYAN ABIRAMAN (16-0630-676)

 ETTAMSETTY RAMESH (16-0736-605)
 EZHILMARAN POOJA (17-0470-788)
 EZHUVATHRA PRITI PRAKASH (17-0077-619)
 FERA MILANKUMAR KANUBHAI (17-0102-287)
 GAGGENAPALLY DRISHYA (16-0285-217)
 GANAPATHY SARAVANAN, NIVEDHA GANGADHAR (16-0588-668)
 GANDIKOTA HEMANARASIMHA (16-0349-310)
 GANDRATH MEGHANA(16-0750-725)

Illustrate the gross anatomy of the liver

 The liver is the largest organ in the body- weighing approximately 1500 g.
 It resides in the right upper abdominal cavity beneath the diaphragm and is
protected by the rib cage.
 It is reddish brown and is surrounded by a fibrous sheath known as Glisson’s
capsule. The liver is held in place by several ligaments.
  The round ligament is the remnant of the obliterated umbilical vein and
enters the left liver hilum at the front edge of the falciform ligament.
 The falciform ligament separates the left lateral and left medial
segments along the umbilical fissure and anchors the liver to the anterior
abdominal wall.
 Arantius’ ligament (ligamentum venosum) - obliterated ductus venosus
 Left and right triangular ligaments- secure the two sides of the liver to
the diaphragm
 Coronary ligaments- extension from the triangular ligaments anteriorly
on the liver.
These ligaments (round, falciform, triangular, and coronary) can be divided in a
bloodless plane to fully mobilize the liver to facilitate hepatic resection.

Attachments of Liver:
 Hepatoduodenal ligament- known as the portahepatis and contains the
common bile duct, the hepatic artery, and the portal vein.
o From the right side and deep (dorsal) to the portahepatis is the foramen of
Winslow, also known as the epiploic foramen.
o This passage connects directly to the lesser sac and allows complete
vascular inflow control to the liver when the hepatoduodenal ligament is
clamped using the Pringle maneuver.
1. Gastrohepatic ligament
Segmental Anatomy
The liver has 2 lobes: Right and Left
Cantlie’s line: divides liver in 2 lobes by the plane from the gallbladder fossa to the
inferior vena cava (IVC).
The right lobe typically accounts for 60% to 70% of the liver mass, with the left lobe (and
caudate lobe) making up the remainder.
The caudate lobe lies to the left and anterior of the IVC and contains three sub
segments:
 The Spiegel lobe
 The paracaval portion
 The caudate process
The falciform ligament does not separate the right and left lobes, but rather it divides the
left lateral segment from the left medial segment.
Vascular Supply:
Hepatic Artery
 arises from the celiac axis
 delivers approximately 25% of the blood supply
 The hepatic artery proper divides into the right and left hepatic arteries.
 This “classic” or standard arterial anatomy is present in only approximately 76%
of cases, with the remaining 24% having variable anatomy.
Anomalies/variants
 replaced or accessory right hepatic artery
 replaced or accessory left hepatic artery
 replaced right and replaced left hepatic arteries
 completely replaced common hepatic artery

