SURGERY LECTURE NOTES BY

MASOOM HAIDER
TOPIC : LIVER
REFERENCE BOOK : BAILEY & LOVE’S EDITION 26

COMPILED BY YASIF ABBAS

LECTURE NOTES SURGERY

A. SURFACE ANATOMY OF LIVER
l. The liver is the largest solid organ in the body, weighing 1 ,500 g -1700 g. It is
smooth, reddish brown, and covered by a fibrous sheath known as Glisson
capsule.
2. It is an intraperitoneal organ lying predominantly in the right upper
quadrant (RUQ) of the abdominal cavity. It is anatomically related to the
diaphragm, the stomach, the duodenum, the right kidney and adrenal gland, and
the right colon. It is fixated in the RUQ by a number of ligamentous attachments,
which include the falciform ligament, the round ligament (obliterated umbilical
vein) , the right and left coronary, and the right and left triangular ligaments.
• Falciform ligament – this sickle-shaped ligament attaches the anterior
surface of the liver to the anterior abdominal wall. Its free edge contains the
ligamentum teres, a remnant of the umbilical vein.
• Coronary ligament (anterior and posterior folds) – attaches the superior
surface of the liver to the inferior surface of the diaphragm and demarcates the
bare area of the liver The anterior and posterior folds unite to form the
triangular ligaments on the right and left lobes of the liver.
• Triangular ligaments (left and right): The left triangular ligament is formed
by the union of the anterior and posterior layers of the coronary ligament at the
apex of the liver and attaches the left lobe of the liver to the diaphragm.
• The right triangular ligament is formed in a similar fashion adjacent to the
bare area and attaches the right lobe of the liver to the diaphragm.
• Lesser omentum – Attaches the liver to the lesser curvature of the stomach
and first part of the duodenum. It consists of the hepatoduodenal ligament
(extends from the duodenum to the liver) and the hepatogastric ligament
(extends from the stomach to the liver). The hepatoduodenal ligament
surrounds the portal triad.
3. The contents of the hepatic hilum are contained in the hepatoduodenal
ligament. These include the bile duct, the hepatic artery, and the portal vein.
The bile duct and hepatic artery lie anterior to the portal vein, with the bile duct
lying lateral to the more medially situated hepatic artery.
4. The space behind the hepatoduodenal ligament is known as the (epiploic)
foramen of Winslow. It communicates directly with the lesser sac and can be
occluded to control the vascular inflow to the liver in what is known as the
Pringle maneuver.

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B. SEGMENTAL ANATOMY
l. The liver has eight distinct liver segments, which are distributed between the
right and left lobes of the liver. The anatomic boundary between the right and left
lobes of the liver is an imaginary line between the gallbladder anteriorly and
the Middle hepatic vein posteriorly. This is known as the Cantlie line.
2. The left lobe of the liver is comprised of segments II to IV. Segments II and
III make up the lateral segments of the left lobe of the liver and lie to the left of
the falciform ligament. Segments IVA and IVB make up the medial segment(s)
of the left lobe of the liver. These lie to the right of the falciform ligament
and to the left of the Cantlie line.
3. The right lobe of the liver is comprised of segments V to VIII. Segments V
and VIII make up the anterior segments of the right lobe of the liver, and segments
VI and VII make up the posterior segments of the right lobe of the liver.
4. Segment I of the liver is known as the caudate lobe. It belongs to neither the
right or left lobes because it has a blood supply and venous drainage pattern
that are distinct from either the right or left systems.
• Caudate lobe – located on the upper aspect of the visceral surface. It lies
between the inferior vena cava and a fossa produced by the ligamentum
venosum (a remnant of the fetal ductus venosus).
• Quadrate lobe – located on the lower aspect of the visceral surface. It lies
between the gallbladder and a fossa produced by the ligamentum teres (a
remnant of the fetal umbilical vein).
• Separating the caudate and quadrate lobes is a deep, transverse fissure –
known as the porta hepatis. It transmits all the vessels, nerves and ducts
entering or leaving the liver with the exception of the hepatic veins

C. VASCULAR ANATOMY
l. The vascular anatomy of the liver is best thought of in terms of the inflow to and
the outflow from the liver. The liver has a unique dual blood supply. Eighty
percent of the blood flowing into the liver comes via the portal venous
circulation. The hepatic portal vein is formed by the confluence of the
superior mesenteric vein and the splenic vein behind the neck of pancreas.
The portal vein bifurcates in the hepatic hilum into the right and left portal veins.
2. There are a number of potential connections between the portal venous
system and the systemic venous system. Under conditions of high portal
venous pressure (cirrhosis, hepatic vein thrombosis, right heart failure, splenic vein
thrombosis), these portosystemic connections may enlarge and clinically manifest
portal hypertension.
3. The more significant locations are:
a. The coronary vein, draining the stomach and the distal esophagus

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b. Umbilical and abdominal wall veins, which recanalize from flow through
the umbilical vein in the ligamentum teres, resulting in caput medusae
c. The superior hemorrhoidal plexus, which receives portal flow from the
inferior mesenteric vein tributaries and may cause large hemorrhoids
d. Retroperitoneal collaterals, ultimately leading back to the vena cava
4. The remaining 20% of the blood flowing into the liver comes via the
hepatic arterial circulation. The common hepatic artery is a branch of the
celiac axis. After the takeoff of the gastroduodenal artery, the common hepatic
artery becomes the proper hepatic artery, which gives off branches to the right and
left lobes of the liver.
• Accessory/completely replaced right hepatic artery (RHA; 22%)
arising from the superior mesenteric artery
• Accessory/completely replaced left hepatic artery (18%) arising from
the left gastric artery
5. The venous drainage, or outflow from the liver, is via three main hepatic
veins: right, middle, and left. These drain directly into the IVC. The right vein
has its own insertion into the IVC, whereas in 95% of patients, the middle and left
veins form a common trunk prior to entering into the IVC.

