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Thin-walled and Anechoic
Posterior enhancement indicates simple cysts (no septations) versus complex cysts (abscesses, hematomas, trauma)
Procedures: Aspiration, excision, or ablation can be performed
US Role:
Identify cyst
Determine location (which lobe/segment)
A dominant genetic disorder resulting in multiple 2-3 cm cysts
60% likelihood of having polycystic renal disease (PRD) - but no two-way correlation
Cysts in porta hepatis may cause obstruction
Differential diagnosis includes abscess; labs should be correlated
PLD is independent, but PRD can cause PLD; PLD cannot cause PRD
Benign liver malformation, disorganized clusters of dilated bile ducts
Surrounded by connective tissue and fibrous stroma
Also known as Von Meyenburg complex
Associated with hepatic fibrosis (too much scar tissue from chronic injury)
Mimics appearance of liver metastases
Pyogenic Liver Abscess: Bacterial pus collection; 50% cause unknown
Amebic Liver Abscess: Caused by parasites
Viral Hepatitis: Inflammation of the liver due to virus
Hydatid Disease: Cysts in the liver caused by tapeworm (Echinococcus)
Types of pathogens: virus (tiny robbers), bacteria (single-celled, may be good or bad), fungi (plant-like), and parasites (hitchhikers)
Common routes include:
Biliary tract (cholangitis & cholecystitis)
Portal venous (from diverticulitis or appendicitis)
Hepatic artery (from osteomyelitis or sub-acute bacterial endocarditis)
Cholangitis: Inflammation of bile duct
Cholecystitis: Inflammation of gallbladder
Variable appearance;
Complex with internal debris or septations
Cystic, well-defined, or irregular borders
Ranges from echo-free to highly echogenic
May appear hypoechoic related to necrosis
Fluid-filled interfaces
Affects liver as infection spreads to other organs
Clinical presentation includes persistent fever in neutropenic patients
US Appearance: “Wheel within wheel” or “bull’s eye target”
Infection by Entamoeba histolytica via fecal-oral route
Sonographic Features:
Round/oval lesions with non-prominent walls
Hypoechoic compared to liver (similar to pyogenic abscess)
Caused by Echinococcus granulosus (3-6 cm tapeworm; definitive host: dogs, intermediate host: sheep)
Transmission via fecal matter containing ova
Simple cysts
Cysts with detached endocyst due to rupture
Cysts with daughter cysts
Densely calcified masses
Most common human parasitic infection
Causes peri-portal fibrosis and enlarged portal veins
Clinical features include:
Initially hepatomegaly, later contraction with portal hypertension
Sonographic Appearance:
Periportal fibrosis and calcification
Most common organism causing opportunistic infection in AIDS patients
Affects patients with bone marrow issues, organ transplants, or who are on chemotherapy
Opportunistic infection: Can cause serious complications due to weakened immune system
Affects hepatocytes and impacts liver function
Measured via liver function tests, specifically ALT levels
Damages hepatocytes, affecting liver enzyme function
Causes include infections, drugs, toxic chemicals, alcohol abuse, and obesity
Fatty infiltration
Acute and chronic hepatitis
Early alcoholic liver disease
Acute and chronic cirrhosis
Viral infections
Drugs and alcohol
Metabolic conditions (e.g., diabetes)
Autoimmune disorders
Transmission routes include fecal-oral, blood products, sexual contact, and transfusions
Types include Non-A, Non-B, and NANB hepatitis
Elevated liver function tests (LFTs): ALT, AST, Bilirubin
Increased WBC count
Presence of viral antibodies
Assess for parenchymal changes
Determine presence of hepatomegaly
Rule out biliary obstruction
Establish baseline liver and spleen size
General parenchymal changes
Decreased echogenicity with accentuated brightness in portal triads
Gallbladder wall thickening
Possible edema
Primarily obesity
Other causes:
Alcoholic liver disease
Diabetes
Chronic illnesses
Steroid use
Pregnancy
Normal
Grade 1: Mild; portal veins still visible