Portal Vein:
Valveless.
 formed by the confluence of the splenic vein and the superior mesenteric vein
 traverses the portahepatis before dividing into the left and right branches
 Left portal vein:
 supplies segments II-IV,
 provides the dominant inflow branch to the caudate lobe
 drains the splanchnic blood from the stomach, pancreas, spleen, small intestine,
and majority of the colon to the liver before returning to the systemic circulation.
 Normal pressure 3-5mmHg
 Hepatic veins: drain the blood to the suprahepatic IVC >>> right atrium
 Right hepatic vein: drains segments V through VIII
 Middle hepatic vein: drains segment IV as well as segments V and VIII
 Left hepatic vein: drains segments II and III
 Inferior accessory right hepatic vein: Occurs in 15% to 20%
Neural Innervation:
Parasympathetic innervation
• Left vagus
• Right vagus
Sympathetic innervation
• greater thoracic splanchnic nerves
• celiac ganglia
Lymphatic drainage:
• hilar cystic duct lymph node
• common bile duct, hepatic artery, and retro-pancreatic and celiac lymph nodes
• also drains cephalad to the cardio-phrenic lymph nodes.
PHYSIOLOGY OF LIVER
• The liver is the largest gland in the body and has an extraordinary spectrum of
functions.
• Process such as metabolism, the liver also is responsible for the synthesis of
most circulating plasma proteins.
• Proteins are albumin, factors of the coagulation and fibrinolytic systems,
and compounds of the complement cascade.
• Process such as storage, metabolism, production, and secretion.
• One crucial role is the processing of absorbed nutrients through the
metabolism of glucose, lipids, and proteins
• The liver maintains glucose concentrations in a normal range over both short and
long periods by performing several important roles in carbohydrate metabolism.
• In the fasting state, the liver ensures a sufficient supply of glucose to the central
nervous system
• The liver can produce glucose by breaking down glycogen through
glycogenolysis and by de novo synthesis of glucose through gluconeogenesis
from noncarbohydrate precursors such as lactate, amino acids, and glycerol.
• In the postprandial state, excess circulating glucose is removed by glycogen
synthesis or glycolysis and lipogenesis.
• The liver also plays a central role in lipid metabolism through the formation of bile
and the production of cholesterol and fatty acids.
• Protein metabolism occurs in the liver through amino acid deamination, resulting
in the production of ammonia
• the liver also is responsible for the synthesis of most circulating plasma proteins.
• Among these proteins are albumin, factors of the coagulation and fibrinolytic
systems, and compounds of the complement cascade.
Bilirubin Metabolism:
• Bilirubin is the breakdown product of normal heme catabolism.
• Bilirubin is bound to albumin in the circulation and sent to the liver.
• In the liver, it is conjugated to glucuronic acid to form bilirubin diglucuronide in a
reaction catalyzed by the enzyme glucuronyl transferase, making it water soluble.
• This glucuronide is then excreted into the bile canaliculi.
• A small amount dissolves in the blood and is then excreted in the urine.
• The majority of conjugated bilirubin is excreted in the intestine as waste because
the intestinal mucosa is relatively impermeable to conjugated bilirubin.
• However, it is permeable to unconjugated bilirubin and urobilinogens, a series of
bilirubin derivatives formed by the action of bacteria.
• Thus, some of the bilirubin and urobilinogens are reabsorbed in the portal
circulation; they are again excreted by the liver or enter the circulation
and are excreted in the urine
Formation of bile
• Bile is a complex fluid containing organic and inorganic substances dissolved in
an alkaline solution that flows from the liver through the biliary system and into
the small intestine.
• The main components of bile are water, electrolytes, and a variety of organic
molecules including bile pigments, bile salts, phospholipids (e.g., lecithin), and
cholesterol.
 • The two fundamental roles of bile are to aid in the digestion and absorption of
lipids and lipid-soluble vitamins and to eliminate waste products (bilirubin and
cholesterol) through secretion into bile and elimination in feces.
• Bile is produced by hepatocytes and secreted through the biliary system.
• In between meals, bile is stored in the gallbladder and concentrated through the
absorption of water and electrolytes.
• Upon entry of food into the duodenum, bile is released from the gallbladder to aid
in digestion.
• The human liver can produce about 1 L of bile daily.
• Bile salts, in conjunction with phospholipids, are responsible for the digestion
and absorption of lipids in the small intestine.
• Bile salts are sodium and potassium salts of bile acids conjugated to amino
acids.
• The bile acids are derivatives of cholesterol synthesized in hepatocytes.
Cholesterol, ingested from the diet or derived from hepatic synthesis, is
converted into the bile acids cholic acid and chenodeoxycholic acid.
• These bile acids are conjugated to either glycine or taurine before secretion into
the biliary system.
• Bacteria in the intestine can remove glycine and taurine from bile salts.
• They can also convert some of the primary bile acids into secondary bile acids by
removing a hydroxyl group, producing deoxycholic acid from cholic acid and
lithocholic acid from chenodeoxycholic acid.
• Bile salts secreted into the intestine are efficiently reabsorbed and reused.
• continuous process of secretion of bile salts in the bile, their passage through
the intestine, and their subsequent return to the liver is termed the enterohepatic
circulation
Drug Metabolism:
• The liver plays an important role in providing mechanisms for ridding the body of
foreign molecules (xenobiotics) that are absorbed from the environment.
• In most cases, a drug is relatively lipophilic to ensure good absorption.
• The liver participates in the elimination of these lipid-soluble drugs by
transforming them into more readily excreted hydrophilic products.
• There are two main reactions important for drug metabolism.
• Phase 1 reactions include oxidation, reduction, and hydrolysis of molecules.
 • These result in metabolites that are more hydrophilic than the original chemicals.
• The cytochrome P450 system is a family of hemoproteins important for
oxidative reactions involving drugs and toxic substances.
• Phase 2 reactions, also known as conjugation reactions, are synthetic reactions
that involve addition of subgroups to the drug molecule.
• These subgroups include glucuronate, acetate, glutathione, glycine, sulfate, and
methyl groups.
• These drug reactions occur mainly in the smooth endoplasmic reticulum of
hepatocytes.
• Many factors can affect drug metabolism in the liver.
• When the rate of metabolism of a drug is increased (i.e., enzyme induction), the
duration of the drug action will decrease.
• However, when the metabolism of a drug is decreased (i.e., enzyme inhibition),
then the drug will circulate for a longer period of time.
• During an overdose, the normal metabolic pathways are overwhelmed, and some
of the drug is converted to a reactive and toxic intermediate by the cytochrome
P450 system
Liver Function Tests:
• Measurement of levels of levels of aspartate transaminase (AST), alanine
transaminase (ALT), alkaline phosphatase (AP), γ-glutamyltranspeptidase
(GGT), and bilirubin
• More accurate measurement of the liver’s synthetic function is provided by serum
albumin levels and prothrombin time (PT)