D. MAIN FUNCTIONS OF THE

LIVER
● Maintaining core body temperature
● pH balance and correction of lactic acidosis
● Synthesis of clotting factors
● Glucose metabolism, glycolysis and gluconeogenesis
● Urea formation from protein catabolism
● Bilirubin formation from haemoglobin degradation
● Drug and hormone metabolism and excretion
● Removal of gut endotoxins and foreign antigens

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E. EVALUATION OF THE LIVER
A. History and physical examination
l. jaundice and icterus refer to the yellow appearance to the skin, sclera,
and mucous membranes as a result of retention and systemic
deposition of bilirubin. jaundice typically does not develop until the serum
bilirubin level exceeds 2.5 to 3. jaundice or icterus is a reflection of liver disease,
including obstruction of the biliary tract, acute hepatic injury from drugs and
toxins, and the chronic loss of hepatic reserve from cirrhosis due to alcohol, the
hepatitis virus(es) ,
iron or copper, and parasitic infection.
2. The triad of splenomegaly, ascites, and caput medusae (dilated
abdominal wall veins) indicates portal hypertension. Other
signs/symptoms of cirrhosis and/or portal hypertension can include a history of
upper GI bleeding from esophageal varices or hepatic encephalopathy from
excessive NH3 levels, testicular atrophy, spider angiomata, pain, and fatigue.
3. A history of pruritus suggests cholestasis, either intrahepatic or
extrahepatic. Causes may be at the hepatocellular level (viral hepatitis), canalicular
level (drugs, total parenteral nutrition, amyloidosis) , or biliary ductal level
(primary biliary cirrhosis [PBC] , primary sclerosing cholangitis [PSC]).

B. Diagnostic laboratory testing

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l. Serum bilirubin levels, both conjugated (direct) and unconjugated
(indirect) , are affected in a number of disease processes and are related to the
metabolism of the bilirubin.
a. Unconjugated bilirubin is generally elevated in hemolysis, drug
hepatotoxicity, inherited enzymatic disorders (Gilbert disease, Crigler-Najjar) , and
the physiologic disorders of the newborn.
b. Conjugated bilirubin is usually elevated in hepatocellular diseases, cholesta-
sis, or biliary obstruction.
2. The serum transaminases alanine aminotransferase (ALT) and
aspartate aminotransferase (AST) are nonspecific indicators of acute
hepatocellular injury. However, an AST:ALT ratio greater than 2:1 is more
suggestive of alcoholic liver disease.
3. Alkaline phosphatase can be used as a marker of cholestasis. Alkaline
phosphatase is released by damaged hepatocytes as a consequence of cholestasis,
but other organ and tissue production of alkaline phosphatase (e.g. , bone,
placenta, kidneys, and leukocytes) make it a nonspecific indicator in the evalua-
tion of liver disease. The heat-stable fraction of alkaline phosphatase is more
suggestive of liver pathology.
4. The synthetic function of the liver is measured by the serum albumin
level and the prothrombin time (PT), the latter of which is reflective of the
vitamin K-dependent clotting factors II, VII, IX, and X. The most sensitive
indicator of deficiency of hepatic synthetic function is an abnormal (prolonged) PT.
No improvement in the PT despite vitamin K administration reflects severe hepatic
functional loss.
The standard method of monitoring liver function in patients with
chronic liver disease is therefore serial measurement of bilirubin,
albumin and prothrombin time.

C. Imaging and diagnostic tests

l. Ultrasound
a. This quick, easy-to-perform, noninvasive test involves no radiation.
b. It is the primary modality to identify cholelithiasis. Focal and diffuse liver
disease can be identified.
c. Doppler ultrasound allows for evaluation of vascular anatomy and pressures.
2. Computed tomography (CT) scan
a. To evaluate the liver for tumors and other pathology, a triple-phase, liver
protocol-contrasted CT scan should be obtained (noncontrasted phase, hepatic
arterial phase, portal venous phase) .
b. It demonstrates hepatic segmental anatomy, focal disease such as tumors, or
diffuse liver disease such as cirrhosis or steatosis.
c. Various benign and malignant tumors of the liver have characteristic features on
triple-phase contrasted CT scans that can help aid in the diagnosis of liver masses.
3. Hepatobiliary iminodiacetic acid (HID A) scan shows excretion of tracer
along the biliary tract and thus is useful for detecting bile leaks or obstruction.

