Definition — Massive Hepatocellular Carcinoma (Massive HCC): A large primary malignant hepatic neoplasm occupying a substantial portion of one hepatic lobe (or the whole liver) and commonly >5 cm in diameter, often showing heterogeneous echotexture, central necrosis or cystic change, irregular margins, arterialised internal vascularity on Doppler, and may be associated with portal or hepatic vein invasion or satellite nodules. Correlate with serum AFP and cross-sectional multiphasic imaging.
Sonographic features — Massive HCC:
- Size & shape: Typically a large (>50 mm, often many cm) solitary mass with irregular, lobulated margins. May produce palpable hepatomegaly and distortion of hepatic contour.
- Echotexture: Heterogeneous echotexture is common — mixed hypoechoic and hyperechoic areas due to viable tumour, necrosis, haemorrhage or fatty change. Central cystic/necrotic zones may be present producing complex internal echoes.
- Internal architecture: Thick internal septations, mural nodularity or solid mural components; layering of blood products may produce fluid-fluid levels in subacute haemorrhage.
- Capsule / pseudocapsule: A peripheral hypoechoic or echogenic rim (pseudocapsule) may be seen; capsule retraction suggests scarring or treated lesion.
- Vascularity (Colour/Power Doppler): Prominent internal arterialised flow and chaotic intralesional vessels are typical — early arterial phase supply and lower-resistance waveform on spectral Doppler. Presence of internal flow helps differentiate solid tumour from simple cyst or avascular collection.
- Vascular invasion: Contiguous echogenic or hypoechoic filling defect in the portal or hepatic vein with internal vascularity (on colour Doppler) suggests tumour thrombus rather than bland thrombus. Look for loss of normal venous flow and expansion of the vessel calibre.
- Contrast-enhanced ultrasound (CEUS) patterns: Typical HCC enhancement pattern on CEUS — arterial phase hyperenhancement (rapid wash-in) followed by washout in the late portal/late phases (timing and degree of washout correlate with lesion grade). CEUS is useful when CT/MRI contraindicated or to characterise indeterminate lesions on B-mode US.
- Elastography: Focal area of increased stiffness compared with surrounding parenchyma; elastography adds supportive information but is not diagnostic on its own.
- Associated findings: Background cirrhosis (coarse, nodular liver), splenomegaly, portal hypertension, ascites. Satellite nodules or multifocal lesions may be present.
- Complications visible on US: Tumour rupture with hemoperitoneum (free fluid with internal echoes), biliary obstruction if centrally located, and spontaneous intralesional haemorrhage producing echogenic clot/heterogeneous areas.
- Size progression / growth pattern: Rapid increase in size over serial exams, new vascularity or new satellite nodules suggests aggressive behavior — compare with prior imaging where available.
- Common pitfalls / mimics: Abscess (systemic sepsis, peripheral hyperemia, gas artifacts), necrotic metastasis (clinical history of other primary), focal nodular hyperplasia (FNH) or haemangioma (typical Doppler/CEUS features differ). Use clinical correlation, AFP and cross-sectional multiphasic CT/MRI to resolve uncertainty.
- Practical reporting tips: Always record lesion segment (Couinaud segment), maximal three-dimensional size (AP × transverse × craniocaudal in mm), number of lesions, relation to major vessels, presence/absence of portal/hepatic vein thrombus, ascites, background liver appearance and comparison with prior studies.
Case Study — 1: Single Massive HCC:
Mr. R., 61 years old, male, known chronic hepatitis B carrier with compensated cirrhosis, presented with progressive right upper quadrant pain, abdominal fullness, and early satiety for the past 6 weeks. He reported unintentional weight loss of 8 kg and intermittent low-grade fever without rigors. No history of alcohol intake in the last 10 years. No prior liver surgery or oncological treatment.
Clinical Examination:
Patient afebrile (37.9 °C), mildly icteric. Abdomen distended with a firm, irregular hepatomegaly palpable 8 cm below the right costal margin, tender to deep palpation. No clinically detectable ascites. No splenomegaly. No stigmata of advanced portal hypertension. Performance status ECOG-1.
Laboratory Findings:
CBC: Hb 11.2 g/dL, WBC 7,800/µL, Platelets 128,000/µL.
