Fig. 16.33 Acutepassivecongestion(“nutmegliver”).(A)Thecutliversection,inwhichmajorbloodvesselsarevisible,isnotableforavariegatedmottledredappearance,representingcongestionandhemorrhageinthecentrilobularregionsoftheparenchyma.(B)Onmicroscopicexamination,thecentrilobularregionissuffusedwithredbloodcells,andatrophiedhepatocytesarenoteasilyseen.Portaltractsandtheperiportalparenchymaareintact.
Circulatorydisordersofthelivercanbecausedbyimpairedbloodinflow,defectsinintrahepaticbloodflow,andobstructionofbloodoutflow.
Portalveinobstructionbyintrahepaticorextrahepaticthrombosismaycauseportalhypertension,esophagealvarices,andascites.
Themostcommoncauseofimpairedintrahepaticbloodflowiscirrhosis.
Obstructionsofbloodoutflowincludehepaticveinthrombosis(Budd-Chiarisyndrome)andsinusoidalobstructionsyndrome,previouslyknownasveno-occlusive disease.
Hepatic masses come to attention for a variety of reasons. They may generate epigastric fullness and discomfort or be detected by routine physical examination or radiographic studies for other indications. Hepatic masses include nodular hyperplasias and true neoplasms.
Solitary or multiple hyperplastic hepatocellular nodules that may develop in the noncirrhotic liver are called focal nodular hyperplasias. These lesions arise from local alterations in hepatic parenchymal blood supply, such as arteriovenous malformations or inflammatory or posttraumatic obliteration of portal vein radicles and compensatory augmentation of arterial blood supply.
MORPHOLOGYFocal nodular hyperplasia appearsasawell-demarcated,poorlyencapsulatednoduleranginguptomanycentimetersindiameter(
Fig.16.34A ).Itpresentsasamasslesioninanotherwisenormalliver,mostfrequentlyinyoungtomiddle-ageadults.Typically,thereisacentralgray-white,depressedstellatescarfromwhichfibrousseptaradiatetotheperiphery(see
Fig.16.34B
Fig. 16.34 Focalnodularhyperplasia.(A)Resectedspecimenshowinglobu-latedcontoursandacentralstellatescar.(B)Low-powerphotomicrographshowingabroadfibrousscarwithmixedhepaticarterialandbileductele-mentsandchronicinflammationwithinhepaticparenchymathatlacksnormalarchitectureduetohepatocyteregeneration.
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Microscopically,thecentralscarcontainslargeabnormalvesselsandductularreactionsalongthespokesofscar.Avascularlesionisprobablytheinitiatinginsult,asitisbelievedthathypoperfusedparenchymacollapsestoproducethesepta,whereashyperperfusedregionsundergohyperplasia.Thehyper-plasticregionsarecomposedofnormalhepatocytesseparatedbythickenedsinusoidalplates.
Cavernous hemangiomas are the most common benign liver tumors (Chapter 10). The chief clinical significance of cavernous hemangiomas is that they must be distinguished radiographically or intraoperatively from metastatic tumors.
Benign neoplasms developing from hepatocytes are called hepatocellular adenomas (