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4. Magnetic resonance imaging (MRI) scan
a. MRI provides exquisite detail of hepatic parenchyma and finer detail of
tumors to differentiate benign (hemangiomas) from malignant.
b. Reconstruction of the biliary tree with great detail is possible, including
recognition of ductal stone disease, biliary damage, or tumors, through magnetic
resonance cholangiopancreatography (MRCP) .
5. Nuclear medicine studies such as sulfur colloid scan or technetium
99 scans can help differentiate hepatic tumors such as focal nodular hyperplasia
(FNH) and hemangioma, respectively, when other imaging modalities are
nondiagnostic/equivocal.
6. PTC Biliary tract imaging when ERCP impossible or failed
7. Angiography To detect vascular involvement by tumour
8. PET scanning To quantify tumour spread

9. Laparoscopy/laparoscopic Ultrasound To detect peritoneal tumour spread

and superficial liver metastases.

F. ACUTE LIVER DISEASE

Scenario
A 40 year old male known case of hepatitis C presented in emergency in
drowsy state he also has jaundice his labs are ALT 430, Bilirubin 6, PH 7.30,
PT 45 second (acute liver disease)

In the early stages, there may be no objective signs, but with severe dysfunction the
onset of clinical jaundice may be associated with neurological signs of liver failure
(hepatic encephalopathy), consisting of a liver flap, drowsiness, confusion
and, eventually, coma.
Causes of acute liver failure
● Viral hepatitis (hepatitis A, B, C, D, E)
● Drug reactions (halothane, isoniazid–rifampicin, antidepressants, non-steroidal
anti-inflammatory drugs, valproic acid)
● Paracetamol overdose
● Mushroom poisoning
● Shock and multiorgan failure
● Acute Budd–Chiari syndrome
● Wilson’s disease
● Fatty liver of pregnancy
Supportive therapy for acute liver failure
● Fluid balance and electrolytes
● Acid–base balance and blood glucose monitoring
● Nutrition
● Renal function (haemofiltration)
● Respiratory support (ventilation)

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● Monitoring and treatment of cerebral oedema
● Treat bacterial and fungal infection
King’s College selection criteria for liver transplantation in acute liver
failure
Paracetamol induced
● pH <7.30 (irrespective of grade of encephalopathy) or prothrombin time
(PT)>100 s + serum creatinine >300 μmol/L + grade 3 or 4 encephalopathy.
Non-paracetamol induced (irrespective of encephalopathy)
● PT >100 s or any three of the following:
● Age <10 years or >40 years
● Aetiology non-A, non-B, halothane or idiosyncratic drug reaction
● More than 7 days’ jaundice before encephalopathy
● PT >50 s
● Bilirubin >300 μmol/L

G. CHRONIC LIVER DISEASE

Scenario
A 45 year old male presented to OPD with abdominal distension, jaundice,
fever and lethargy. On examination he has splenomegaly and fluid thrill
positive, palmer erythema and flapping tremors of hand. His labs are
Bilirubin 25 umol/L, ALT 470, AST 360 and Albumin 28g/L (Chronic liver
disease)
Features of chronic liver disease
● Lethargy
● Fever
● Jaundice
● Protein catabolism (wasting)
● Coagulopathy (bruising)
● Cardiac (hyperdynamic circulation)
● Neurological (hepatic encephalopathy)
● Portal hypertension
• Ascites
• Oesophageal varices
• Splenomegaly
● Cutaneous
• Spider naevi
• Palmar erythema

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Quantifying the severity of chronic liver disease
Two prognostic models commonly used to assess the severity of chronic liver
disease and perioperative risk are the Child–Turcotte–Pugh (CTP)
Classification and the Model for End-Stage Liver Disease (MELD) score.
The original Child classification was developed to predict mortality following shunt
surgery in cirrhotic patients, with the modified CTP classification developed to
predict mortality after any surgery.
In the MELD model the survival probability of patients with end-stage liver
disease is computed based on the patient’s international normalised ratio
(INR), serum bilirubin and serum creatinine.

Surgery in the presence of chronic liver disease

Patients with liver disease are at greater risk of surgical and anaesthetic
complications, with the magnitude of risk dependent on size of procedure, degree
of liver impairment and type of anaesthesia. Overall surgical mortality rates are
generally considered to be increased by 10% in CTP A disease, 30% in CTP B and
75–80% in CTP C. MELD score also correlates with operative mortality, with a 1%
increase for each MELD point up to 20, with a further 2% for each point above 20.

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H. ACUTE LIVER INFECTION
Scenario’s
1. A 25-year-old male complains of generally feeling unwell with fever and
weight loss. He has had bloodstained motions on and off for the last 6
weeks after he returned from the subcontinent where he was working for 6
months. On examination he has a tender right upper quadrant with
hepatomegaly. US shows a hypoechoic cavity in the right lobe with ill-
defined borders. (Amoebic liver abscess)
Explanation:
Classic features of amoebic liver abscess
Residence or travel in endemic areas, symptoms of 2-week duration,
RUO pain, abrupt onset of fever (38° to 40° C). tender hepatomegaly,
dysentery and solitary hypoechoic or mixed echogenic liver lesion,
Leucocytosis with greater than 1 5,000/ micro L, and positive serology.