CASES

A 30year old male who just returned from vacation came in

with right upper quadrant pain and fever.

a. What pertinent data will you elicit in the history and physical examination?
General data:
Name
Age- 30Y
Gender- male
occupation

History of Present illness:

Chief Complaint: Right Upper Quadrant Pain & Fever
 When did the pain started (sudden or gradual)?
 What is the quality of the pain (Sharp or dull or colicky)?
 What is the intensity of the pain (on a scale from 1-10)?
 Does the pain is radiating?
 What makes it worse and makes better?
 Is that the pain is constant or intermittent? How long does it last?
 How long you experiencing the fever? Is the fever Intermittent or constant?
 Did you take any medication for fever or pain (Acetaminophen)?
 Does it come with any other symptoms? (vomit, Nausea, weight loss, loss of
appetite, Fatigue, Malaise, Cough)
 How about the bowel movements?
 stool color and consistency? Any recent episodes of Diarrhea?
 Do you have any problem in urinating (To rule out kidney problem)?
 Color of the Urine?
 Have you noticed any change sin the color of your eyes/skin?
 Have you had any recent blood transfusions?

Past Medical History:

Ask if they have any medical problems (Congenital Jaundice, Heart Disease, Asthma,
Hypertension?)
Are you taking any medication in regular basis?
Have you undergone any surgery before?
Any diagnosis pf sexually transmitted infections?

Family History:
Any family History of Cancer or gallstones?

Personal History and Social History:

Are you allergic to any medication or food?
Smoking Hx: Do you smoke? If yes then how many packs daily?
Alcohol Hx: Do you drink Alcohol? If yes the ask how much and how often he consume?
Do you have any habit of using illicit Drugs?
Did you have any recent Tattoos done?
When and where was your last vacation to?
Details about patients sexual life?

