Essam Abdul Wahab Lecturer of Internal Medicine Hepatogastroenterlogy Unit

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Essam Abdul Wahab Lecturer of Internal Medicine Hepatogastroenterlogy Unit Focal Hepatic Lesions Focusing On Hepatocellular Carcinoma

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Essam Abdul Wahab Lecturer of Internal Medicine Hepatogastroenterlogy Unit. Objectives. Focal hepatic Lesions. Benign Liver Lesions. Hemangioma. The commonest liver tumor 5 % of autopsies Usually single small with demarcated capsule. Usually asymptomatic. - PowerPoint PPT Presentation

Transcript of Essam Abdul Wahab Lecturer of Internal Medicine Hepatogastroenterlogy Unit

Page 1: Essam Abdul Wahab Lecturer of Internal Medicine  Hepatogastroenterlogy  Unit

Essam Abdul WahabLecturer of Internal Medicine

Hepatogastroenterlogy Unit

Focal Hepatic Lesions

Focusing On Hepatocellular Carcinoma

Page 2: Essam Abdul Wahab Lecturer of Internal Medicine  Hepatogastroenterlogy  Unit

@ Identify the common focal hepatic lesions.

@ Know the risk factors, Diagnosis, and management of hepatocellular carcinoma.

Home message.

Objectives

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Focal hepatic Lesions

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Focal Hepatic Lesions

Hemangioma

Focal nodular hyperplasia

Adenoma

Liver cysts

1- Primary liver cancers

Hepatocellular carcinoma

Fibrolamellar carcinoma

Hepatoblastoma

2. Metastases

Benign Malignant

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Benign Liver Lesions

Hemangioma

Focal nodular hyperplasia

Adenoma

Cysts

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Hemangioma

The commonest liver tumor 5% of autopsies

Usually single small with demarcated capsule.

Usually asymptomatic.US: well demarcated echogenic spot.CT: venous enhancement from periphery to centerMRI: high intensity areaNo need for FNANo need for treatment ??

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Focal Nodular Hyperplasia (FNH)Benign nodule formation of normal liver with Central stellate scar.

Common in young and middle age women

No relation with sex hormones.

Asymptomatic, may cause minimal pain.US: Nodule with varying echogenicityCT: Hypervascular mass with central scarMRI: iso or hypo intense FNA: Normal hepatocytes and Kupffer cells with central core.No treatment necessary.Pregnancy and hormones----- OK.

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Benign neoplasm ---- normal hepatocytes but no portal tract, central veins, or bile ducts.More common in women.Usually asymptomatic but may have RUQ pain.May presents with rupture, hemorrhage, or malignant transformation (very rare).US: filling defectCT: Diffuse arterial enhancementMRI: hypo or hyper intense lesionFNA : may be neededStop hormones, Observe every 6m If no regression then surgical excision.

Hepatic Adenoma

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Liver Cysts

May be single or multiple

May be part of polycystic kidney disease.

Patients often asymptomatic.

No specific management required.

Hydated cyst.

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Leader

1928-----2001

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Malignant Liver Tumors

Hepatocellular carcinoma (HCC) 90%

Fibro-lamellar carcinoma of the liver

Hepatoblastoma

Intrahepatic cholangiocarcinoma

Secondary liver tumors.

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US: HCC Jaundiced

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‘Time’ is the best kept secret of the rich..!

Jim Rohn

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HCC: Risk FactorsThe most important risk factor is cirrhosis from any cause.

Hepatitis B (integrates in DNA) regress now in Egypt

Hepatitis C(common in our country)

Alcohol

Aflatoxin

Hemochromatosis

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Patients for Whom HCC Surveillance Is Recommended

HBV carrier with HCC family history

Cirrhotic HBV carriers

Hepatitis C with cirrhosis

Stage 4 primary biliary cirrhosis

Genetic hemochromatosis and cirrhosis

Alpha-1 antitrypsin deficiency and cirrhosis

Other cirrhosis

80% of patients with HCC have underlying cirrhosis

Bruix J, et al. AASLD HCC guidelines. July 2010. Simonetti RS, et al. Dig Dis Sci. 1991;36:962-972.