MCQ: AMOEBIC INFECTION REACHES TO LIVER THROUGH PORTAL

ROUTE

Management
Investigation :
• CECT ABDOMEN shows edema, no rim enhancement and leucofective
necrosis.
• Positive serology to E. histolytica is indicative of tissue invasion. Higher
antibody titers are seen in initial stages of disease, but elevated levels are seen
up to 3 years after infection occurred.
• Stool examination plus isolation of parasites
• Amoebic lecithin antigen test
Treatment:
• oral metronidazole up to 1 g PO bid for 10 days in adults.
• Drainage of abscess is not part of initial therapy but may be needed if a
rapid response does not occur (antibiotic therapy fails).
Complications
• include extension of the amoebic abscess to the peritoneum, pericardium,
diaphragm, abdominal organs, great vessels (IVC, aorta) , and rupture into
pleural space with amoebic empyema.

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2. A 50-year-old female patient has had recurrent attacks of colicky right
upper quadrant and epigastric pain with jaundice, high temperature
with rigors and itching. Ten months ago she underwent an uneventful
laparoscopic cholecystectomy. On examination she is jaundiced with
scratch marks all over her body and hepatomegaly. She has raised serum
bilirubin and the ALP is 1100 IU/L. US shows a dilated common bile duct
with stones. (Ascending cholangitis)
Explanation
This patient has classical Charcot’s intermittent hepatic triad almost certainly
from a retained stone as seen on the US. The LFTs will show an obstructive picture.
She needs to be treated with antibiotics, vitamin K and an ERCP and endoscopic
papillotomy.

3. A 35-year-old male patient presents with general ill-health, weight loss,

anorexia and malaise for several weeks. He has developed jaundice for
the last 2 weeks; he has no pruritus. Abdominal examination shows a tender
hepatomegaly. Liver function tests show raised bilirubin and
transaminases. (Acute viral hepatitis)
Explanation
Viral hepatitis can be due to hepatitis A, B and C. Hepatitis C is one of the most
common causes of liver disease worldwide. Hepatitis B is the most serious
and later can cause a hepatoma. Some patients may present acutely with
fulminating liver failure or at a late stage with cirrhosis, variceal bleeding and
ascites. Diagnosis is confirmed by the antibody titre to the infective agent.

4. A 75-year-old male diabetic patient complains of anorexia, fever,

malaise and right upper quadrant discomfort. On examination there is
weight loss and tender hepatomegaly. US shows a multiloculated cystic
mass, a finding confirmed on CT scan. (Acute pyogenic liver abscess)
Explanation
Classic features of pyogenic liver abscess
Fever (90%), malaise, rigors, and RUQ pain. Chills and weight loss may
be seen in 50% of patients. Symptom duration is typically less than 2
weeks. Jaundice is uncommon, unless biliary tract obstruction is also
present. At the time of presentation, 50% of patients have positive blood
cultures. Risk factors (immunocompromised : old age , child , DM ,
HIV)

MCQ Points :
• Most pyogenic hepatic abscesses are caused by infection originating from
the G I tract or the biliary tract.

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 • The potential routes of hepatic exposure to bacteria are the biliary
tree, portal vein, hepatic artery, direct extension from nearby foci
of infection (gallbladder, kidney) , and trauma.
• Common intra-abdominal sources of pyogenic abscesses include
appendicitis, diverticulitis, cholecystitis, infected
pancreatitis/pancreatic abscess, and perinephric abscess.
• Pyogenic abscesses with no identifiable primary infection are called
cryptogenic hepatic abscesses
• Diagnosis is made most commonly with CT scan (93% accurate).
• Organisms cultured include gram-negative aerobes, which are found 68%
of the time. Escherichia coli and Klebsiella species are most
commonly isolated. Aerobic Streptococcus and Staphylococcus are
seen in 20% and 1 2% of pyogenic abscesses, respectively.
• Increased use of indwelling biliary stents and broad-spectrum
antibiotics has led to an increased prevalence of Pseudomonas,
anaerobic Streptococcus, and fungi.

Management
Investigation:
• CECT ABDOMEN : clusters, rim enhancement, microabscess
• Confirmed by aspiration for culture and sensitivity
Treatment is with antibiotics and ultrasound-guided Percutaneous abscess
aspiration and drainage
• First-line antibiotics to be used are a penicillin, aminoglycoside and
metronidazole or a cephalosporin and metronidazole.
• Treatment of the primary intra-abdominal source of infection is
mandatory (e.g. , surgical management of appendicitis, diverticulitis) . Surgical
co-drainage of hepatic abscess during laparotomy is still required in up to one-
third of patients.

5. A 50-year-old male patient, a native of Cyprus, presents with a painful mass in

the right upper quadrant. The pain is a continuous dull ache and has the
features of a mass arising from the right lobe of the liver. The blood count
shows raised eosinophils. The CT scan shows a smooth space-occupying
lesion with multiple septa within it. (Hydatid liver disease)

Explanation
Classic features of hydatid liver disease
Most common presenting symptom is RUQ pain and palpable
hepatomegaly. Eosinophilia and positive serology with indirect
hemagglutination or enzyme-linked immunosorbent assay is positive in
90% of cases. Casoni skin test is 85% sensitive. Parasitic eggs are not
seen in human stool.

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MCQ Points:
• The causative tapeworm, Echinococcus granulosus, is present in
the dog intestine, and ova are ingested by humans and pass in the
portal blood to the liver.