Physical Examination:
 Inspection: skin color(yellow), scar, striae, any bulged mass, distended abdomen,
Lesions,

 Auscultation: Note the pitch and frequency of the bowel sounds, If any rubs are
hear over RUQ indicates Inflammation of Liver.

 Percussion: The purpose of liver percussion is to measure the liver size. Liver
span: commonly clinically under estimated.
o Midclavicular line: normally 6-12cm.
o Midsternal line: normally 4-8cm.
False positives for enlarged liver span: right pleural effusion, consolidated lung.

 Palpation: The purpose of liver palpation is to approximate liver size, feel for
tenderness and masses.
Tenderness:
The normal liver may be slightly tender.
Greater tenderness suggests inflammation (e.g. hepatitis) or congestion (e.g.
congestive heart disease).

Consistency
Firm, bluntness/rounding or irregularity of liver edge suggest an abnormality.
Obstructed, distended gallbladder may be palpable on the inferior liver edge.
Nodules may be palpable; rock hard and umbilicated (central dimple) nodules
suggest malignancy.

b. What are your differential diagnoses? Explain.

DIFFERENTIAL RULE IN RULE OUT

DIAGNOSIS
Hepatic abscess Right upper Jaundice
quadrant pain Clay-colored stools
Fever Dark urine
Nausea, vomiting
 Unintentional weight loss

Acute Cholecystitis RUQ pain, fever Nausea, vomiting,

Pain radiates to shoulder
Acute cholangitis Right upper Nausea, vomiting
quadrant pain jaundice
fever
ACUTE VIRAL Right upper quadrant
HEPATITIS abdominal pain
Fever
Travel history

c. What further diagnostics (include labs and diagnostic interventions) will you
request?
a. Key Labs (NON Imaging)
 CBC
 Liver function Test - AST, ALT, Alkaline Phosphatase, Bilirubin Direct & Indirect,
Prothrombin time/INR
 Viral Serology
 Metabolic Panel

b. Imaging study: UTZ of abdomen, CT Scan

A liver biopsy should be performed if certain disease entities such as autoimmune

hepatitis or lymphoma are a possibility.

d. How will you manage your patient?

TREATMENT FOR HEPATITIS A:

 treatment is usually supportive
 Patients who develop fulminant infection require aggressive therapy and
should have a liver transplantation.

TREATMENT FOR CHOLECYSTITIS

Nonsurgical  NPO, IV fluids

 IV antibiotics for severe acute cholecystitis: guided by the most
common organisms likely to be present (E. coli, Klebsiella spp. and
Streptococcus spp.)
 Meperidine or NSAIDs: usually employed for analgesia because they
may produce less spasm of the sphincter of Oddi than drugs such as
 morphine
Surgical  Definitive management: early cholecystectomy (2-3days)
 If patient unfit for surgery: cholecystostomy plus elective lap
cholecystectomy
Management based on grade of cholecystitis:
Grade I Early laparoscopic cholecystectomy (within 72 hours) is
(Mild) preferred

Grade II Early cholecystectomy (laparoscopic or open) is

recommended; early gallbladder drainage
(Moderate)
(percutaneous or surgical) if with severe local
inflammation

Grade III Urgent management of organ dysfunction and

(Severe) gallbladder drainage (delayed elective cholecystectomy
2-3 months later when general conditions are
improved)

2. A 32 year old woman presents with abdominal pain and a

right upper quadrant mass. She is on birth control pills and
has a past history of hepatitis B infection?

a. What is the most appropriate work-up? Why?

