Definition — Liver Calcification (Hepatic Calcification):
Deposition of calcium salts within the hepatic parenchyma or within focal hepatic lesions. Calcifications may be dystrophic (in necrotic or treated tumours), granulomatous (healed infection), parasitic, vascular, or related to prior surgery/trauma. Sonographically calcifications appear as brightly echogenic foci; large calcifications cast posterior acoustic shadowing while tiny microcalcifications may create comet-tail or reverberation artifacts.
Sonographic features — Liver Calcification:
Appearance: Bright echogenic foci within the liver parenchyma or within lesions. Dense calcifications produce strong posterior acoustic shadowing; microcalcifications may cause comet-tail/reverberation artifacts.
Location & distribution: Solitary or multiple; segmental, lobar or diffuse distribution. Note relation to bile ducts, vessels, prior surgical sites or focal lesions.
Associated lesion: Calcification within a mass may indicate dystrophic change (treated or necrotic tumour), healed abscess, hydatid cyst (inactive), or calcified metastasis (eg mucinous primaries).
Doppler: Calcified foci are avascular; assess surrounding tissue for increased vascularity which may indicate active inflammation or viable tumour.
Acoustic shadowing vs enhancement: Dense calcifications cast shadowing; biliary or gas artifacts may mimic shadowing — correlate with patient history and other imaging.
Comet-tail/reverberation: Typical of small intraparenchymal calcifications or biliary microstones and helpful to distinguish from surgical clips or gas.
Mimics: Surgical clips, gallstones in an intrahepatic duct, phleboliths, gas — cross-check prior imaging (CT/X-ray) to confirm true calcification.
Clinical relevance: Calcification usually indicates chronicity/healing. New calcification within a lesion requires further characterisation to exclude treated tumour vs progressing disease.
Reporting tips: Document number, size, segmental location (Couinaud), presence/absence of posterior shadowing, relation to adjacent structures, and comparison with prior imaging.
Case Study — 1: Hepatic Calcification/Solitary Calcified Granuloma:
48-year-old female with intermittent right upper quadrant discomfort. No fever. History of prior pulmonary tuberculosis.
Ultrasound:
Single 10–12 mm intensely echogenic focus in segment IV with posterior acoustic shadowing; no surrounding hypoechoic halo, no internal vascularity.
Interpretation:
Appearance most consistent with a healed calcified granuloma. Recommend correlation with prior chest imaging and clinical history; no evidence of active infection or viable tumour on ultrasound.
Ultrasound Report — Line
Liver shows a solitary 12.22 mm echogenic focus in segment IV with strong posterior acoustic shadowing — appearance consistent with hepatic calcification/old granuloma. No adjacent mass or intra-lesional vascularity identified. Background liver echotexture within normal limits. Recommend correlation with prior CT or radiographs to confirm chronicity.
Conclusion
Focal hepatic calcification in segment IV, most likely a healed granuloma. No sonographic evidence of active abscess or viable tumour.
Recommendation
Correlate with prior imaging (non-contrast or contrast CT) to confirm calcific density and chronicity.
If calcification is new or associated with a mass, obtain contrast-enhanced CT for full characterisation.
If infection suspected clinically (fever, raised inflammatory markers), consider CT and clinical management; aspiration only if abscess suspected and accessible.
Right kidney shows A tiny echogenic foci in the mid calyx , consistent with microlithiasis. No significant hydronephrosis noted.
Left kidney demonstrates a single echogenic calculus measuring ~3.7 mm in the mid calyx with posterior acoustic shadowing and twinkle artifact on Doppler. No associated hydronephrosis observed.
Most hepatic calcifications are asymptomatic and incidental findings.
If due to active abscess — RUQ pain, fever, leukocytosis and raised CRP.
Mass effect symptoms only when associated with large lesion.
Diagnostic Strategy
Identify echogenic focus and characterise artifact (shadowing vs comet-tail).
Use Doppler to confirm lack of internal vascularity.