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Malignant Transformation

Potential Targets

Oxidative stress and inflammation

Viral oncogenes

Carcinogens

Growth factors Telomere shortening

Cancer stem cells

Loss of cell cycle checkpoints

Antiapoptosis Angiogenesis

Normal liver

Liver cirrhosis

Hepatitis C,BEthanolNASH

Epigenetic alterationsGenetic alterations

HCC[2]

Dysplastic nodules[1]

1. Tornillo L, et al. Lab Invest. 2002;82:547-553. 2. Verslype C, et al. AASLD 2007. Abstract 24.

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Diagnosis of HCC

Clinical

Examination

AFP

Detection

Radiological

Assessment Biopsy

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C/p1- HCC usually have no symptoms other

than those related to their chronic liver

disease.

2- Sudden decompensation as

ascites, encephalopathy,

jaundice, or variceal bleeding.

3- Mild to moderate -upper abdominal pain, weight loss, early satiety, or a

palpable mass in the upper abdomen.

4- Hypercalcemia , hypoglycemia,

erythrocytosis, and watery diarrhea

5- features of metastases

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HCC: labs…AFP (Alfa Feto Protein)

HCC tumor marker since 1968.

> 200 ng/ml are highly suggestive of HCC.

Elevation seen in more than 70% of pt.

Serum level increase also in chronic hepatitis and liver cirrhosis.

Sensitivity 60 % and specificity 94 %.

Small HCCs are usually non AFP secreting.

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Radiology

HCC can be diagnosed radiologically, without the need for biopsy if the typical imaging features are present.

Requires a contrast-enhanced study:• 1- CEUS

• 2- Dynamic CT.

• 3- Dynamic MRI.

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Contract enhanced US (CEUS)

Using microbubble structure, consisting of gas bubbles stabilized by a shell.

The sizes of the bubbles are not small to be lost by lung or large to pass to extracellular like CT and MRI.

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CEUS allows visualization of the arterial ,portal phase and late phase that differs from the late phase of extracellular (CT) and (MRI) agents in that it is prolonged more than 5 minutes and may reflect sinusoid pooling and RES or Kupffer cell uptake

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Enhanced CT arterial phase

Venous phase Delayed phase

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Biopsy Often not necessary. Most focal liver lesions have characteristic radiological findings on CT or MRI.

Recommended in uncertain cases.

Many debates regarding tunneling of tumor cells. .

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HCC: Prognosis

Tumor size

Spread

Underlying liver disease

Patient status

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HCC Management

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Surgical resection

Liver

Transplantation Percutaneous

ablation...

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HCC: Liver Transplantation

Best available treatment.

Removes tumor and liver.

Only if single tumor less than 5cm or less than 3 tumors less than 3 cm each.

Recurrence rate is low.

Not widely available.

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HCC: Resection

Feasible for small tumors with preserved liver function (no jaundice or portal HTN)

Recurrence rate is high.

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HCC: Loco -Regional Ablation

• For non respectable pt. temporary measure only as bridge for liver transplantation.

• For pt. with advanced liver cirrhosis:• Percutaneous Ethanol injection(PEI)• Radiofrequency ablation(RFA)• Tran arterial chemoembolization (TACE)• Microwave Coagulation.

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Ethanol InjectionIt is the best known and best studied approach.

It achieves necrosis rate of:

90-100% of the HCC smaller than 2 cm

70% in tumors between 2 and 3 cm

50% HCC between 3 and 5 cm.

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Radio Frequency Ablation

Deliver heat around the tip induces a wide region of

tumor necrosis.

The efficacy of RFA in tumors <2 cm is similar to that

of ethanol but requires fewer treatment sessions. The

efficacy in tumors >2 cm is better than with ethanol

.

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Follow up The efficacy of percutaneous ablation is assessed

by dynamic CT or MR one month after therapy

The absence of contrast uptake within the tumor

reflects tumor necrosis, while the persistence of

contrast uptake indicates treatment failure

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HCC: ChemoembolizationInject chemotherapy selectively in hepatic artery

Then inject an embolic agent……

Only in pts. with early cirrhosis….

No role for systemic chemotherapy

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Chemoembolization

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Systemic Chemotherapy

• For advance HCC with accepted liver function:

• HCC has been considered to be a relatively chemo and radio-resistant.

• Survival is often determined by degree of hepatic dysfunction.

• Systemic chemotherapy is not well tolerated by most patients.

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HCC is an evolving and explosive problem in Egypt.

HCC is tightly related to chronic HCV infection.

Early diagnosis of respectable of loco regional eligible HCC is a major interest.

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