● Radiologic imaging is vital for the assessment of cyst size, type of cyst, location within
the liver and the anatomic relations with biliary and vascular structures.
● Ultrasound can differentiate a simple cyst from other cystic lesions.
● Laboratory examination generally includes hepatic function panel, CBC (to evaluate
for anemia and thrombocytopenia), HCV antibody, HBsAg, alfa-fetoprotein, and Ca19-9.
● A biopsy of liver away from the lesion is sometimes performed to establish the
presence of cirrhosis

b. How do you differentiate an adenoma of the liver from hepatocellular

carcinoma?
Hepatic adenoma
  Hepatic adenomas are benign solid tumors. Long-term estrogen exposure
corresponds to an increased risk of developing hepatic adenoma
 For this reason, these rare tumors occur most commonly in premenopausal
women who are between 30 and 50 years of age and who have a long-
standing history of oral contraceptive use.
 Prior or current use of estrogens (oral contraceptives) is a clear risk factor
for development of liver adenomas, although they can occur even in the
absence of oral contraceptive use
 The clinical presentation may be abdominal pain, and in 10% to 25% of
cases, hepatic adenomas present with spontaneous intraperitoneal
hemorrhage
 On gross inspection, adenomas are soft and appear tan to light brown in
color.
 On microscopic examination, adenomas are composed of swollen
hepatocytes filled with glycogen.
 Adenomas lack bile ducts and Kupffer cells that would be characteristic of
normal liver tissue.
 On CT imaging, an adenoma will appear as a well-circumscribed, hypo-
intense lesion. Adenomas carry the risk of sudden spontaneous bleeding
as well as malignant transformation.
 Discontinuation of oral contraceptives may lead to involution of some
adenomas, but for adenomas larger than 4 cm surgical resection is
recommended

Hepatocellular carcinoma:-

 Hepatocellular carcinomas (HCC) are most common primary liver

malignant tumors
 An estimated 70-90% of HCC arises in the setting of cirrhosis, so patients
with hepatitis B, hepatitis C, alcoholic cirrhosis, non-alcoholic
steatohepatitis (NASH), or other chronic liver disease are at increased risk.
 Microscopically, it is characterized by thickened cell plates, malignant
tumor cell cytology, capillarization of sinusoids and evidence of invasion
 HCC tends to have a hypervascular blood supply from the hepatic artery.
 On CT scan with IV contrast, there will be diffuse enhancement of the
lesion with arterial phase contrast, followed by washout during delayed
venous images. And the presence of an enhancing portal vein thrombus is
highly suggestive of HCC.
 Alpha-fetoprotein (AFP) may already be chronically elevated in patients
with underlying cirrhosis, however, an AFP level above 500 mg/dL should
raise concern for the presence of HCC
 Resection or liver transplant are the two primary surgical treatments for
HCC. This tumor is prone to vascular invasion, particularly into the portal
 venous circulation; the larger the size of the tumor, the greater the risk of
vascular spread
 Lung and bone are the most common sites of metastases
 For patients with more advanced cirrhosis, or with larger disease burden,
but still without evidence of extrahepatic disease, liver transplant can treat
both their cancer and their underlying liver dysfunction

c. Does the presence or absence of cirrhosis impact your therapeutic

decision? Why?
● Although cirrhosis is not present in all cases, it has been estimated to be present
70% to 90% of the time.
● In a person with cirrhosis, the annual conversion rate to HCC is 2% to 6%.79 In
patients with chronic HCV infection, cirrhosis usually is present before the HCC
develops; however, in cases of hepatitis B virus infection, HCC tumors can occur
before the onset of cirrhosis.
● For patients without cirrhosis who develop HCC, resection is the treatment of
choice. For patients with Child’s class A cirrhosis with preserved liver function
and no portal hypertension, resection also is considered.
● If resection is not possible because of poor liver function and the HCC meets
transplant criteria (discussed later), liver transplantation is the treatment of
choice.

