Imaging in Cirrhotic Patients Undergoing Surgical Procedures

Fig. 4.1

Spectrum of morphologic changes in the cirrhotic liver. (a) Nodular liver contour and fissural widening, in this case the fissure for the ligamentum venosum (*). Ascites is also present. (b) Classic lobar findings of cirrhosis, including atrophy of the right lobe and medial segment of the left lobe, and hypertrophy of the caudate and the lateral segment of the left lobe. There is also widening of the hilar periportal space (arrow)

Additionally, the ratio of caudate lobe width to right lobe width can also be used to assist in the diagnosis of cirrhosis. As the caudate lobe enlarges and the right lobe becomes atrophic, this ratio increases and several researches have used this ratio as a quantifiable measure of cirrhosis [2, 7].

Confluent hepatic fibrosis can also be seen as wedge-shaped areas along the periphery of the liver, classically in segments IV, V, or VIII, with associated capsular retraction and delayed enhancement on contrast enhanced CT and MRI [5, 8].

In a few instances, the etiology of cirrhosis can be suggested by the imaging findings. The classic example is primary sclerosing cholangitis-induced cirrhosis, which is manifested by atrophy of the peripheral hepatic segments, and mass-like caudate enlargement, as well as multifocal regions of intrahepatic ductal prominence created by irregular bile ducts stricture (Fig. 4.2) [5].

Fig. 4.2

Primary sclerosing cholangitis-related cirrhosis. Mass-like caudate enlargement and central regeneration, lateral segment atrophy (*) and multiple mildly dilated right lobe intrahepatic bile ducts (arrow) created by irregular ductal strictures (Note the splenomegaly due to portal hypertension)

Of note, there are several entities that induce morphologic changes in the liver that resemble cirrhosis radiographically but are not cirrhosis histologically. Examples would include “pseudocirrhosis,” which is the name given to the scarred and fibrotic appearance of the liver that occasionally occurs after treating hepatic metastases with chemotherapy, and the “atrophy-hypertrophy complex,” which refers to the changes in hepatic morphology induced by portal vein thrombosis and cavernous transformation in patients without cirrhosis (Fig. 4.3). Therefore, it is important to keep these potential mimickers of cirrhosis in mind when evaluating any liver with altered morphology [9, 10].

Fig. 4.3

Mimickers of cirrhosis. Pseudocirrhosis in a woman with breast cancer metastatic to liver before (a) and after chemotherapy (b) The nodular liver contour on the later image (b) developed in a 9-month timeframe and is a treatment affect unrelated to cirrhosis. Atrophy-hypertrophy complex (c, d) in a noncirrhotic patient with hypercoagulable state. The caudate lobe (*) and right lobe are enlarged and the left lobe is atrophic (a different pattern than what is classically observed in cirrhosis). The portal vein is thrombosed (*) and there is cavernous transformation, evidenced by numerous tortuous collaterals in the porta hepatis (arrow). While cirrhosis is often the cause of these venous changes, it was not the etiology in this case

In addition to the anatomic/morphologic information described thus far, MRI provides additional diagnostic information in the evaluation of cirrhosis. For example, MRI has improved contrast resolution and is superior to CT and US in the visualization of cirrhotic nodules and intervening bands of fibrosis (Fig. 4.4). It can also be used to assess and quantify fat and iron deposition [2, 11].

Fig. 4.4

MRI in cirrhosis. Dark lines throughout the liver in a somewhat lace-like pattern are created by bands of fibrosis surrounding regenerative nodules in a patient with primary biliary cirrhosis. The superior contrast resolution of MRI enables visualization of cirrhotic nodules, which are not routinely apparent on CT

MR elastography (MRE) is a relatively new MR imaging technique that can quantify liver stiffness by analyzing propagation of mechanical waves through the liver parenchyma. These stiffness measurements are used as a marker for liver fibrosis, that is, liver stiffness measured by elastography increases with increased stages of fibrosis (Fig. 4.5) [4]. MRE is emerging as a reliable and noninvasive alternative to biopsy for grading liver fibrosis [12].

