The use of duplex sonography in the detection of colorectal hepatic metastases

Abstract

Summary Conventional imaging techniques are of limited value in identifying small liver metastases. Indirect methods of measuring blood-flow have shown that metastases may be associated with subtle changes in liver blood-flow. Doppler ultrasonography has the ability to measure liver blood-flow directly. In this study, the role of duplex sonography in the detection of hepatic metastases was evaluated. Hepatic arterial and portal venous blood-flows were In 1983, Parkin and colleagues suggested that changes in liver blood-flow occurring in patients with intra-hepatic tumour could be measured indirectly by dynamic scintigraphy. They described an increase in the ratio of hepatic arterial: total liver blood-flow in patients with overt hepatic metastases. However, this technique has not been widely used in clinical practice because of difficulties in interpretation and reproducibility (Laird et al., 1987).In contrast, duplex sonography has the capacity to measure liver blood-flow directly. In this study, the crosssectional area and velocity of blood-flow within the hepatic artery and portal vein were measured and blood-flow calculated. This technique is less invasive, independent of hepatic function and can be more readily standardised.The aim of this study was to assess the value of duplex sonography in the detection of colorectal liver metastases. StatisticsThe data were analysed using a Mann-Whitney test.

Splanchnic blood flow changes in the presence of hepatic tumour: evidence of a humoral mediator

“…This occurred both in patients with overt metastases and in those who, despite having an ostensibly normal liver at the time of primary surgery, manifested hepatic tumour within 1 year of follow-up. We have recently confirmed these findings using the more direct and quantitative technique of duplex ultrasonography (Leen et al, 1991;1993a).…”

“…This occurred both in patients with overt metastases and in those who, despite having an ostensibly normal liver at the time of primary surgery, manifested hepatic tumour within 1 year of follow-up. We have recently confirmed these findings using the more direct and quantitative technique of duplex ultrasonography (Leen et al, 1991;1993a).The mechanisms underlying this effect are unknown. Liver metastases derive their blood supply predominantly from the hepatic artery (Breedis & Young, 1954), and initially it was assumed that the primary change was an increase in hepatic arterial flow to meet demand from rapidly growing tumour tissue.…”

“…Liver metastases derive their blood supply predominantly from the hepatic artery (Breedis & Young, 1954), and initially it was assumed that the primary change was an increase in hepatic arterial flow to meet demand from rapidly growing tumour tissue. Quantitative flowmetry has confirmed that hepatic arterial flow is increased, but has shown that a substantial reduction in portal venous blood flow also contributes to the elevation of the perfusion index (Leen et al, 1991). Experiments in rat liver tumour models have demonstrated a similar rise in the HPI that is due entirely to reduced portal venous inflow secondary to increased splanchnic vascular resistance (Nott et al, 1989;Hemingway et al, 1991;1993).…”

“…Whether this is a tumour product or an endogenous agent remains unclear, and we are currently undertaking further studies to identify it. The haemodynamic changes underlying the increase in the HPI in patients with liver metastases consist of both a reduction in portal venous blood flow and an increase in hepatic arterial flow (Leen et al, 1991). The latter feature does not appear to be reproduced in experimental models for reasons that are unknown.…”

Contrast‐Enhanced Doppler Perfusion Index

“…t is known from experimental animal studies [1][2][3] and clinical patient studies [4][5][6][7][8][9] that the presence of even microscopic liver metastases is associated with changes in hepatic hemodynamics. The mechanism is not clear, although changes have been shown to originate from the early nonvascular phase of the metastases 3 and may be mediated by circulating vasoactive agents as a response to neoplastic growth.…”