Compare with prior imaging (CT or radiographs) — CT is gold standard to confirm mineral density.
If infection suspected, correlate with labs (CBC, CRP) and treat/aspirate as indicated.
Risk Factors
History of granulomatous disease or endemic infections.
Prior hepatic abscess, parasitic disease, or liver trauma.
Prior hepatic tumour treatment (ablation, chemo) leading to dystrophic calcification.
Metastatic disease from calcifying primaries (less common).
Declaration:
I, R. K. Mouj, declare that the material presented in this document titled "Liver Calcification — Sonographic Guide" has been prepared for educational purposes. Patient data should be anonymised and clinical correlation is required.
Author: ____________________ Name: R. K. Mouj [Radio-imaging Technologist] Supervisor / Guide: Department radiologist Department: Radiology Institution: ____________________ Date: 25-09-2025
"Every cyst tells a story — knowing the benign from the sinister is the art of ultrasound."
Gall bladder sonography — Table of Contents (Topic-wise)
Contents (Topic-wise)
Agenesis of Gallbladder
Gallbladder not visualized despite adequate scanning and patient repositioning; normal biliary tree — features consistent with gallbladder agenesis. Conclusion: Gallbladder agenesis suspected — correlate with MRCP if clinically indicated. Recommendation: Clinical correlation and/or cross-sectional imaging (MRCP) to confirm agenesis and assess biliary anatomy.
Definition — Hepatic Simple Cyst:
A benign, developmental, non-parasitic cystic lesion of the liver lined by cuboidal epithelium, usually containing clear serous fluid. Sonographically, it appears as a well-defined, anechoic lesion with thin, imperceptible walls, posterior acoustic enhancement, and without internal septations, solid components, or vascularity. Typically asymptomatic and incidentally detected, but large cysts may cause mass effect symptoms. Differentiation from hydatid cyst or cystic neoplasm is important in relevant clinical contexts.
Sonographic features — Hepatic Simple Cyst:
Size & shape: Usually round or ovoid, variable in size (few mm to several cm), with smooth and well-defined margins.
Wall characteristics: Thin, imperceptible wall without irregularity, calcification, or nodularity.
Internal contents: Anechoic (completely echo-free) fluid content without septations or internal echoes.
Vascularity: No internal vascularity on color Doppler imaging.
Distribution: May occur singly or as multiple simple cysts; usually asymptomatic and found incidentally.
Case Study — 1: Hepatic Simple Cyst:
Mrs. S., 54 years old, female, presented for routine health check-up with nonspecific abdominal bloating. She had no history of jaundice, fever, weight loss, or liver disease. No history of alcohol intake or prior abdominal surgery. No relevant family history.
Clinical Examination:
Patient afebrile, no pallor or icterus. Abdomen soft, non-tender, no palpable hepatomegaly, no ascites. No stigmata of chronic liver disease. General and systemic examination unremarkable.
Laboratory Findings:
CBC: Hb 12.8 g/dL, WBC 6,400/µL, Platelets 220,000/µL.
LFT: Bilirubin 0.8 mg/dL, AST 28 U/L, ALT 32 U/L, ALP 86 U/L, Albumin 4.2 g/dL.
INR 1.0. Serum AFP within normal limits. Viral markers (HBsAg, anti-HCV) negative.
Ultrasound Examination:
Transabdominal ultrasound performed using 3.5–5 MHz convex probe.
A well-defined anechoic round cyst in the right hepatic lobe (segment V/VII) measuring 67 x 46 mm.
Imperceptible thin wall, no septations or mural nodules.
Prominent posterior acoustic enhancement.
No internal vascularity on color Doppler.
Ultrasound Report — Hepatic Simple Cyst:
A solitary, well-circumscribed, thin-walled anechoic lesion with posterior acoustic enhancement, measuring 67 x 46 mm in the righ hepatic lobe, without septations, solid component, or vascularity. No intrahepatic biliary dilatation or additional focal hepatic lesion seen. Findings consistent with a Hepatic Simple Cyst.