3. A 64year old male presented with persistent vomiting

and weight loss of 6kgs in 3 months.

a. The vomiting was intermittent once in 2-3 days in the beginning, but
progressively increased to 2- 3times daily in the last one month.
b. He was a known case of hepatitis B virus carrier for the last 3 years.
c. On examination patient was dehydrated, there was fullness in the
upper abdomen with visible peristalsis and non-tender hepatomegaly
3 cms, below the right coastal margin.
d. Routine hematological investigations showed anemia, hypokalemic
hypochloremic alkalosis.
e. Liver function tests showed mild elevation of liver enzymes, and the
rest of liver function tests were normal.
f. Child-pugh score 5.
g. Endoscopy showed normal oesophagus, no varices, hugely dilated
stomach with edematous mucosa, and old food material, endoscope
could not be passed beyond 1st part duodenum, suggestive of
gastric out obstruction.
 h. CT scan of abdomen showed a large tumor in the right lobe of liver,
of size 10.5x 8.4 x 7.2 cms, with area of central necrosis and early
washout in arterial phase.
i. The lesion was compressing the duodenum, leading to huge
dilatation of the stomach, likely malignant morphology causing
gastric outlet.
j. No other lesions were seen in other segments of liver or in the
abdomen.
k. Spleen was normal in size and there were no features of portal
hypertension or ascites.

l. AFP level significantly elevated.

m. CA 19-9 and CEA were within normal limit.

a. What are the pertinent data you can extract in the case given? Why are they
pertinent?
Age – 64Y (Mostly commonly Patients presenting with HCC are 4th to 6th decade of
life)
• Gender – Male (HCC is 8 times more common in Male compared to females)
• Vomiting, Cachexia – These are Non specific Symptoms of HCC are also common.
• Mass in upper abdomen present in HCC.
• Hep –B carrier
• In general HCC arises from a precursor condition including chronic hepatitis B or C or
liver cirrhosis
• Elevated liver enzymes reflect active hepatitis due to viral infection, current alcohol
use, or other causes
• Anemia - Low hemoglobin may be related to bleeding from varices or other sources
• CT of Abdomen showed large tumor with Necrosis in Early Wash out arterial Phase
• This helps to differentiate HCC from other metastasis.
• Serum AFP levels increase
• AFP levels may be elevated because of production by the tumor or by regenerating
hepatocytes
• Gastric outlet obstruction.
• CT image showing grossly dilated stomach with tumor mass seen compressing the
duodenum.

b. What are your differential diagnoses? Rule in? Rule out?

Differentials Rule in Rule out
Pancreatitis Vomiting Fever.
Tenderness when
touching the
abdomen
Metastatic liver loss of appetite. Dardark colored
disease weight loss. urine.
abdominal jaundice, a
swelling or yellowing of the skin
bloating. or the whites of the
eyes.
pain in the right
shoulder.
pain in the upper
right abdomen.
Cholangiocarcino Yellowing of
ma Unintended weig your skin and the
ht loss. whites of your eyes
(jaundice)
Intensely itchy skin.
White-colored stools.
 Hepatocellular Vomiting
carcinoma
Weight loss
Fullness in upper
abdomen
Dehydration
Visible peristalsis
Non tender
hepatomegaly
anemia

c. What is your Impression?

Hepatocellular carcinoma
 Upper abdominal pain.
 Abdominal pain that radiates to your back.
 Abdominal pain that feels worse after eating.
 Rapid pulse.
Nausea

d. How do you plan to manage this patient? If you plan do surgery, what are
the considerations for resectability?

For patients with Child’s class A cirrhosis with preserved liver function and no portal
hypertension, resection also is considered.
 Class A
 5 to 6 points
 Least severe liver
disease
 One to five year
survival rate : 95%
 The treatment of HCC is complex and is best managed by a multidisciplinary liver
transplant team.
 For patients without cirrhosis who develop HCC, resection is the treatment of
choice.
 If resection is not possible because of poor liver function and the HCC meets
transplant criteria.
 Living donor liver transplantation also is an alternative for patients with HCC
awaiting transplantation to avoid dropout as a candidate for cadaveric donor liver
transplantation due to tumor progression.
 Surgery for hepatocellular carcinoma (HCC) includes partial liver resection (LR)
and liver transplantation (LT). Although LT represents the most efficient
treatment in patients with small HCC, <30% of patients are eligible for LT
because of restrictive criteria (one nodule <5 cm or two to three nodules <3. )