Liver pathology Flashcards
Haemangioma
Now called venous malformations
Most common benign vascular liver lesion
Much more common in females 5:1
They are rarely seen in young children, but infantile hepatic haemangioma is the most common, benign hepatic vascular tumour in infants.
Appearance: Hyperechoic, well defined, CD peripheral feeding vessels, CEUS arterial phase peripheral nodular discontinuous enhancement, portal venous and delayed phases: continued “filling in” of the lesion, until the entire haemangioma is hyperechoic relative to background liver
A peripheral location within the liver is most common
Symptoms:
Mostly asymptomatic
Outcome:
Benign
6 month follow up/ CT or MRI confirmation
Differential diagnosis:
Focal hepatic steatosis
Hepatic metastases
HCC
Adenoma
Benign generally hormone induced, predilection for haemorrhage
Appearance:
Solitary, well-demarcated, heterogeneous, hypo halo FFS often seen, large 5-15cm, sub capsular location RLL, CEUS arterial phase-hypervascular same as FNH, portal venous/delayed phase- centripetal filling (opposite to FNH-centrifugal filling)
Symptoms/cause:
Asymptomatic until rupture resulting in abdominal pain
Rapid bleeding into peritoneal cavity can sometimes lead to massive exsanguination and death
Oral contraceptive
Men
Obesity
Metabolic syndrome
Outcome:
Complications- rupture
Rarely degenerate into HCC in men
Generally resected
Differential diagnosis:
HCC
Fibrolamellar HCC- radiating central scar, more often calcification and lymph node enlargement
FNH- T2 bright central scar with late enhancement
HCC
Most common primary malignancy of the liver
2nd in children after hepatoblastoma
Strongly associated with cirrhosis
5th most common cancer in the world
3rd most common cancer-related death (lung/stomach)
Increase is attributed to rise of Hep C rates
Appearance:
Small focal hypoechoic
Larger lesions heterogeneous due to fibrosis, fatty change, necrosis and calcification
Peripheral hypo halo
Diffuse HCC may be difficult to visualise
CEUS- arterial phase neovascularity
Portal venous decreased echogenicity relative to liver
Tumour thrombus may be visible
Symptoms/Causes: Jaundice Portal hypertension Hepatomegaly Haemorrhage from tumour Often late middle age 65YO average Men 75% Hep B Hep C Alcoholism Biliary cholangitis Food toxins Congenital biliary atresia Haemachromatosis Obesity/diabetes
Outcome:
If small resection is possible
Up to 2/3 of liver can be resected due to regeneration
Transplant
Chemo/TACE/Thermal Ablation/SIRT
If resectable then 5year survival ~45%
Mets occur late with a poor prognosis- lung, adrenal, lymph nodes, bone
Differential diagnosis:
Hypervascular Hepatic Mets
FNH
Hepatic adenoma
Fibrolamellar Hepatocellular Carcinoma
Histological variant of HCC
Different demographic and risk factors to HCC
Often don’t produce AFP
Appearance: Variable appearance Hepatomegaly as masses usually large CEUS- arterial phase heterogeneous Portal venous decreased echogenicity compared to liver
Symptoms/Cause: Non specific symptoms Occasionally gynaecomastia Young adults (20-40YO) No gender predilection No association with cirrhosis, alcoholism or Hep B/C
Outcome: Less aggressive than HCC but due to lack of symptoms often becomes sizeable Usually advanced at presentation Resection usual with 5year 76% If unresectable it is usually fatal
Differential diagnosis: HCC FNH Hepatic Adenoma Hepatic Mets
Portal hypertension
Hepatic venous pressure gradient (HVPG) greater than 5 mmHg
Prehepatic causes: Portal vein thrombosis Extrinsic compression of PV Congenital PV stenosis Arteriovenous fistula SVC obstruction (downhill varices)