Conclusion:
Benign hepatic simple cyst. No features to suggest parasitic, neoplastic, or complicated cyst.
Recommendation:
No active intervention required. Symptomatic management if bloating persists. Follow-up ultrasound only if lesion enlarges or symptoms develop.
Causes / Etiology — Hepatic Simple Cyst:
Congenital biliary microhamartomas with cystic dilatation.
Embryological maldevelopment of intrahepatic bile ducts.
Non-parasitic, non-neoplastic origin.
Symptoms / Clinical Features — Hepatic Simple Cyst:
Most are asymptomatic and discovered incidentally.
Large cysts may cause abdominal fullness, discomfort, or early satiety.
Rarely, pain due to cyst hemorrhage, rupture, or infection.
Diagnostic Strategy — Hepatic Simple Cyst:
Ultrasound: Anechoic, thin-walled, well-defined, posterior enhancement, no septa or nodules.
CT/MRI: Simple fluid attenuation/signal, no enhancement.
Differentiation: Important to exclude hydatid cyst, cystic neoplasm, or abscess in symptomatic or atypical cases.
Declaration:
I, R. K. Mouj, hereby declare that the material presented in this document titled "Hepatic Simple Cyst: 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. Sources and references have been acknowledged where appropriate.
Ethics / Patient Data Statement: Any patient images, case material, or ultrasound examples included here are for academic use only, anonymised, and used with ethical consideration.
Author: ____________________ Name: R. K. Mouj [Radio-imaging Technologist] Supervisor / Guide: Department radiologist Department: Radiology Institution: ____________________ Date: 16-09-2025
"Every cyst tells a story — knowing the benign from the sinister is the art of ultrasound."
Bilingual Quiz - Hepatic Simple Cyst Sonography
Note: Select English to answer in English, या हिंदी चुनें तो प्रश्नों के उत्तर हिंदी में दीजिए।
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.
Ultrasound Report — Multiple Massive HCCs:
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.
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."
Liver showing posterior acoustic enhancement without internal septations, solid components, or mural nodules. No distortion of hepatic architecture or compression of vascular structures noted. Features are consistent with Polycystic Liver Disease – Type I.
Polycystic Liver Disease (PCLD) Type II
Multiple cysts with distortion of hepatic architecture — PCLD Type II.
Polycystic Liver Disease (PCLD) Type III
Extensive cystic involvement with gross distortion and hepatomegaly — PCLD Type III.
Congenital Hepatic Fibrosis (CHF)
Hepatomegaly with increased periportal echogenicity and irregular fibrotic bands — suggestive of CHF.
Caroli Disease
Multiple cystic/dilated intrahepatic bile ducts communicating with the biliary tree (central dot sign) — Caroli disease.
Simple Caroli Disease
Multiple cystic, tubular intrahepatic structures communicating with bile ducts (central dot sign) — simple Caroli disease.
Caroli Syndrome
Intrahepatic bile duct dilatations with periportal fibrosis/portal hypertension — Caroli syndrome.
Aberrant Hepatic Veins / Accessory Fissures
Anomalous course of hepatic veins with variant drainage.
Hepatic Simple cyst
A solitary, well-circumscribed, thin-walled anechoic lesion with posterior acoustic enhancement, measuring 67 x 46 mm in the righ hepatic lobe, without septations, solid component, or vascularity. No intrahepatic biliary dilatation or additional focal hepatic lesion seen. Findings consistent with a Hepatic Simple Cyst. Conclusion: Benign hepatic simple cyst. No features to suggest parasitic, neoplastic, or complicated cyst. Recommendation: No active intervention required. Symptomatic management if bloating persists. Follow-up ultrasound only if lesion enlarges or symptoms develop.