Grade 2: Moderate; portal veins not visible
Grade 3: Severe; significant attenuation with minimal portal vein visibility
Normal liver tissue mixed with fatty tissue
Can mimic mass lesions
Chronic damage leading to degradation of liver architecture
Liver function diminishes, potentially leading to failure
Causes include:
Alcohol
Chronic hepatitis
Drugs
Biliary obstruction
Cardiac diseases
Metabolic/storage diseases
Symptoms include jaundice, hepatomegaly, and ascites
Variable based on disease stage;
Initially large, later small right lobe with prominent caudate and left lobe
Coarse echotexture
Surface nodularity (often seen with ascites)
Loss of intrahepatic vasculature delineation
Decreased amplitude of phasic oscillations
Narrowed hepatic veins with high-velocity areas and turbulence
Splenomegaly
Ascites
Portal vein hypertension and thrombosis
Collaterals (recanalized umbilical vein)
Possible development of HCC (hepatocellular carcinoma)
Couinaud’s Segment I
Typically spared or hypertrophied in cirrhosis
Has its own blood supply
Falciform ligament houses umbilical vein, carries maternal blood to fetal liver
Ligamentum teres is the obliterated umbilical vein remnant
Intrahepatic: Caused by cirrhosis
Extrahepatic: Caused by thrombosis of portal or splenic veins
In Children: Thrombosis due to umbilical vein catheterization, omphalitis, or sepsis
In Adults: Trauma, HCC, or sepsis
Splenomegaly
Ascites
Recanalized umbilical vein
Porto-systemic venous collaterals
Reverse flow on Doppler (hepatofugal)
Determine direction of flow
Evaluation challenges for ill patients with ascites or contracted livers
Major sites include:
Gastroesophageal junction
Paraumbilical veins
Splenorenal and gastrorenal veins
Intestinal-retroperitoneal veins
Hemorrhoidal veins
Commonly associated with malignancies (e.g., HCC, pancreatic cancer)
Echogenic thrombus within the portal vein lumen
Increased diameter of portal vein (>13 mm)
Presence of collateral channels, indicating alternate pathways due to blockage
Collateral channels develop in chronic portal vein obstruction
Diagnosed by visualization of extrahepatic portal veins not present
Occlusion of some or all hepatic veins and inferior vena cava (IVC)
Can result from:
Chronic leukemia
Trauma (e.g., extension from HCC, RCC)
Pregnancy
Congenital anomalies
Coagulation abnormalities
Hepatic vein occlusions
Enlarged, bulbous liver
Possible infarcted liver areas
Ascites presence
Intrahepatic collateral formations
Redirects blood flow from collaterals to reduce pressure on hepatic veins and treat varices or refractory ascites
TIPS: Transjugular Intrahepatic Portosystemic Shunt
Warren Shunt: Distal spleno-renal
Portal Caval and Mesocaval Shunts
Typically placed between portal vein and hepatic vein to manage complications of portal hypertension
Assess patency of shunt
Identify stenosis or occlusion
Determine direction of flow in stent
Evaluate flow direction in portal and hepatic veins
PSV (Peak Systolic Velocity) between 135-200 cm/sec
Potentially turbulent flow
Hepatofugal flow patterns in right/left portal veins (abnormal)
No flow indicates possible thrombus or occlusion
PSV <90 cm/sec or >200 cm/sec indicates critical issues
Changes in velocity by >50 cm/sec may indicate a problem
Cavernous hemangioma (most common)
Focal nodular hyperplasia (FNH)
Lipoma
Angiomyolipoma
Often asymptomatic
Most common benign liver lesion
More prevalent in women (5:1 ratio)
Sonographic Appearance:
Small (<3 cm), well-defined, homogeneous, hyperechoic, extremely slow blood flow
Second most common benign liver mass
Hormonal stimulation may be a contributing factor
Generally asymptomatic
Sonographic Appearance:
Solitary with central scar
Majority <5 cm
May displace normal vessels
Useful Doppler assessment for vessels
More common in women in childbearing years
Associated with oral contraceptives and glycogen storage diseases
Symptoms can range from asymptomatic to RUQ pain
Similar US appearance to FNH but less common
Varies in size and composition
