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CMH BWP
HEPATOCELLULAR CARCINOMA
By
Dr. Danish Rauf
HOUSE SURGEON, CMH Bahawalpur
Supervisor
Col Malik Saeed Awan
Consultant General and Laparoscopic Surgeon
CMH BWP
CMH BWP
SEQUENCE
Case Presentation
Case Discussion
CASE PRESENTATION
CMH BWP
• A 24-year-old patient was admitted to our hospital with a 2-month
history of right hypochondriac pain and fever. He also reported
decreased appetite, significant weight loss, and occasional
vomiting but there were no other symptoms. He gave no history
of chronic medical illnesses; there was no drug or family history
of note. He denied cigarette smoking or alcohol consumption.
Before presenting here, the patient was already previously seen
in another hospital in which a diagnosis of liver abscess was
made.
GENERAL PHYSICAL
EXAMINATION
• Pulse: 98/ min
• Blood Pressure: 100/60 mmHg
• Respiratory rate: 15/ min
• Temperature: 103 ºF
CMH BWP
ABDOMINAL EXAMINATION
1 )palpable liver (10 cm below the right costal margin, irregular, firm
and tender)
2) No ascites or splenomegaly
3) no peripheral stigmata of chronic liver disease
4) No hepatic failure r disease
CMH BWP
SYSTEMIC EXAMINATION
Unremarkable
CMH BWP
INVESTIGATION
Laboratory
Radiological
CMH BWP
LABORATORY
CBC : Hb 14.6 gm/dL,
WBC of 11300/cmm,
platelets of 291,000/cmm.
LFTs : total bilirubin of 35 mmol/L (reference range 0-17),
ALT 54 IU/L (30-65),
AST 74 U/L (15-37),
alkaline phosphatase 344 U/L (50-136),
GGT 646 U/L (1-94),
albumin 33 g/L (34-50)
CMH BWP
• Serum alpha-fetoprotein : >1000 ng/L
• Hepatitis Profile : Negative
• RFTs : Normal
RADIOLOGY
Ultrasound Abdomen : multiple hypodense hepatic
lesions
CT : multiple hypodense hepatic lesions with ring
enhancemen
CMH BWP
DIAGNOSIS
Hepatocellular Carcinoma
CMH BWP
CASE DISCUSSION
CMH BWP
INCIDENCE
⚫28/100000 in SEA
⚫10/100000 in SE
⚫5/100000 IN NE
⚫ Incidence is increasing day bydaydue to -chronic
hepatitis B &C virus infection.
⚫-cirrhosis due toanycause.
⚫Thedisease is morecommon in male(4:1)usually in
middleage group(50years).
PATHOGNESIS
⚫Theexact pathogenesis is unknown.
⚫Thedisease seems tooccur in stages:
Chronic liver injury > cell death >regeneration>
cellular metabolicdysfunction> release of
inflammatory mediators> increase risk of
transforming mutation of hepatocytes.
• Preneoplastic changes –hepatocytes dysplasia can
be seen.
CLINICAL
PRESENTATION
Symptoms:
 Weakness,
 malaise,
 abdominal
 chest
pain,vomiting,jaundice,haematemesis.
 Anorexia,weightloss –incaseof metastasis.
CONTD….
Sign:
 Jaundice
 Ascites
 Hepatomegaly
 Periumbilical collateral veins
 Variceal bleeding
 Easy bruising
 Hepaticencephalopathy
 Shock
CONTD…
Local examination:
 Palpable mass in right upperabdomen which is
hard,irregular,tender/nontender.
 Hepatic bruit
SPREAD
 invasion into vasculature mostly portal
vein.
 lymphnode.
Lung and bone metastasis in terminal
cases.
DIAGNOSIS:
Diagnosisof HCC is done by
:
1. Clinical presentation
2.Investigation
3. Staging
IMAGES OF
INVESTIGATION
El-Serag HB. N Engl J Med 2011;365:1118-1127
MRI Studies Showing the Effects of Hepatocellular Carcinoma at
Different Stages of the Disease.
A: Very early stage (one lesion 1.7cm), B: early stage (2 lesions 2.4 and 1.2 cm)
•C: Intermediate stage (multiple lesions, Childs B), D: Advanced
•(large mass and ascites)
CONTD..
 Tumormarkers:
AFP- measurement
-viral marker
 Liverradio isotope scans
 Liverfunction test:
-serum bilirubin
-AST
-ALT
-ALP
-Prothrombin time
-Serumalbumin
TNM STAGING
SCREENING FOR HCC
 Methods:
 AFP (every 6 month) & Ultrasound
 Indications
 Forpatientat risk for HCC:-
• -Cirrhosis
• -Hepatitis B,C
• -Alcohol consumption
• -Genetic hemachromatosis
• -Autoimmune hepatitis
• -Non alcoholic steatohepatitis
• -Primary biliarycirrhosis
• -Alpha1antitrypsin deficiency
TREATMENT
A. Surgical approach
B. Non surgical therapy
SURGICAL APPROACH
a. Segmental or local resection
b. Lobectomy or partial hepatectomy
c. Extended lobectomy
d. Livertransplantation
IMAGES OF
SURGICAL
TREATMENT
B.NONSURGICAL
THERAPY
Majorityof HCC not be amenable tosurgical
resection because of :-
=Advanced stageof thecarcinoma &
=Severity of the underlying liverdisease
CONTD..
Theoptions are:
Ablative
-Ethanol injection
-Aceticacid injection
-Thermal(cryotherapy,readiotherapy,microwave)
Transarterial
-Embolization
-Chemoembolization
Systemic
-Chemotherapy
-Radiotherapy
-Imunotherapy
RADIOFREQUENC
Y ABLATION
TRANSARTERIAL CHEMO
EMBOLIZATION
MCQS
PROGNOSIS AFTER
TREATMENT:
o5 yearsurvival rate:- 30-40% after liver
resection
o5yearsurvival rate:- 75% in liver
transplantation
o2 yearsurvival rate :- 60% in transarterial
chemoembolization
CONCLUSION
In brief ,preventing and treating viral
hepatitis may help to reduce the risk of
developing liver cancer.Childhood hepatitis
vaccinationof hepatitis B may reduce risk of
it.Proper nutrition,rest,good habits(avoid
alcohol) and safer practises makes a man
healthy.
hcc20-8-15-150824200958-lva1-app6892.pptx

