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home - Liver - Liver Masses - Focal Nodular Hyperplasia Written by Dr Sebastian Zeki
Knowledge


Knows the epidemiology pathology clinical presentation and natural
history of benign tumours of the liver

Can define a programme of investigation and characterisation of
benign liver lesions including haemangioma focal modular
hyperplasia and adenoma

Skills
Demonstrates ability to make an appropriate differential diagnosis
Formulates appropriate plan of management
Behaviours
Recognises importance of the role of multidisciplinary team in
diagnosis and management

Also...

Knowledge


Understands the epidemiology risk factors pathology prevalence
and range of presentations of HCC

Knows the appropriate investigation and staging of the disease
Aware of treatment options including trans-arterial
chemoembolisation (TACE) radiofrequency ablation (RFA) local
ethanol injection

Appreciates the indications and contraindications of each and how
the most appropriate is selected Aware of surgical treatment options

Aware of role of surveillance and referral for specialist multidisciplinary management including liaison with oncology

Skills
Appreciates the indications and contraindications of each modality of
treatment and how the most appropriate is selected

Understands the process of selection of patients for liver resection or
transplantation

Behaviours
Appreciates Involvement of multi-disciplinary team in management
decisions close liaison with surgical radiology oncology and
pathology colleagues

Focal Nodular Hyperplasia

Normal bile ducts are absentBile ductules present (derived from hepatocyte metaplasia) The minimal microscopic criteria to diagnose FNH: Nodular architectureAbnormal vesselsBile ductule proliferation Nodules contain abnor-mally large portal tracts including large feeding arteries, portal veins, and bile ducts. Central stellate scar with inappropriately large, branched artery radiating to the periphery. Usually solitary (95 %), and <5 cm in diameter.Sharp margin,no capsule and may be pedunculated. Focal nodular hyperplasia(=solitary hyperplastic nodule, hepatic hamartoma, focal cirrhosis, hamartomatous cholangio-hepatoma, and hepatic pseudotumor.) ManagementLesions are usually stable- can enlarge with OCP and pregnancy.There is no evidence for malignant transforma-tion of FNH.If suspected, follow up at 3 and 6m and if stable, no further follow-up needed.OCP’s can usually continue but get follow-up imaging in 6-12m.No risk to pregnancy tho’ need close observa-tion. Resection may be prudent for large (>8 cm) FNH. Ultrasound — Variably hyper, hypo, or isoechoic. Central scar seen in 20 % onlyOnly doppler US can distinguish in FNH (art flow) from HA(venous flow)CT scan — No contrast: Isodense; Art phase: Hyperdense; venous phase: hypodense Central scar may also be present in the fibrolamellar variant of HCC.Technetium sulfur colloid scanning — Kupffer cells take this up; HA (no Kupffer cells) don’t.MRI — T1: Isointense T2: Isointense to slightly hyperintense mass- scar is hyperintenseGadolinium iv gives arterial enhancement therefore early hyperintensity Se:70%/Sp: 98%.Angiography —Spoked wheel appearance though rarely used Pathology:It is associated with HHT and and hepatic hemangiomas.Multiple FNH’s are assoc. with hemihypertrophy and vascular malformations (Klippel-Trénaunay-Weber syndrome)The use of OCPs is not required for the development of FNH but FNH may be responsive to oestrogens.Those on OCPs have larger, more vascular tumors, have more symptoms, and more haemorrhage or rupture.FNH is a hyperplastic (regenerative) response to hyperperfusion by anomalous acentral arteries.Sinusoids and Kupffer cells are present, (as opposed to hepatocellular adenoma (HA)).Lymphocyte infiltration, canalicular bile plugs, copper deposition, and feathery degeneration of hepatocytes may suggest cholestasis and/or an inactive cirrhosis.Irregular intimal fibrosis or hypertrophy of the media may be seen in large arteries and veins, at times even occluding the lumen.When present, portal veins are dilated and/or stenotic.Non-classical variants: Always contain bile ductular proliferation and lack acharacteristic central scar. Pathology Non-nodular architecture ; single, quite regular plates of hepatocytes separated by sinusoids fed directly by anoma-lous arteries.Risk of bleeding similar to hepatic adenoma. Symptoms — Usually asymptomatic.Laboratory testsMild transaminitis; Normal AFPImaging tests Written by Dr Sebastian Zeki Types:1. Telangiectatic type-often presents with multiple FNH.2. A mixed hyperplastic and adenomatous form-may be difficult to distinguish from HA due to its subtle vascular and bile ductular findings.3. FNH with cytologic atypia- resembles dysplasia of large cell type.

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