Hepatic/Sinusoidal causes: Cirrhosis Viral hepatitis Schistosomiasis Congenital hepatic fibrosis Polycystic liver disease Nodular regenerative hyperplasia Idiopathic portal hypertension
Posthepatic causes: Budd-Chiari syndrome Sinusoidal obstruction syndrome Congestive cardiac failure Constrictive pericarditis
Subtypes:
Sinistral portal hypertension
Appearance: Dilated PV >13mm non-specific Biphasic or reverse flow PV Recanalisation of paraumbilical vein- pathognomonic Portal-systemic collateral pathways Splenomegaly Ascites
Complications
Ascites
Oesophageal/gastric varices
Hepatic encephalopathy
Symptoms:
Outcome:
Lifestyle change- sodium restriction
Medication for varices, diuretics for ascites
Interventional procedure TIPS (Transjugular Intrahepatic Portosystemic Shunt), balloon hepatic vein, splenic artery embolisation, liver transplant
Differential diagnosis:
Immune response can lead to splenic vein dilatation at splenic hilum with splenomegaly
Metastases
18-40 times more common than primary liver tumours
Multiple post-contrast CT or MRI are necessary
Most common primaries: GI tract via portal circulation Breast Lung Genitourinary Melanoma Sarcomas Adrenocortical carcinomas Essentially all metastatic solid malignancies Testicular
Appearance:
Wide range of appearances and with fatty livers definitive statements are difficult
Rounded/well-defined
Positive pass effect-vessel distortion
Hypoechoic 65%
Hypo halo
Possibly cystic, calcified, infiltrative and echogenic
CEUS- distinguishes between hyper and hypovascular lesions
Symptoms/causes: Usually asymptomatic Found in work up of malignancy which presented in other ways If large metastatic burden- localised pain due to capsular stretching disordered liver metabolic function ascites low-grade fever Demographic mirrors underlying primaries Increase in age
Outcome:
If from colorectal adenocarcinoma, hepatic metastasectomy is possible with 20% disease free
Transarterial chemo or radioembolisation are other options
MRI guided adaptive radiation therapy is new
Differential diagnosis: Haemangioma Cysts HCC FNH Adenoma Transient Hepatic Attenuation Differences (THAD) FFS
Focal Nodular Hyperplasia
Regenerative mass lesion- second most common benign liver lesion
Associated with: Haemangiomas Hereditary haemorrhage telangiectasia AVM Anomalous venous drainage Congenital absence of PV/atresia Budd-Chiari syndrome Portal hypertension
Appearance:
Usually solitary
Some well marginated, some isoechoic
When seen usually contains central scar with peripheral vascular displacement- only in 20%
CEUS- early arterial phase- enhanced, centrifugal filling, prominent feeding vessel
Late arterial- centrifugal filling- opposite to haemangioma and adenoma
Portal venous phase- sustained enhancement as opposed to adenoma, unenhanced scar may be present
Symptoms/causes:
Asymptomatic typically
Mass effect causing RUQ pain 20%
Uncommon to rupture
Most frequently found in young to middle aged adults
Only 15% in men
Exogenous oestrogen does not cause FNH or increase size
Outcome: Benign No malignant potential Minuscule risk of complication Require no treatment
Differential diagnosis: Adenoma HCC FL HCC Hypervascular hepatic mets Hepatic haemangioma Intrahepatic cholangiocarcinoma
Focal Fatty Sparing
Localised absence of increased intracellular hepatic fat, in a liver otherwise fatty in appearance i.e. diffuse hepatic steatosis
Appearance:
Usually adjacent to vessels, gallbladder and falciform ligament
May be found adjacent to metastases
Absence of mass effect
CEUS- varied in arterial phase, is-enhancement most common
Portal venous and late phase- never demonstrates washout, remains iso to surrounding liver
Symptoms:
Asymptomatic benign phenomenon
May be symptomatic from fatty liver