Multiloculated hepatic cyst with multiple peripheral daughter cysts arranged in a rosette pattern, suggestive of hydatid cyst (CE2 stage). Conclusion: 00 Recommendation: 00
Full-Text___________ ↑ Top
Multivesicular / Septated Cyst (Cartwheel sign or Honeycomb appearance) (CE2)
Cystic lesion with multiple internal septations and daughter cysts arranged in a cartwheel / honeycomb pattern, suggestive of multivesicular hydatid cyst (CE2).
Cyst with Detached Membrane (Water-lily sign) (CE3a)
Well-defined cystic lesion in the liver showing internal floating membranes (‘water-lily sign’), suggestive of hydatid cyst with detached endocyst.
Hydatid cyst (Serpent Sign) (CE3a)
Cystic lesion in the liver with floating wavy undulating membranes (‘serpent sign’), suggestive of hydatid cyst with detached endocyst.
Cyst with Solid Matrix & Daughter Cysts (Ball of wool sign) (CE3b)
Cystic lesion with heterogeneous solid matrix containing multiple daughter cysts, showing ‘ball of wool’ appearance, suggestive of hydatid cyst (transitional stage, CE3b).
Cyst with Snowstorm / Hydatid Sand (CE4)
Liver shows a well-defined cystic lesion with internal echogenic mobile echoes producing a ‘snowstorm / hydatid sand’ appearance, suggestive of Hydatid Cyst (CE4).
Hepatomegaly with multiple tiny (<2 mm) hypoechoic nodules; some with central caseation and necrosis — miliary hepatic TB.
Acute Viral Hepatitis
Liver is enlarged with hypoechoic parenchyma and accentuated periportal echogenicity (‘starry sky’ sign). Features suggestive of acute viral hepatitis.
Chronic Viral Hepatitis
Liver shows mild hepatomegaly with coarse parenchymal echotexture. Portal tracts appear echogenic. Features consistent with chronic viral hepatitis.
Perihepatitis / Fitz-Hugh-Curtis Syndrome
Liver parenchyma appears normal. Hepatic capsule shows thickening with subtle perihepatic fluid/adhesions. Features are suggestive of perihepatitis (Fitz-Hugh-Curtis Syndrome) in the setting of pelvic inflammatory disease.
Diffuse hepatic steatosis Grade-i (Fatty liver)
Increased echogenicity with posterior attenuation; blunted portal margins.
Diffuse hepatic steatosis Grade-i (Fatty liver)
Increased echogenicity with posterior attenuation; blunted portal margins.
Diffuse hepatic steatosis Grade-ii (Fatty liver)
Increased echogenicity with attenuation and blurring of portal/hepatic vein margins.
Diffuse hepatic steatosis Grade-iii (Fatty liver)
Marked echogenicity with poor diaphragm/vessel visualization due to attenuation.
Non-alcoholic fatty liver disease
Diffuse increased echogenicity with attenuation and blurring of vessel margins (NAFLD).
Focal hepatic fat (Focal hepatic steatosis)
Focal increased echogenicity without mass effect; vessels traverse normally.
Nodular focal fat sparing
Well-defined hypoechoic area without mass effect; normal vessels through it.
Multiple hyperechoic nodules without mass effect; preserved vascular architecture.
Autoimmune Hepatitis
Liver is enlarged with coarse echotexture and periportal hyperechogenicity. Findings may be suggestive of autoimmune hepatitis; correlation with serology advised.
Glycogen Storage Disease
Marked hepatomegaly with increased echogenicity; homogeneous texture — GSD.
Type I – Von Gierke Disease
Hepatomegaly with diffuse echogenicity — GSD Type I.
GSD Type II – Pompe Disease
Echogenic liver ± cardiomegaly — GSD Type II.
GSD Type III – Cori / Forbes Disease
Enlarged echogenic coarse liver — GSD Type III.
GSD Type IV – Andersen Disease
Coarse, heterogeneous echotexture with fibrosis/cirrhosis features — GSD IV.
GSD Type V – McArdle Disease
Normal liver sonographically; muscle changes may be seen — GSD V.