Management:
Investigation:
• Diagnosis is suggested by the finding of a multiloculated cyst on
ultrasound and is further supported by the finding of a floating
membrane within the cysts on CT scan.
• Clinical and radiological diagnosis can be supported by serology for
antibodies to hydatid antigen, in the form of an enzyme-linked
immunosorbent assay (ELISA)
Treatment :
• The cysts should not be aspirated to avoid spillage of the organisms and
development of new cysts.
• Antihelminthic therapy with mebendazole, praziquantel, or albendazole is
given three times daily for up to 16 weeks. Toxicity results in alopecia,
leucopenia, and elevated transaminases.

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 • Percutaneous treatment (PAIR) constitutes of an intial course of
albendazole followed by puncture of the cyst under image guidance,
aspiration of the cyst’s contents, instillation of hypertonic saline in the cyst
cavity and reaspiration. PAIR should only be attempted if there is no
communication with the biliary tree.
• Failure to respond to medical treatment or percutaneous treatment usually
requires surgical intervention. The surgical options range from liver
resection or local excision of the cysts to deroofing with evacuation
of the contents.
• Contamination of the peritoneal cavity at the time of surgery with active
hydatid daughters should be avoided by continuing drug therapy with
albendazole and adding peroperative praziquantel. This should be combined
with packing of the peritoneal cavity with 20% hypertonic saline-
soaked packs and instilling 20% hypertonic saline into the cyst before
it is opened.
• A biliary communication should be actively sought and sutured.
• The residual cavity may become infected, and this may be reduced, as may bile
leakage, by packing the space with pedicled greater omentum (an
omentoplasty)

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I. SUMMARY OF ACUTE LIVER
INFECTIONS

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J. CHRONIC LIVER DISEASES
Scenario’s

1. A 30-year-old patient has a history of recurrent attacks of fever with

rigors, right upper quadrant pain and jaundice with itching. Biochemistry
shows a jaundice of obstructive nature. CT scan shows intrahepatic ductal
dilatation with stones. (Caroli’s Disease or choledochal cyst type v)

Explanation :
This patient has recurrent attacks of obstructive jaundice with features of
sepsis – typical of bile duct stones. The CT scan confirms the diagnosis of
this congenital condition.

2. A 40-year-old female presents with recurrent episodes of right upper

quadrant pain with jaundice. Biochemistry shows an obstructive pattern of
the jaundice. Five years ago she underwent a panproctocolectomy for
ulcerative colitis and has been well since, except for these attacks. Endoscopic
retrograde cholangiopancreatography (ERCP) shows irregular
narrowed intra- and extrahepatic bile ducts. (Primary sclerosing
cholangitis)

Explanation
Clinical features of primary sclerosing cholangitis
This condition often presents in young adults with mild non-specific symptoms,
and biliary disease is suggested by the finding of abnormal liver function
tests. The disease process results in progressive fibrous stricturing and
obliteration of both the intrahepatic and the extrahepatic bile ducts.
Although the aetiology is unknown, a genetic predisposition is likely, owing to its
association with ulcerative colitis (UC). There is a strong predisposition to
cholangiocarcinoma (CCA) and gallbladder cancer, and this should be
considered in any patient with PSC in whom a new or dominant stricture is
demonstrated on cholangiography, or in whom gallbladder polyps are identified
Management:
Investigation
• cholangiography, in which irregular, narrowed bile ducts are demonstrated
in both the intrahepatic and the extrahepatic biliary tree.
• If the radiological appearances are equivocal, a liver biopsy is required to
demonstrate the fibrous obliteration of the biliary tracts.
• Diagnosis of CCA in PSC is greatly facilitated by biliary brush cytology
and direct endoscopic inspection.
• Serum CA 19-9 level may be increased but the sensitivity of CA 19-9 in
detecting CCA in PSC is only 60%.

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Treatment:
The only useful treatment modality is liver transplantation, which is
associated with excellent results if carried out before bile duct cancer has
developed. Temporary relief of obstructive jaundice due to a dominant bile
duct stricture can be achieved by biliary stenting, although there is
considerable risk of cholangitis from the introduction of bacteria to the biliary tract

3. A 50-year-old female complains of general malaise, lethargy, pruritus

and jaundice, the latter being present over the last 3 months. The LFTs show
a rise in bilirubin, the transaminases and prothrombin time. She has had
recurrent small haematemesis and has ascites. (Primary biliary
cirrhosis)

Explanation
Presentation of patients with primary biliary cirrhosis (PBC) is often hidden,
with general malaise, lethargy and pruritus prior to the development of
clinical jaundice or the finding of abnormal liver function tests. The
condition is largely confined to females.
• Diagnosis is suggested by the finding of circulating antismooth muscle
antibodies and, if necessary, is confirmed by liver biopsy. The condition
is slowly progressive, with deterioration in liver function resulting in lethargy
and malaise. It may be complicated by the development of portal
hypertension and the secondary complications of ascites and
variceal bleeding.
• The mainstay of Treatment is liver transplantation, which should be
considered when the patient’s general condition starts to deteriorate with
inability to lead a normal lifestyle.