Outcome:
When not related to hepatic focal mass, prognosis is diffuse hepatic steatosis
Differential diagnosis:
HCC
Metastases
Hepatic Hydatid Cyst
A parasitic zoonosis caused by the Echinococcus tapeworm. In the liver, two agents are recognised as causing disease in humans:
Echinococcus granulosus
Echinococcus multilocularis
Appearance:
Septated cyst with daughter cysts and echogenic material between the cysts
CT better at visualising
Symptoms: Lump in RUQ 88% Ascites 6% Right epigastric pain 38% Jaundice 12% Splenomegaly Fever
Outcome: Complicated by rupture into: biliary tree peritoneal space bloodstream lung Sometimes sample of cyst taken for presence of tapeworm Blood tests to check immune response to parasite
Differential diagnosis:
Simple cyst if hard to visualise
Secondary Hepatic Involvement with Lymphoma
Common
More common in non-Hodgkin lymphoma 20% to 5%
Appearance: Liver is normal in ~25% of cases Features are non-specific Well-defined small nodular hypo lesions (occasionally may be a target lesion) Diffuse infiltrative disease Hepatomegaly 30% Splenomegaly Abdominal lymphadenopathy
Symptoms: Hepatomegaly Deranged LFTs Jaundice Rarely acute liver failure Systemic symptoms of fever, night sweats, and weight loss.
Outcome:
Chemo dictated by histological subtype
Differential diagnosis:
Primary hepatic lymphoma (rare)
Cirrhosis
Common endpoint of many chronic liver disease processes causing hepatocellular necrosis
Appearance:
Hypertrophy of the caudate lobed lateral segments of the left lobe 2/3 with concomitant atrophy of posterior segments 6/7 of the right lobe
Surface nodularity
Overall coarse and heterogeneous echotexture
Signs of portal hypertension:
enlarged PV >13mm
Slow PV flow <15cm/s
Reversal or to and fro PV flow
PV thrombosis
Enlarged SMV and splenic vein >10mm measured during deep inspiration
Recanalisation and hepatofugal paraumbilical venous flow
Portalisation of hepatic vein waveform
Hepatic arteries corkscrew appearance
Splenomegaly
Ascites
Fatty change
Sonoelastography- >7kPa advanced fibrosis
12.5-15kPa cirrhosis
CEUS diminished mean hepatic venous transit time is similar to that of perfusion CT
Symptoms/Causes: Liver failure Alcoholism Viral hepatitis from IV drug use Cryptogenic/ NASH Biliary disease PSC Cystic fibrosis
Complications:
Portal hypertension
HCC
Outcome:
6 month- 1 year ultrasound surveillance scans
IR very helpful treating portal hypertension and complications- TIPS, chemoembolisation or radio frequency ablation of HCC
Differential diagnosis:
Wide spread liver metastases
Budd Chiari syndrome particularly chronic
Hepatic sarcoidosis
Acute Hepatitis
Acute hepatitis is a general term encompassing diffuse hepatocyte injury with resulting inflammatory change- may affect whole liver or portions
Occurs when liver suffers an injury resulting in inflammatory response
Requires a clinical diagnosis and a normal appearance on ultrasound does not exclude it
Appearance:
Hepatomegaly (most sensitive sign)
Starry sky appearance- poor sensitivity and specificity
Gallbladder wall thickening- may be more Hep A
Periportal oedema
Accentuated brightness of PV radicle walls
Colour doppler normal
Overall echo texture usually decreased
Symptoms/Causes: Fever Abdominal pain Jaundice Raised AST, ALT, GGT High temperature Feeling/being sick
Viral hepatitides (HAV, HCV, HBV)- acute distinguished from chronic by duration and differing histopathological injury patterns Parasites Drug/toxin induced Autoimmune Steotohepatitis Metabolic disease
Outcome:
Depends on aetiology
Potential liver failure through cirrhosis, HCC
Differential diagnosis:
Simple Cyst
Appearance:
Symptoms:
Outcome:
Differential diagnosis:
