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The Liver Metastases

The Liver Metastases

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Published by Caren Chan

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Published by: Caren Chan on Mar 20, 2011
Copyright:Attribution Non-commercial


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HEPATIC METASTASESThe liver receives blood via the hepatic artery and portal vein. The hepatic arterycarrier arterial blood, whereas the portal vein drains venous blood from the GI tract and other parts of the splanchnic area. The dual blood supply makes hepatic infarcts uncommon exceptin hepatic surgery, affecting the hepatic vasculature. Portal and hepatic venous flow isessential for normal hepatic function. The acinus is the basic unit function. The hepaticlobule consists of plates of liver parenchymal cells acquires a classic hexagonal lobule. TheKupffer cells anchor to the vessel walls by pseudopodia, while platelets adhere to Kupffer cells; designed to trap foreign material from blood passing through the sinusoid. The space of Disse is the space subjacent to the endothelial cells. Circulating tumour cells, emboli enteringthe sinusoids or both appear to be physically obstructed by the Kupffer cells; or else theybecome lodge in the portal venous branches if tumour emboli are large.Malignant tumours in the liver is classified as primary (cancers that originate in theliver) or metastatic (cancers which spread to the liver from an extrahepatic primary site). Thetrue prevalence of metastatic liver disease is unknown because most data derive fromautopsies reflect the end-stage of a disease process. Depending on the site of the primarytumour, 30-70% of patients dying of cancer have liver metastases.
The most commontumour seen in the liver is metastatic colorectal cancer.The liver provides a fertile soil in which metastases may become established, not onlybecause of rich, dual blood supply but also because of humoral factors that promote cellgrowth. The fenestrations in the sinusoidal endothelium allow a foothold into the space of Disses for tumour emboli arriving via the blood stream.
Tumour emboli entering thesinusoids through the liver¶s blood supply appear to be physically obstructed by the Kupffer cells, but if tumour emboli are large, this may lodge in the portal venous branches.The presence of stasis-damaged endothelium and normally fenestrated endothelium isconducive to the implantation of tumour emboli. Access to underlying collagen in the spaceof Disse provides attachment points for cancer emboli at the sinusoid, but not all of thesecells progress to develop liver metastases. The fenestration in the sinusoidal lining aids incancer implantation.
The liver is the second most commonly involved organ by metastatic disease, after thelymph nodes. A focal liver lesion deposition in the liver may be the site of metastasis fromvirtually any primary malignant neoplasm, but the most common primary sites are the eye,colon, stomach, pancreas, breast, and lung. In children, the most common liver metastases arefrom a neuroblastoma, a Wilms tumor, or leukaemia.Several factors influence the incidence and pattern of liver metastases such as age,sex, primary site, histologic type, and duration of the tumour. Colonic carcinoma, carcinoid,and hepatocellular carcinoma (HCC) are the common metastasis confined to the liver. Other tumours which metastasize to the liver are breast and lung cancers, spread to other sites at thesame time.Most liver metastases are multiple. In 77% of patients with liver metastases, bothlobes are involved, in only 10% of cases is metastasis solitary. Multiple tumours often vary insize; suggesting that tumour seeding occurs in episodes. Growing metastases compressadjacent liver parenchyma, causing atrophy and forming a connective tissue rim.Approximately 50% of the patients with liver metastases have clinical signs of hepatomegalyor ascites, liver function tests tend to be insensitive and nonspecific.The destruction of liver tissue by cancer cells and their metastases is contributed by avariety of proteinases from the cancer cells. The main factors which enables tumour cellsliver invasion are: (1) the tendency to retain a round shape, (2) the adhesiveness of differenttypes of tumour cells and to adhere to hepatocytes, (3) the inability of some tumour cells tosurvive and proliferate in the bloodstream for long periods, (4) the pressure on thesurrounding tissues, (5) the formation of tumour cell and hepatocyte junction, (6) tumour celllocomotion, and (7) host tissue destruction by enzymes elaborated by tumour cells.The pathologic-anatomic characteristics of metastases resemble that of the primarytumour. They often have the same degree of vascularity as that of primary tumour. Mostmetastases are hypovascular, whereas hypervascular metastases are seen in primary tumours.Blood flow is said to increase relative to the normal parenchyma in all metastases, evenhypovascular tumours. Large metastases tend to displace the surrounding vessels, and maycompress or occlude the portal venous branches. Large metastases often outgrow their bloodsupply, causing hypoxia and necrosis at the centre of the lesion.
Metastatic tumours of liver may be expansive or infiltrative. They vary in size, shape,vascularity, and growth pattern in accordance in blood supply, haemorrhage, cellular differentiation, fibrosis, and necrosis. Metastatic carcinoma of the breast and pancreas incitean intense fibrous or sclerosing reaction around the tumour acini, leading to fibrous scar formation. Tumour thrombi occlude the portal vein, the hepatic vein, or both. In the presenceof mucin secretion, necrosis, and phosphate activity, metastases may develop calcificationwhich is detectable radiographically.
 The blood supply patterns of the liver metastases are of considerable clinicalimportance because a number of diagnostic and therapeutic approaches depend on the degreeof neovascularity and the source and type of the blood supply. Some focal lesions may besurgically resectable or treated by means of ablation techniques and several minimallyinvasive techniques. These treatments have been successful, especially in treating colorectalcancers, for which hepatic resection may offer potential cure. Chemotherapy is now a feasibleoption in patients with more extensive disease. However, it has little success in treating of liver metastases from the breast, lung, or pancreas due to their presence at the time of diagnosis.
Imaging plays a vital role in the diagnosis of liver metastases and in theassessment of the response to treatment. The recognition of a liver lesion as a metastaticfocus may significantly influence the patient¶s treatment and prognosis. Many patients die of cancer as a result not only of metastases but also recurrence of their primary tumour andtreatment with cytotoxic drugs.Over 50% of patients diagnosed with colorectal cancel will develop hepaticmetastases during their lifetime. Resection for metastatic colorectal cancer to the liver shouldbe performed only for fewer than four metastases, technically.
Improved chemotherapeuticregimens and surgical techniques produced aggressive strategies for the management of thisdisease. Many groups now consider volume of future liver remnant and the health of theliver, and not actual tumour number, as the primary determinants in selection for an operativeapproach.
Therefore, resectability is indicative for what will remain after resection.
 Use of neoadjuvant chemotherapy, portal vein embolization, two-stage hepatectomy,simultaneous ablation, and resection of extrahepatic tumour in selected patients haveincreased the number of patient eligibility for a surgical approach.
Studies has shown anacceptable 5-years survival rates in the 20-40% range for resection of hepatic metastasesfrom breast, renal, and other GI tumours.

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