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LIVER CANCERS
Dr. MANISH DUTT
• ANATOMY
• EPIDEMIOLOGY
• ETIOLOGY
• PATHOLOGY
• PROGNOSTIC FACTORS
• WORKUP
• STAGING
anatomy
Couinaud segments
Clinical significance
Each segment can be resected without
damaging those remaining
resections must proceed along the
vessels
Dual blood supply:
Portal vein: 3/4
Hepatic artery:1/4
Venous outflow:
Hepatic veins: left, right and middle
Drains into IVC
HEPATIC LOBULES
EPIDEMIOLOGY
• 782,000 new cases worldwide 2012
• fifth most common cancer in men, 7.5% of
the total) and the ninth in women (3.4%)
• high incidence in Eastern and South-Eastern
Asia (ASRs 31.9 and 22.2 respectively)
• lowest rates in Northern Europe (4.6) and
South-Central Asia (3.70
• second most common cause of death from
cancer 746,000 deaths in 2012 (9.1% of the
total)
• prognosis very poor (overall ratio of mortality
to incidence of 0.95
INDIAN STATS
• men 0.9-7.5 per 100,000
• women 0.2 -2.2 per 100,000
• male:female ratio for HCC in India is 4:1
• age of presentation 40 to 70 years
• highest AAIR was reported from Sikkim(7.5)and
Mizoram(6.4)
• 4–8% of the cancers were due to HCC
• annual incidence rate of 1.6% (Paul et al) in cirrhotics
• age standardized mortality rate for men is 6.8 ,women
5.1/100,000.
• incidence of HCC in cirrhotics in India is 1.6% per year
• 70–97% of patients with HCC at the time of diagnosis
had underlying cirrhosis of liver
• incidence of HCC is increasing in India
ETIOLOGY
• Viral hepatitis- HBV
1. 98 fold greater risk
2. Asymptomatic HbsAg+ - 12
times RR
3. MECHANISM-indirect/direct
4. 70% HBV related HCC- with
cirrhosis
5. Risk of HCC in hepB cirrhotic
0.5%
• HCV-
1. Chronic infection(60-80%)
2. 20 fold more and advanced
cirrhosis
3. Risk of HCC in hepC cirrhotic
5%
Mi-R-155 accumulation
Etiology contd.
• Alcohol- carcinogenic, acetaldehyde, oxidative stress
• NASH(24%)
• METABOLIC DISEASES-haemochromatosis, Wilson,
alpha1 AT def.
• Chemical carcinogens- aflatoxin
• Anabolic steroids, estrogens
• Pesticides, insecticides
• Obesity, DM
• Cumulative tobacco use
• Male, old age, specific promotor mutations, higher
viremia levels
STAGING
PROGNOSTIC FACTORS
• large size,
• multiple tumors
• vascular invasion
• lymph node spread
• Macroscopic or microscopic
vascular invasions
• severity of underlying liver
disease- CHILD PUGH, CLIP, V-
CLIP, (JIS), BCLC
DIAGNOSTIC W/U
• Labs: CBC, LFTs, chemistries,
coagulation panel, serum
AFP(10–15% false negative),
Hepatitis B/C panels.
• Abdominal CT scan (special
contrast protocol).
• FNAC can be performed but is
not always needed.
W/U Contd.
Radiological/non invasive
• Lesions>2cm-
• arterial hyperenhancement on two
different imaging modalities, or on one
imaging modality alongside with a serum
AFP of 400 ng/dL
• both arterial hyperenhancement and
venous washout in a single imaging
modality concomitant with an AFP >200
ng/mL
• sensitivity and specificity of 64.9% and
62.8%
pathological
• Core biopsies- liver/portal vein
• stromal invasion
• sensitivity and specificity of 89.1%
and 100%

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Hepatocellular carcinoma premanagement

  • 2. • ANATOMY • EPIDEMIOLOGY • ETIOLOGY • PATHOLOGY • PROGNOSTIC FACTORS • WORKUP • STAGING
  • 5. Clinical significance Each segment can be resected without damaging those remaining resections must proceed along the vessels Dual blood supply: Portal vein: 3/4 Hepatic artery:1/4 Venous outflow: Hepatic veins: left, right and middle Drains into IVC
  • 7.
  • 8. EPIDEMIOLOGY • 782,000 new cases worldwide 2012 • fifth most common cancer in men, 7.5% of the total) and the ninth in women (3.4%) • high incidence in Eastern and South-Eastern Asia (ASRs 31.9 and 22.2 respectively) • lowest rates in Northern Europe (4.6) and South-Central Asia (3.70 • second most common cause of death from cancer 746,000 deaths in 2012 (9.1% of the total) • prognosis very poor (overall ratio of mortality to incidence of 0.95
  • 9.
  • 10. INDIAN STATS • men 0.9-7.5 per 100,000 • women 0.2 -2.2 per 100,000 • male:female ratio for HCC in India is 4:1 • age of presentation 40 to 70 years • highest AAIR was reported from Sikkim(7.5)and Mizoram(6.4) • 4–8% of the cancers were due to HCC • annual incidence rate of 1.6% (Paul et al) in cirrhotics • age standardized mortality rate for men is 6.8 ,women 5.1/100,000. • incidence of HCC in cirrhotics in India is 1.6% per year • 70–97% of patients with HCC at the time of diagnosis had underlying cirrhosis of liver • incidence of HCC is increasing in India
  • 11. ETIOLOGY • Viral hepatitis- HBV 1. 98 fold greater risk 2. Asymptomatic HbsAg+ - 12 times RR 3. MECHANISM-indirect/direct 4. 70% HBV related HCC- with cirrhosis 5. Risk of HCC in hepB cirrhotic 0.5% • HCV- 1. Chronic infection(60-80%) 2. 20 fold more and advanced cirrhosis 3. Risk of HCC in hepC cirrhotic 5% Mi-R-155 accumulation
  • 12. Etiology contd. • Alcohol- carcinogenic, acetaldehyde, oxidative stress • NASH(24%) • METABOLIC DISEASES-haemochromatosis, Wilson, alpha1 AT def. • Chemical carcinogens- aflatoxin • Anabolic steroids, estrogens • Pesticides, insecticides • Obesity, DM • Cumulative tobacco use • Male, old age, specific promotor mutations, higher viremia levels
  • 14. PROGNOSTIC FACTORS • large size, • multiple tumors • vascular invasion • lymph node spread • Macroscopic or microscopic vascular invasions • severity of underlying liver disease- CHILD PUGH, CLIP, V- CLIP, (JIS), BCLC
  • 15. DIAGNOSTIC W/U • Labs: CBC, LFTs, chemistries, coagulation panel, serum AFP(10–15% false negative), Hepatitis B/C panels. • Abdominal CT scan (special contrast protocol). • FNAC can be performed but is not always needed.
  • 16. W/U Contd. Radiological/non invasive • Lesions>2cm- • arterial hyperenhancement on two different imaging modalities, or on one imaging modality alongside with a serum AFP of 400 ng/dL • both arterial hyperenhancement and venous washout in a single imaging modality concomitant with an AFP >200 ng/mL • sensitivity and specificity of 64.9% and 62.8% pathological • Core biopsies- liver/portal vein • stromal invasion • sensitivity and specificity of 89.1% and 100%