Can present as round/oval, well-defined borders, homogeneous, and echogenic
Rare benign mass, isolated and asymptomatic
Sonographic Appearance:
Well-defined, echogenic; CT shows fatty nature
Most common primary malignant liver tumor
Strongly associated with cirrhosis (especially in the USA)
Increased levels of alpha-fetoprotein (AFP)
Clinical Factors:
50-60% of cirrhotic patients develop HCC
Often solitary, multiple, or diffuse
Later stages present with:
Elevated AFP levels
RUQ pain
Weight loss
Ascites
Laboratory values confirmed presence of AFP
Most common primary liver tumor in children
Associated with Beckwith-Weidemann syndrome and hemihypertrophy
Sonographic Appearance:
Single, large solid mass with mixed echogenicity
18-20 times more common than primary liver tumors
Detection significantly alters prognosis
25-30% of liver cancer patients also have metastatic disease
Colon
Stomach
Pancreas
Breast
Lung
Gallbladder
Hyperechogenic = Hepatocellular carcinoma (HCC)
Hypoechoic = breast, lung cancers, lymphoma
Target or bull's-eye = often seen with lung cancer
Mixed or cystic lesions = may indicate complex pathology
Can involve hematoma, lacerations, free fluid, contusions, active bleeding, or ruptured capsule
Most common site affected is the posterior segment of the right lobe
Most frequent indications:
Hepatitis C
Alcoholic liver disease/cirrhosis (post-recovery)
Biliary cirrhosis
Sclerosing cholangitis
Contraindications for Liver Transplantation:
Compensated cirrhosis
Extrahepatic malignancy
Cholangiocarcinoma
Active untreated sepsis
Advanced cardiopulmonary disease
Active alcoholism/substance abuse
Anatomical abnormalities
Hepatic Artery: Anastomosis occurs between donor's and recipient's blood vessels
Portal Vein: End-to-end connection between donor and recipient
IVC: End-to-end connections above and below the liver
Biliary complications:
Stricture
Thrombosis
Sclerosing cholangitis
Hepatic artery complications:
Stenosis, thrombosis
Portal vein complications:
Stenosis or thrombus formation
Collections:
Abscess vs. infarct
Ascites
Tardus Parvus: Aliasing with high peak, distorted waveforms
Can lead to ischemia of the liver due to reduced blood supply
Right hepatic vein divides the right lobe into segments
Reidel’s lobe: A tongue-like projection of the right lobe
Patent umbilical vein found in the left lobe of the liver
Useful liver lab values: AST, ALT
Caudate lobe (Couinaud’s Segment I) has its own blood supply
Left lobe segment landmarks: Segment I (caudate), II (superior lateral), III (inferior lateral), IVa (superior medial), IVb (inferior medial)
Right lobe segment landmarks: Segment V (inferior anterior), VI (inferior posterior), VII (superior posterior), VIII (superior anterior)
Landmarks dividing the right and left lobes seen on ultrasound: Middle hepatic vein, imaginary line from gallbladder to IVC
Three landmarks for left lobe segmentation:
Left hepatic vein
Left portal vein
Ligamentum teres
Landmarks showing caudate lobe area:
Anterior (ligamentum venosum)
Posterior (IVC)
Inferior (porta hepatitis)
Alcohol
Drugs
Ischemia
Viral infections
ALT
AST
Bilirubin
Candidiasis appears as a “wheel within a wheel” on ultrasound.
Hydatid disease
Pneumocystis carinii
Obesity
Alcohol
Drugs
Hepatitis
Biliary obstruction
Cardiac/metabolic diseases
Caudate lobe sparing and hypertrophy
Exhibits narrowing and aliasing
Splenomegaly
Ascites
Portal vein hypertension and thrombosis
Collaterals (including recanalized umbilical vein)
Possible development of HCC
Cirrhosis
Portal vein thrombosis
Hepatofugal flow indicated on Doppler studies.
Identified as the ligamentum teres remnant
Known as Budd Chiari Syndrome
Specifically between the portal vein and the hepatic vein
Assess patency, stenosis, occlusion, and flow direction
Approximately 135 to 200 cm/sec
Cavernous hemangioma
Appearance: Small, well-defined, homogeneous, hyperechoic, and extremely slow blood flow
Focal Nodular Hyperplasia (FNH)
Hepatic adenoma
Cirrhosis
Tardus parvus pattern.