Size, Shape, Echotexture, and Contour

The measurement of liver diameters does not seem to be a significant parameter to specify and its use has been abandoned in general practice, as suggested by international guidelines (see also Chapter 3) [1]. It is preferable to give a general description of hepatic enlargement, and hypertrophy or hypotrophy/atrophy of segments/lobe that might influence the shape and general appearance of the liver. In general, although there might be some variability among different aetiologies, morphological signs of cirrhosis include hypotrophy/atrophy of the right liver lobe, and compensatory hypertrophy of the caudate and left lobe. At first glance the morphological appearance is sufficient usually to suggest cirrhosis, although a caudate to right liver lobe width ratio >0.65 using the main bifurcation of the portal vein (PV) as a landmark between the two lobes is more precise and has high accuracy in diagnosing an advanced fibrotic process (Figure 8.1) [2]. Other morphological signs are related to retraction and hypertrophy of different areas of the liver and include enlargement of the gallbladder fossa secondary to atrophy of the right liver lobe, medial segment of the left lobe, and hypertrophy of the caudate lobe; enlargement of the periportal space secondary to atrophy of the left lobe’s medial segments [3]; focal capsular retraction, which might be more pronounced in certain areas as it is observed eventually along the posterior margin of the liver adjacent to the right kidney and is known as ‘notch sign’ [4]; and areas of confluent fibrosis corresponding to wedge‐shaped areas with capsular retraction that might be seen in advanced cirrhosis.

One of the most common findings in CLD is the heterogeneity of liver echotexture as an expression of the backscattering of the ultrasound beam on uneven surface, secondary to inflammatory changes, fibrosis, and nodular regeneration. The heterogenic echotexture can vary from mild to very pronounced (‘coarse echopattern’), usually according to the severity of CLD (Figure 8.2). However, it is also of note that the underlying aetiology has an impact on tissue damage, inflammatory response, and distribution of fibrosis, and hence can influence the echotexture heterogeneity, as will be described later in this chapter. In addition, the inappropriate regeneration of the hepatocytes in response to tissue damage is associated with nodularities, which can be very subtle, more obvious, or sometimes so pronounced as to be confounded with a lesion of a different nature, requiring contrast imaging for differential diagnosis.

In normal conditions the margins of the liver are usually sharp, while in CLD and advanced cirrhosis they become rounded and the outline is typically irregular or even nodular (Figure 8.3). The hepatic veins and gallbladder contour irregularities are also very sensitive signs of CLD (Figure 8.4). It is of note that sometimes irregularities of the liver outline and parenchymal changes might be very subtle. The accuracy of ultrasound in detecting early stages and micronodular regeneration can be missed in about 30% of cases [5]. Along these lines, magnifying the liver surface with a high‐frequency transducer will highlight structural modifications and help to avoid false‐negative results (Figure 8.5) [1].

Echogenicity

The echogenicity of liver parenchyma refers to its brightness, a feature that is most commonly found and used to describe steatosis. Although the most common cause of steatosis is nutrition‐related lipid dysmetabolism, steatosis can also be found in different hepatopathies such as alcohol‐related liver disease, viral hepatitis [6], hemochromatosis, or be drug induced [7]. According to its ultrasound appearance, steatosis can be classified as grade I or mild, when liver echogenicity is more pronounced than the renal cortex but there is no or very mild attenuation of the ultrasound beam through the liver parenchyma; grade II or moderate, where fat‐induced attenuation reduces the visibility of the posterior segments and the contour of the hepatic veins and portal venous system; or grade III or severe, when posterior attenuation is so severe that the posterior segments of the liver and the outline of the diaphragm cannot be seen or are barely visible (Figure 8.6) [8, 9].

Hepatic steatosis can be diffuse, focal, multifocal, or have a very irregular and ill‐defined distribution named the ‘geographical’ pattern (Figure 8.7). Steatosis in some cases can be well defined as a single area or scattered throughout the liver and mimic neoplastic lesions, sometimes requiring second‐level imaging for diagnostic certainty. Nevertheless, a differential criterion between focal steatosis and a focal lesion is that steatosis never deforms the hepatic structures, in particular the liver capsule, bile ducts, and vasculature (Figure 8.8).

In cases of diffuse steatosis, there might be fat‐sparing areas that can be located anywhere in the liver parenchyma, but most typically near the PV bifurcation, sub‐capsular regions, or around the gallbladder and hepatic veins (Figure 8.9).

It should be borne in mind that increased echogenicity can also be secondary to fibrotic changes, which can be more diffuse or localised according to the underlying liver pathology. As will be further described, periportal and peribiliary fibrosis is typically characterised by peribiliary and perivascular hyperechoic thickening that might extend to the adjacent liver parenchyma.

Ultrasound Features of Portal Hypertension

Increased pressure in the portal venous system accompanies the structural changes of CLD, while haemodynamic factors subsequently contribute to its further progression. The gold standard for PH assessment in cirrhosis is measurement of the hepatic venous pressure gradient (HVPG) obtained by evaluating the difference between wedged hepatic venous pressure and free hepatic venous pressure by means of hepatic vein catheterisation. An HVPG ≥10 mmHg defines the threshold of CSPH, which is associated with the risk of clinical decompensation and onset of the most feared complications such as ascites, variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome [10–12]. However, HVPG is invasive, costly, implies risks, and is not widely available. Although more innovative methods such as elastography have been validated to non‐invasively assess CLD in its different stages (see Chapter 9), ultrasound also has an important role in the diagnosis of PH. In fact, not only can ultrasound highlight the presence of signs of CLD, but it can distinguish features that are in keeping with other chronic conditions suggesting an alternative diagnosis, distinguish features that are more specific of certain aetiologies, and evaluate the presence of PV thrombosis, which can be a cause of non‐cirrhotic PH as well as a complication of cirrhosis [10].