4. A 30-year-old female complains of abdominal discomfort and di

stension. She has had 3 episodes of small haematemesis in the past 6
months. On examination she has hepatomegaly and ascites. All the LFTs are
deranged. CT scan of the liver shows a large congested liver. (Budd Chiari
syndrome)

Explanation
• Budd–Chiari syndrome (BCS) is a condition principally affecting young
females, in which the venous drainage of the liver is occluded by
hepatic venous thrombosis or obstruction from a venous web. As a result
of venous outflow obstruction, the liver becomes acutely congested,
with the development of impaired liver function and, subsequently, portal
hypertension, ascites and oesophageal varices

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 • The cause of the venous thrombosis needs to be established, and an
underlying myeloproliferative disorder or procoagulant state is
commonly found, such as antithrombin 3, protein C or protein S
deficiency.
• The diagnosis is commonly suspected in a patient presenting with ascites, in
whom a CT scan shows a large congested liver or a small cirrhotic
liver in which there is gross enlargement of segment I (the caudate lobe);
this feature results from preservation and hypertrophy of the segment
with direct venous drainage to the IVC in the face of atrophy of the
rest of the liver due to venous obstruction. IVC compression or
occlusion from the segment I hypertrophy is also a common feature, as is
portal vein thrombosis.
• Treatment of BCS must be tailored to the individual patient and, in
particular, to the stage of disease at presentation. Patients presenting in
fulminant liver failure should be considered for liver
transplantation, as should those with established cirrhosis and the
complications of portal hypertension. Those in whom cirrhosis is not
established may be considered for portosystemic shunting by
TIPSS. IVC compression may be relieved by the insertion of a
retrohepatic expandable metallic stent.
• If the BCS is treated satisfactorily, the prognosis of this patient group is
largely dependent on the underlying aetiology and whether this is amenable to
treatment. Patients are usually left on lifelong anticoagulation.

5. A fit-looking 50-year-old male complains of recent onset of dull,

aching, right upper quadrant pain of 3–4 months’ duration. Examination
shows no abnormality. Liver function tests are normal, as is an upper
gastrointestinal endoscopy. An ultrasound of the liver shows a 6 cm solitary
cystic lesion. (Simple cystic disease of liver)

Explanation
• Simple cysts are generally solitary, and occur more frequently in
women.
• Most are incidental findings, and have a characteristic blue hue when
seen at laparoscopy.
• Indications for surgical intervention include symptoms, rupture,
haemorrhage, infection or indeterminate diagnosis.
• Surgical resection typically involves laparoscopic deroofing, with oversewing of
the cyst wall

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K. SUMMARY OF CHRONIC LIVER
DISEASES

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L. TUMORS OF LIVER
1. A 35-year-old woman who is on the contraceptive pill presents with
right upper quadrant aching pain. She is fit without any physical
findings. Her LFTs and other blood tests are normal. US of the liver
shows a single well-demarcated hyperechoic mass and CT scan
demonstrates a well-circumscribed vascular solid tumour.
(Hepatic adenoma)
Explanation
• Hepatic adenomas are uncommon solid lesions seen in women of
childbearing age, usually with antecedent use of more than 5 years of
high-dose estrogen oral contraceptives. Ninety-three percent of
adenomas occur in this segment of the population.
• On triple-phase CT scan, hepatic adenomas are hypervascular
tumors on arterial phase that become isodense or even hypodense to the
background liver on portal venous phase.
• Most patients (52%) present with right upper abdominal pain due to
local compression, but they rarely hemorrhage into the tumor, or
rupture leads to an acute presentation with hypotension and shock
from bleeding.
Management:
• (l) Spontaneous regression is observed in smaller adenomas with
withdrawal of oral contraceptives. Asymptomatic smaller adenomas may
also be observed.
• (2) Increasing alpha-fetoprotein (AFP) , an enlarging mass, or one with
irregular borders should prompt surgical resection because malignant
transformation is associated with these characteristics in hepatic
adenomas. Furthermore, size greater than 4 em is associated with increased
rates of malignant degeneration as well as spontaneous rupture and should be
used as a criterion for surgical resection in and of itself.
• (3) If a larger hepatic adenoma is not resected, pregnancy should be
avoided due to an increased risk of tumor growth, hemorrhage, or rupture
during pregnancy.

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2. A 40-year-old male patient presents with dull, persistent upper
abdominal pain, weakness, weight loss and occasional fever. He had one
episode of haematemesis. Abdominal examination shows an enlarged liver
with a mass in the right lobe. Liver function tests show elevation of the
transaminases and much raised alpha- fetoprotein (AFP).
(Hepatocellular carcinoma)
Explanation:
Risk Factors
• Cirrhosis ~ 80% of hepatocellular carcinoma cases arise in cirrhosis Patients
with cirrhosis from any etiology are at risk for developing hepatocellular
carcinoma
• Chronic viral Infection: Chronic hepatitis B (about 50% cases), Chronic
hepatitis C (about 25% cases)
• Toxins: Chronic alcoholism, Aflatoxins- (fungus Aspergillus flavus),
Chemicals (thorotrast)
• Metabolic: Non-alcoholic steatohepatitis (NASH), Tyrosinemia, Glycogen
storage disease, Hemochromatosis, α1-antitrypsin deficiency
Presentation
• Includes weight loss, abdominal swelling, and RUQ abdominal pain.
In a patient known to have stable cirrhosis, sudden hepatic
decompensation may be an indicator of HCC development.
• HCC may also present with paraneoplastic syndromes caused by
ectopic hormonal production (sexual changes, hypercalcemia, carcinoid-like
syndrome) , metabolic changes (hypoglycemia, hypercholesterolemia, acute
porphyria) , skin changes (vitiligo, pityriasis, thrombophlebitis migrans), as
well as fever, leukocytosis, and cachexia.
Diagnosis
• Imaging (ultrasound, CT [arterial phase of CT shows HCC lesion to be
hypervascular while the portal venous phase demonstrates washout of the
lesion compared to the background liver] , and MRI) is used for diagnosis.
Because of the abnormal appearance of the cirrhotic liver on imaging,
diagnostic tissue biopsy confirming HCC may sometimes be required.
• Serum AFP level can be a useful tumor marker for HCC; however, it is
elevated in only 50% of patients with HCC. It may also be elevated in benign
conditions such as chronic active hepatitis, cirrhosis, and pregnancy. An AFP
level greater than 400 ng/mL, however, is considered diagnostic for
HCC.