GSD Type VI – Hers Disease
Mild–moderate hepatomegaly with homogeneous increased echogenicity — GSD VI.
GSD Type VII – Tarui Disease
No significant hepatic abnormality; muscle findings may be present — GSD VII.
GSD Type IX – Phosphorylase Kinase Deficiency
Hepatomegaly with diffusely echogenic parenchyma — GSD IX.
GSD Type 0 (Hepatic Glycogen Synthase Deficiency)
Normal sonographic liver; correlate clinically — GSD 0.
Amyloidosis
Hepatomegaly with diffusely heterogeneous increased echogenicity.
Hemochromatosis
Hepatomegaly with diffusely increased echogenicity; coarse texture.
The short axis view of the IVC and the hepatic veins show dilation: measures of 29 mm IVC & 15 mm main hepatic vein dilation. Features are compatible with Stag head sign. Oblique subxiphoid window showing pleural anechoic collection compatible with right pleural effusion.
Portal Vein Thrombosis
Echogenic thrombus with cavernoma and periportal collaterals — chronic PVT.
3-Budd-Chiari Syndrome
HV/IVC thrombus with reduced/absent flow; hepatomegaly; heterogeneous parenchyma.
Congestive Hepatopathy
Hepatomegaly with coarse texture; dilated hepatic/portal veins; loss of venous phasicity.
Portal Hypertension
Dilated PV with reduced hepatopetal flow; splenomegaly; collaterals.
Focal Arteriovenous Malformation
High-velocity, low-resistance arterial flow with early venous filling — AVM.
Hepatic Arteriovenous Malformation
Multiple anechoic channels with turbulent color flow; arterialized venous waveforms.
Echogenic Hemangioma
Well-defined, homogeneously hyperechoic lesion with enhancement; no internal Doppler flow.
Hypoechoic Hemangioma
Well-defined hypoechoic lesion with enhancement; minimal/no internal Doppler flow.
Heterogeneous Hemangioma
Predominantly hyperechoic lesion with enhancement; peripheral Doppler flow — atypical; consider CE imaging.
Full-Text
Massive HCC (single lesion)
Finding (Ultrasound report line_)
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.
Finding (Ultrasound report line_)
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.
Finding (Ultrasound report line_)
Liver is enlarged in size with rounded inferior margin. Parenchymal echotexture is homogeneous with normal echogenicity. No focal lesion is identified. Intrahepatic biliary radicles are not dilated. Portal vein and hepatic veins are patent with normal flow. Conclusion: Heptomegaly
Liver shows coarse, heterogeneous echotexture with irregular parenchymal pattern. No focal SOL identified. Findings are suggestive of chronic parenchymal liver disease.
Chronic liver failure/Liver cirrhosis
Liver shows increased parenchymal echogenicity with coarse echotexture (fatty fibrotic pattern) and decreased definition of the portal vein wall. Features are suggestive of chronic liver disease / chronic liver failure or cirrhosis.
Acute liver failure
Liver shows irregular contour with diffuse heterogeneity of parenchymal echotexture giving a starry night appearance, along with posterior sound attenuation. Multiple ubiquitous hyperechoic and hypoechoic micro- and macronodules are noted. These features are compatible with fulminant hepatic failure.
Atrophy of Liver Segment
Volume loss and parenchymal thinning of [segment] — segmental atrophy.
Regenerative Nodules
Multiple small iso–mildly hypoechoic nodules on coarse background — regenerative nodules.
Post-Surgical/Transplant Changes type-i
Localized parenchymal atrophy with architectural distortion — post-surgical change.
Post-Surgical/Transplant Changes type-ii
Linear echogenic bands/scar — post-operative changes.
Right lobe of liver shows a focal heterogeneous lesion of indeterminate nature. Margins are ill-defined. No definite internal calcification or cystic change noted. Color Doppler shows minimal/absent internal vascularity. Features are indeterminate; recommend further evaluation with contrast-enhanced CT/MRI for characterization.