LFT: Bilirubin 2.1 mg/dL, AST 98 U/L, ALT 82 U/L, ALP 310 U/L, Albumin 3.0 g/dL.
INR 1.4. Serum AFP markedly elevated at 2,450 ng/mL.
HBsAg positive, anti-HCV negative. Renal function normal.
Ultrasound Examination:
Transabdominal ultrasound performed with a 3.5–5 MHz convex probe.
- Right lobe shows a large heterogeneous hypoechoic mass in segments V–VIII. with lobulated margins and central necrosis.
- Colour Doppler demonstrates chaotic intralesional arterial flow with evidence of early venous shunting.
Ultrasound Report — Single Massive HCC:
Liver shows a large heterogeneous hypoechoic mass lesion in the right lobe (segments V–VIII) measuring 114x92 mm, with lobulated margins, central necrosis and prominent intralesional arterial flow on colour Doppler. Right portal vein demonstrates an intraluminal echogenic filling defect with internal vascularity, consistent with tumour thrombus. Background liver is coursed in appearance. No significant ascites.
Conclusion:
Large heterogeneous hepatic mass with arterialised vascularity and portal vein tumour thrombus — findings are most consistent with a Single Massive Hepatocellular Carcinoma (HCC).
Recommendation:
Triphasic contrast-enhanced CT or MRI liver for staging and treatment planning. Correlation with serum AFP. Multidisciplinary team (MDT) review (hepatology / oncology / surgery) advised for management decision — surgical resection vs locoregional therapy (TACE/ablation) vs systemic therapy. Assess transplant eligibility if criteria are met.
Case Study — 2: Multiple Massive HCC:
Mr. K., 69 years old, male, known case of chronic hepatitis C with established cirrhosis, presented with progressive abdominal distension, dull right upper quadrant pain, early satiety, and significant weight loss (10 kg over 2 months). He also complained of intermittent low-grade fever and generalized fatigue. No prior history of hepatic surgery or locoregional therapy. Alcohol abstinent for the last 12 years.
Clinical Examination:
Patient mildly icteric, afebrile (37.5°C). Abdomen distended with massive hepatomegaly, firm irregular liver palpable up to 12 cm below the right costal margin, crossing midline. Shifting dullness positive indicating ascites. Mild splenomegaly. No pedal edema. ECOG performance status 2.
Laboratory Findings:
CBC: Hb 10.4 g/dL, WBC 9,600/µL, Platelets 102,000/µL.
LFT: Bilirubin 3.5 mg/dL, AST 132 U/L, ALT 97 U/L, ALP 410 U/L, Albumin 2.7 g/dL.
INR 1.6. Serum AFP markedly elevated at 5,800 ng/mL.
Anti-HCV positive, HBsAg negative. Renal function preserved.
Ultrasound Examination:
Transabdominal ultrasound performed with a 3.5–5 MHz convex probe.
- Multiple large heterogeneous masses identified in both hepatic lobes.
- The dominant right lobe mass (segments V–VIII) measures 85 × 56 mm with central necrosis and lobulated margins.
- A left lobe lesion (segments II–III) measures 35 x 32 mm.
- Several satellite nodules present bilaterally.
- Colour Doppler shows chaotic arterialised intralesional flow with arterioportal shunting.
- Right portal vein shows intraluminal echogenic thrombus with internal vascularity — consistent with tumour thrombus.
- Background cirrhotic liver with coarse echotexture and nodular surface.
- Moderate ascites and splenomegaly (131 mm) present.
Liver appears cirrhotic with coarse, nodular echotexture. Multiple large heterogeneous masses are noted in both hepatic lobes, the dominant lesion in the right lobe (segments V–VIII) measures 85 x 65 mm, and another large lesion in the left lobe (segment II–III) measures 35 × 32 mm. Additional satellite nodules are seen in both lobes. Lesions are predominantly hypoechoic with central necrotic areas and irregular lobulated margins. Colour Doppler shows prominent chaotic arterial flow within the dominant masses. Right portal vein shows intraluminal echogenic filling defect with internal vascularity, consistent with tumour thrombus.
Conclusion:
Multifocal massive hepatocellular carcinoma involving both lobes of the liver, with vascular invasion (portal vein tumour thrombus) in a cirrhotic background.