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Management
• One of the keys to treatment of HCC is prevention, because the
reduction or improvement of chronic liver damage by treatment of
the underlying etiology reduces the risk of HCC development. For
example, HBV infection can be prevented by vaccination. Screening in the Far
East has been successful in identifying HCC earlier by screening patients with
cirrhosis, a family history of HCC, chronic active hepatitis with elevated viral
loads, or increasing AFP .
• Treatment options for HCC include the following: Liver
Transplantation, surgical resection, ablative techniques, regional
liver-directed therapies, or systemic treatments.
• The specific type of treatment chosen is influenced in a large part by the stage
of the disease as well as the health of the background liver.
• b. Liver transplantation is the optimal curative treatment for HCC
because it removes the cancer as well as the underlying background liver.
Candidacy for LT in patients with HCC is defined by the Milan
criteria.
Milan criteria.
One lesion smaller than 5 em
Up to three lesions smaller than 3 em
No extrahepatic spread
No vascular invasion
• c. Surgical resection is the next best curative treatment option for
HCC but is often not possible due to excessive postoperative morbidity and
mortality associated with liver insufficiency/failure in patients with cirrhotic
back-ground livers.
• d. Unfortunately, 75% of patients with HCC are not candidates for
either LT or surgical resection at the time of their diagnosis.
Untreated, unresectable HCC carries with it a grim prognosis (median survival
of 6 to 12 months) . Therefore, local ablative therapy (most commonly
radiofrequency ablation or microwave ablation) can provide
acceptable local control under certain circumstances. The utility of this
method is limited in large tumors (>5 em) or in those that are
centrally located and near important hilar structures (particularly the
main or segmental right and left bile ducts). Ablation can also be used as a
"bridge to transplantation" to avoid having patients drop off of the LT
waiting list due to progression of the disease.

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 • e. Regional liver-directed therapy for HCC includes transhepatic
arterial chemoembolization (TACE) or selective internal
radiotherapy (SIR) spheres. These techniques take advantage of the
unique dual blood supply to the liver (hepatic arterial and portal venous) as
well as the fact that HCCs derive their blood supply predominantly from the
arterial circulation while the background liver derives its predominantly from
the portal venous system. In TACE, chemotherapy (given in higher doses
than that which can be delivered systemically) is injected into the
hepatic arterial system in combination with embolization of the
feeding vessel(s) to the tumor(s) . In SIR spheres, 32 micron in
diameter, Yytrium-90 containing beads are injected into the
hepatic arterial circulation and eventually get lodged in the
capillary network supplying the tumor(s), where they emit local
radiation. Response rates to each approach are roughly 50% to 60% and can
extend patients' life expectancy by years. Candidates for these approaches
must have enough hepatic reserve to tolerate the associated toxicity. These
treatments can also be used as a "bridge to transplantation."
• f. Systemic treatment for HCC is limited with only one FDA-approved
drug (sorafenib, an anti-vascular endothelial growth factor [anti-
VEGF] anti-body that inhibits angiogenesis) . Median survival for
patients with un-resectable HCC was significantly improved in sorafenib-
treated patients compared to placebo (Study of Heart and Renal Protection
[SHARP] trial) ; however, the benefit was minimal (3 months) .

3. A 60-year-old male patient presents with dragging pain in the right

upper quadrant for 3 months and weight loss. On examination he is slightly
jaundiced. He has an enlarged liver. Three years ago he underwent a right
hemicolectomy for cancer of the caecum. LFTs show elevation of all the
parameters. US shows a solid mass in the right lobe and a CECT
confirms the mass with lack of enhancement. (Secondary liver
metastases)
Explanation
• The liver is the most common site of metastatic disease for a variety of
cancers.
• Isolated liver metastases are more commonly seen in association with
colorectal cancer, neuroendocrine tumors of the GI tract, stromal tumors of
the GI tract, and ocular melanomas.
• b. Hepatic metastases from colorectal cancer are often asymptomatic and
rarely yield jaundice or liver function derangement at presentation.
2. Colorectal cancer with liver metastases:
Management