B‐Mode Signs of Portal Hypertension

Abundance of the accumulated fibrous tissue, nodular regeneration, and parenchymal distortion result in resistance to blood flow through the liver with increased pressure in the portal venous system and its tributaries.

The portal venous flow velocity decreases proportionally with the severity of PH, while its calibre often becomes wider (>13 mm) (Figure 8.10) [13, 14] as well as for the splenic and superior mesenteric veins (>11mm) [10].

It is of note that less commonly a normal or even slightly narrow PV can be found despite the severity of PH in cirrhosis (Figure 8.11). Increased pressure in the portal venous system leads to congestion of splanchnic organs such as stomach, bowel, gallbladder (Figure 8.12) and spleen (Figure 8.13) [15].

Splenomegaly is one of the most common signs of PH and its increase in size over time is described as a marker of PH progression. It is defined by a bipolar cranio‐caudal diameter > 13 and an anteroposterior diameter > 4 cm. In some individuals spleen morphology might differ being longer but thinner or shorter but wider. Under these circumstances measuring the area with a cutoff of > 45cm² to define splenomegaly might be of help. However, spleen size variability has been described among different CLD aetiologies and in 20–30% of cases it might be normal in size despite the presence of CSPH, especially in alcohol‐related liver disease [16, 17]. The presence of hyperechoic foci without acoustic shadowing, of a size of less than a millimetre, scattered throughout the splenic parenchyma can sometimes be seen in patients with both severe cirrhotic or non‐cirrhotic PH. These findings are remnants of focal splenic microhaemorrhages, histologically proven to be calcific‐fibrosiderotic nodules known as Gamna‐Gandy bodies. Magnetic resonance imaging (MRI) has been approved as the most sensitive imaging modality for the detection of these nodules due to their iron content (drop‐out signal in T1). Nevertheless, sonographic features are also quite typical (Figure 8.14) [18, 19]. Ascites can be one of the first signs of clinical decompensation in cirrhosis with severe PH (Figure 8.15). Nevertheless, in the presence of ascites other signs of advanced cirrhosis and PH should be looked for in patients with CLD, since intraperitoneal fluid might be the consequence of other pathologies such as heart failure, severe hypoalbuminemia, peritoneal carcinomatosis, renal failure, and serositis.

Colour Doppler Signs of Portal Hypertension

In normal physiological conditions portal blood has a constant monophasic or slightly biphasic hepatopetal flow. However, with the worsening of PH, portal vein velocity progressively and proportionally decreases (Figure 8.16a) and it might even become stagnant (Figure 8.16b), with a high risk of thrombosis, or be completely inverted to hepatofugal flow, representing one of the most specific signs of severe PH [13, 20]. Because of the reduced portal venous flow, arterial buffering takes place leading to hepatic parenchymal arterialisation (Figure 8.17). With severe PH, there is an increase in arterial peak systolic velocity and diminished hepatic artery end‐diastolic velocity (EDV), resulting in an increased hepatic artery resistive index (RI >0.7) (Figure 8.18a). However, in cases where a shunt between hepatic artery and hepatic vein has been formed, the RI diminishes due to the drop in the peripheral resistance to arterial blood flow, and the resultant waveform in the hepatic artery changes with both high PSV and EDV (Figure 8.18b).

The hepatic veins are typically narrowed and compressed by collagen deposition and nodular regeneration, therefore the Doppler waveform loses its triphasic appearance and becomes progressively flattened and linear [20]. The flattening of the hepatic vein waveform has been found to correlate with the severity of CLD [21]. Owing to congestion, but also to the hypertrophy and hyperplasia of some tissue elements, resistance to arterial blood flow in the spleen increases together with portal pressure. Therefore, the intrasplenic arterial waveform becomes stretched, with increased PSV and diminished EDV, resulting in a high RI and pulsatility index (PI). The splenic artery PI is easily obtained, automatically calculated by the ultrasound software, and has been demonstrated as a reliable parameter for PH with a cut‐off value for significant PH when ≥1 (Figure 8.19) [22]. Owing to splanchnic vasodilation, the RI of the superior mesenteric artery diminishes during fasting. On the other hand, systemic vasodilation results in diminished renal perfusion, leading to intrarenal vasoconstriction and increased intrarenal RI (>0.7). An increase in renal RI in cirrhosis might be one of the first indicators of imminent hepato‐renal syndrome [23]. The congestive index is a quite complex Doppler‐related measurement obtained by the ratio between the cross‐sectional area of the PV and its mean flow velocity (cut‐off value of 0.1 cm/s) [24]. Although resistance and pulsatility indexes together with the congestion index are described and have been used in the past, they are considered ancillary findings to be eventually used as integration and not independently for PH diagnosis.

Vascular Modifications as a Sign of Portal Hypertension

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