Recommendation:
Triphasic contrast-enhanced CT or MRI liver for staging and treatment planning. Correlation with serum AFP. Multidisciplinary team (MDT) review advised to assess options — liver transplantation (if within criteria), locoregional therapy (TACE/TAE), systemic therapy, or palliative care depending on tumour burden, vascular invasion, and hepatic reserve.
Causes / Etiology — Massive HCC:
- Chronic hepatitis B infection with cirrhosis — most frequent cause of massive solitary HCC.
- Chronic hepatitis C infection with long-standing cirrhosis.
- Alcohol-related cirrhosis in advanced disease stages.
- Metabolic dysfunction–associated steatohepatitis (NASH) with fibrosis/cirrhosis, increasingly common cause.
- Aflatoxin B1 exposure leading to aggressive, large single tumours.
- Hereditary liver disorders (hemochromatosis, Wilson’s disease, α1-antitrypsin deficiency) occasionally progress to massive HCC.
Symptoms / Clinical Features — Massive HCC:
- Right upper quadrant or epigastric pain due to large mass stretching the capsule.
- Palpable abdominal mass or hepatomegaly crossing the midline.
- Early satiety and abdominal fullness from mass effect on stomach and bowel.
- Unintentional rapid weight loss, anorexia and generalised weakness.
- Jaundice if tumour compresses bile ducts or in decompensated cirrhosis.
- Fever may occur with tumour necrosis or secondary infection.
- In advanced cases: ascites, variceal bleed (due to portal hypertension), or acute abdominal pain if tumour ruptures.
Diagnostic Strategy — Massive HCC:
- Initial suspicion: Large space-occupying liver lesion detected on routine ultrasound in a cirrhotic patient or with high AFP.
- Ultrasound: Identifies a single dominant mass >5 cm (often >10 cm), heterogeneous with necrosis, irregular margins, and arterialised flow.
- Doppler: Demonstrates chaotic intralesional arterial flow and vascular invasion (portal/hepatic vein thrombus).
- Cross-sectional imaging: Triphasic CT or MRI shows arterial phase hyperenhancement and portal/delayed washout — diagnostic hallmark.
- AFP correlation: Often markedly raised (>400 ng/mL in many massive lesions).
- Staging: Evaluate for vascular invasion, extrahepatic spread, ascites and performance status — crucial for therapy planning.
Risk Factors — Massive HCC:
- Chronic HBV infection — directly oncogenic, can cause massive HCC even without cirrhosis.
- HCV with cirrhosis — progressive, often multifocal, but may present as one massive lesion.
- Alcohol-related cirrhosis with large tumour burden.
- NASH/MAFLD cirrhosis — rising cause of massive HCC in older adults with metabolic syndrome.
- Aflatoxin exposure (Asia/Africa) — associated with very large single tumours.
- Male sex, age > 55 years, poor compliance with surveillance (leading to late, massive presentation).
- Genetic liver disease (rare) — hemochromatosis, Wilson’s disease, α1-antitrypsin deficiency.
Declaration:
I, R. K. Mouj, hereby declare that the material presented in this document titled "Massive Hepatocellular Carcinoma (HCC): Definition, Sonographic Features, Case Studies, and Risk Assessment" has been prepared and compiled by me for educational purposes only. It is intended for learning, training, and academic reference, and not for submission toward any formal degree or qualification. Sources and references used have been acknowledged where appropriate. This is my own original work. This thesis has not been submitted, either in whole or in part, for a degree at this or any other university. All sources and contributions from other authors have been clearly acknowledged and cited in the references. Where material from other authors has been used, permission has been obtained and is indicated in the text or figure captions.
Ethics / Patient Data Statement: Any patient images, clinical data, or case material included in this thesis have been used in accordance with applicable ethical guidelines and with appropriate consent or institutional approval. All identifying patient information has been removed or anonymised.
Author: ____________________
Name: R. K. Mouj [Radio-imaging Technologist]
Supervisor / Guide: Department radiologist
Department: Radiology
Institution: ____________________
Date: 15-09-2025
"Learning never stops — every question answered brings you one step closer to mastery, and every mistake is a doorway to deeper understanding."
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