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 • Sixty percent of patients diagnosed with colorectal cancer will at
some point in their disease course develop liver metastases. In
selected patients, surgical resection of colorectal liver metastases offers 5-year
survival rates of up to 40%.
• b. Systemic multidrug chemotherapy regimens show promising ability to
significantly reduce liver tumor volume and/or prevent the development of
extrahepatic disease. Chemotherapy alone, however, is not a cure, and
therefore, surgical resection should be offered to all patients who are
candidates.
• Unfortunately, only 25% of patients with liver metastases from colorectal
cancer are operative candidates. Evaluation by a trained liver surgeon at the
time of the diagnosis of the liver metastases to determine their resectability is
critical.
• c. Management of hepatic metastases from neuroendocrine tumors, ocular
melanomas, and specific GI tract stromal tumors is individualized and based
on the patient's clinical course, extent of disease, and symptoms.
• d. Local tumor ablation with cryoablation or radiofrequency
ablation achieves local destruction of active cancer tissue and is
useful in palliative disease control but does not improve overall survival.
• e. Aggressive surgical or ablative management of liver metastases
from gastric, pancreatic, or small intestine adenocarcinomas; soft-tissue
sarcomas; and skin melanomas has no oncologic benefit. Patients should be
managed with palliative systemic chemotherapy.

4. In a 30-year-old female patient, during laparoscopic cholecystectomy,

the surgeon noticed that the under-surface of the liver has several lesions
which are blue in colour. (Hemangioma)
Explanation
• a. Hemangioma is the most common benign mesenchymal tumor.
These tumors vary in size from l to 20 cm, and if they are greater than 4 cm,
they are called giant hemangiomas. Sixty percent to 80% of these are found in
women in the third to fifth decade of life. If greater than 10 cm, 90%
present with symptoms of liver capsule distension and pain.
• b. On triple-phase CT scan, hemangiomas are not hypervascular on arterial
phase and show asymmetric, centripetal filling on portal venous phase.
• c. MRI is the most accurate noninvasive test, with sensitivity greater
than 90%. Hemangiomas have a low Tl signal and a high T2 signal.
Technetium pertechnetate liver scans are also useful in identifying
hemangiomas. Percutaneous biopsy is potentially dangerous,
inaccurate, and not recommended.

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 • d. Hemangiomas do not require treatment and may be left alone.
Spontaneous rupture of even giant hemangiomas is very rare, even in
pregnancy. Surgical enucleation of the hemangioma is preferred to
surgical resection, yielding less blood loss and fewer transfusion
requirements

5. A 45-year-old female patient underwent an US for suspected biliary

pain. The US of the biliary tract was normal but showed a solid lesion in
the liver. Therefore she had a CECT scan which showed a vascular lesion
surrounding a solid mass with central scarring. (Focal nodular
hyperplasia)
Explanation
• FNH is the second most common benign solid tumor of the liver.
Seen in all ages and both sexes, it is slightly more common in women
from age 20 to 50 years. The incidence of FNH is not increased with
prolonged oral contraceptive use; however, it tends to be seen
slightly more frequently in women who take oral contraceptives.
• b. FNHs are non-neoplastic solid tumors characterized by a central fibrous
scar with radiating septa, often lobulated, and sharply demarcated from
adjacent liver, without a capsule. The central scar often contains a large artery
that branches out in a spoke-wheel pattern. These tumors arise as a
hyperplastic, hepatocellular response to either hyperperfusion or vascular
injury from the anomalous central artery in the lesion, which is not
accompanied by a portal vein or bile duct branch.
• c. Regenerative nodules resembling FNH tumors may be seen in chronic
advanced liver disease. These nodules have the hallmark of vascular inflow
reduction, liver cell atrophy centrally in the nodule, and regeneration around
the intrahepatic portal triads.
• d. Patients with FNH are usually asymptomatic, but those who do present with
pain are more commonly women who take oral contraceptives.
• e. Physical examination and liver function tests are normal. Liver
nuclear scan with 99-Tc sulfur colloid shows FNH tumors to be "hot,"
with increased presence of Kupffer cells. Both CT and MRI may
accurately demonstrate the classic central scar in a solid liver
tumor as the characteristic finding of an FNH tumor. Another
hallmark of FNH on cross-sectional imaging studies (CT or MRI) is
a hypertrophied feeding artery supplying the tumor.
Management
• Because rupture and malignant transformation are not seen with FNH tumors,
they may be left alone. Rarely, the enlarging FNH tumor or a patient with
severe pain from liver capsule distension should be taken for surgical
resection.

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M. SUMMARY OF LIVER TUMORS
• IOC FOR LIVER TUMORS IS TRIPHASIC CT SCAN

• FOR HEMANGIOMA MRI IS IOC

• EARLIEST INVESTIGATION FOR LIVER TUMOR IS USG

• FNAC IS CONTRAINDICATED IN LIVER TUMOR

• TOC FOR HEMANGIOMA IS ENUCLEATION

• FEMALE WITH HISTORY OF COCPS -- HEPATIC ADENOMA

• PATIENT PRESENTS WITH CONGESTIVE HEART FAILURE ---

HEMANGIOMA

• HEPATIC ADENOMA CAN PROGESS TO HEPATOCELLULAR

CARCINOMA

• TUMOR INVOLVED KUPFFER CELLS: FOCAL NODULAR

HYPERPLASIA

• BENIGN TUMORS COMMON IN FEMALE

• CARCINOMA COMMON IN MALES

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