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hcc20-8-15-150824200958-lva1-app6892.pptx

Editor's Notes

  1. Worthy commandant, respected teachers and fellow colleagues, Asalam-o-Alikum.
  2. Her general physical examination revealed a middle aged lady oriented in time, place and person with stable vital signs.
  3. On breast examination there was obvious asymmetry of the breast. Right breast was more prominent and had a visible swelling of approximately 6cm x 5cm, which was hard in consistency, present in the outer quadrant of right breast at around 9 o’clock position.THE LUMP HAD IRREGULAR MARGINS AND WAS FIXED TO THE CHEST WALL but no fixity to the skin Nipple was retracted.No peau d’orange or ulceration was seen. there was no dimpling of skin.There was a mobile, firm pectoral lymph node palpable in the right axilla. Supra clavicular fossa was clear. Contralateral breast, axilla and supraclavicular fossa were normal too
  4. There was no evidence of pleural effusion or consolidation No hepatomegaly, ascites or abdominal swelling noticed. PELVIC ,Skull and spine were normal TOO
  5. There was no evidence of pleural effusion or consolidation No hepatomegaly, ascites or abdominal swelling noticed. PELVIC ,Skull and spine were normal TOO
  6. There was no evidence of pleural effusion or consolidation No hepatomegaly, ascites or abdominal swelling noticed. PELVIC ,Skull and spine were normal TOO
  7. There was no evidence of pleural effusion or consolidation No hepatomegaly, ascites or abdominal swelling noticed. PELVIC ,Skull and spine were normal TOO
  8. On the basis of the history, examination and investigations a final diagnosis of INVASIVE DUCTAL CARCINOMA of the right breast was made. She was staged as T4aN1M0 (locally advanced) as it was lump more than 5cm, fixed to chest wall with few mobile axillary LN
  9. Now the case discussion