Absent arterial flow in all arteries on a technically adequate Doppler imaging study is nearly always indicative of thrombosis. False positives may occur due to severe hepatic edema, systemic hypotension, or in a suboptimal ultrasound study. Reduced flow, whether secondary to spasm or to low cardiac output, can also cause non visualization of flow at Doppler US. A loss of diastolic flow or diastolic flow reversal has been suggested as a sign of impending thrombosis [5, 6], especially if it occurs in the main HA.

Microbubble contrast material-enhanced US may help to improve flow visualization in the HA [7]. In patients in whom no flow is identified in the HA, angiography, computed tomography (CT), or magnetic resonance (MR) angiography are usually required to definitely diagnose thrombosis. The treatment of HA thrombosis usually consists of emergent thrombectomy or retransplantation.

HA stenosis occurs in 2–11 % of transplantations [8, 9]. The most common site of stenosis is the anastomosis, which is often difficult to detect by US, being frequently obscured by bowel. In the very early postoperative period (<72 h after transplantation), increased HA RI (>0.8) is frequently observed, although it usually returns to normal within a few days [10]. Increased RI is associated with fibrotic livers and a prolonged period of ischemia [10]. HA stenosis may be treated with percutaneous angioplasty or surgical intervention [11].

HA pseudoaneurysm is an uncommon complication and can be classified as either extrahepatic or intrahepatic. Extrahepatic pseudoaneurysm most commonly occurs at the arterial anastomosis or arises as a complication of angioplasty, whereas intrahepatic pseudoaneurysm may result from percutaneous biopsy, biliary procedures, or infection [12, 13].

A pseudoaneurysm is identified on US as a cystic structure in communication with the HA with a disorganized ‘‘to and fro’’ color and spectral Doppler pattern as the arterial blood flows into and out of the pseudoaneurysm (Fig. 10.9).

US detection of a fluid collection near the arterial anastomosis requires further evaluation with pulsed Doppler US to rule out pseudoaneurysm. Contrast-enhanced CT demonstrates a focal lesion with central enhancement that follows arterial blood-pool attenuation. Treatment consists of embolization for both types of aneurysms, as well as stent placement or surgical resection for an extrahepatic pseudoaneurysm [13, 14]. A ruptured intrahepatic pseudoaneurysm can lead to a portal or biliary fistula.

Intrahepatic arterioportal fistula is usually secondary to liver biopsy of other invasive procedures. On US, the inflowing hepatic arterial RI will be lower than the contralateral normal vessel on the opposite side. In addition, reversed flow in particular portal vein (PV) radicals (considered a rare finding), arterialized PV waveform as well as a focus of turbulence with aliasing at the site of the arterioportal fistula can also be seen [12, 15–17].

In orthotopic whole LT, the PV anastomosis is usually performed in an end-to-end fashion between the donor and the recipient portal trunks (Fig. 10.10). In split grafts, the anastomosis is usually performed between the donor and recipient right or left portal branches. In the case of preoperative PV thrombosis and/or portal hypoplasia, PV thrombectomy (Fig. 10.11) and anastomosis on different recipient sites are possible solutions. In this latter case, the anastomosis can be performed on enlarged tributaries of the PV, on the superior mesenteric vein through a donor vascular graft, on the left renal vein or on the recipient inferior vena cava (IVC) (cavoportal hemitransposition). PV complications are less common than arterial complications. They occur in 1–13 % of whole transplantations, and include thrombosis and stenosis [18]. Technical errors, insufficient thrombectomy, discrepancy between the sizes of the donor and recipient PVs, hypercoagulable state, and insufficient flow due to spontaneous portosystemic shunts are the main causes of complications [18]. Intraoperatively, a scarce portal flow can be increased with ligation of collaterals of PV or of the left renal vein, in order to reduce the flow through portosystemic shunts. Postoperatively, angioplasty, thrombolysis, thrombectomy, redo anastomosis or retransplantation can be required.

In split LT, the use of small-for-size grafts (especially left-sided grafts) is often associated with liver congestion and dysfunction. This condition is attributable to excessive portal flow in relationship with the reduced hepatic mass, causing endothelial disruption, and secondarily parenchymal injury with cholestasis. The portal flow can be reduced with splenic artery ligation, splenectomy, or creation of a hemi-portocaval shunt (Figs. 10.12, 10.13, 10.14).