Fig. 4.5

MR elastography (Courtesy of Dr. Ajit Goenka, Mayo Clinic). (a) MR elastogram images demonstrate normal liver stiffness (<2.5 kPa). (b) MR elastogram images demonstrate significantly elevated liver stiffness, which was consistent with patient’s known biopsy-proven stage 3–4 liver fibrosis

In addition to assessing for parenchymal and morphologic changes of cirrhosis with grayscale US, Doppler ultrasound has proven to be a valuable tool in the cirrhotic population. Most commonly, it is used to detect alterations in portal venous flow. While normal portal flow is hepatopetal (or directed towards the liver), cirrhosis and portal hypertension can result in slower portal venous flow, hepatofugal (or retrograde) flow (Fig. 4.6), or absent flow due to stagnation or thrombosis.

Fig. 4.6

Ultrasound in cirrhosis. Doppler evaluation of the main portal vein demonstrates hepatofugal flow. The blue color within the vein indicates flow away from the ultrasound transducer and away from the liver; the corresponding spectral venous waveform is below the baseline, also consistent with retrograde flow. Incidentally, note the nodular liver contour, the perihepatic ascites, and the gallbladder wall thickening (arrow), commonly present in the setting of cirrhosis and portal hypertension

Altered hepatic venous and hepatic arterial flow can also be detected in the setting of cirrhosis. For example, altered hepatic vein waveforms can be seen in up to 50% of patients with cirrhosis and may correlate with the severity of the disease. Usually this manifests as a monophasic, or flat, hepatic vein flow pattern since the stiff or fibrotic liver does not permit transmission of cardiac pulsation, which is responsible for the tri-phasic waveform in normal individuals. The hepatic arteries may show increased caliber and flow to compensate for the relatively decreased portal flow that develops in the setting of cirrhosis and portal hypertension [13–15].

Additionally, Doppler interrogation is the study of choice for initial and follow-up evaluation of transjugular intrahepatic portosystemic shunts (TIPS) [14–16].

US elastography is an additional sonographic tool used as a noninvasive technique for quantifying liver fibrosis, sometimes in lieu of liver biopsy. Although specific details are beyond the scope of this discussion, elastography attempts to correlate liver stiffness with the different pathologic stages of liver fibrosis in patients with chronic hepatitis, similar to MRE [17].

Extrahepatic Imaging Manifestations

Portal Hypertension and Portosystemic Collaterals

Portal hypertension is the major clinical manifestation of cirrhosis. In addition to being a major risk factor for postoperative mortality [18], portal hypertension is as associated with increased incidence of intraoperative complications, especially in abdominal surgery, largely related to bleeding. This is especially true in patients with prior abdominal surgery and adhesions [19]. Not unexpectedly, extreme care must be taken during surgical procedures when handling varices as they have thin walls and high pressure, which can result in massive bleeding if injured [1]. As such, collateral venous pathways should be described on preoperative imaging studies.

Interestingly, some advocate the placement of a TIPS in cirrhotic patients with portal hypertension before abdominal surgery in order to reduce the likelihood of intraoperative bleeding. However, there is currently insufficient evidence to support the routine use of TIPS preoperatively [20, 21].

Classically, collateral pathways are believed to develop due to passive opening of preexisting portosystemic channels or anastomoses in the setting of increased portal pressure. More recently some research suggests that portosystemic circulation may also be due to endothelial growth factor–induced angiogenesis [22].

While conventional angiography was historically the procedure of choice for detection of varices [23], CT and MRI are less intrusive alternatives now commonly used in the delineation of portosystemic collaterals that develop secondary to portal hypertension.

As described previously, Doppler ultrasound is an additional technique to evaluate portal hypertension, especially in situations where contrast enhanced CT and MRI are contraindicated (e.g., acute kidney injury). Ultrasound features of portal hypertension include increased diameter of the main portal vein, hepatofugal portal vein flow, and identification of collateral vessels.

As portal hypertension progresses, there is gradual slowdown in the portal vein velocity secondary to elevated intrahepatic resistance. As reversal of portal venous flow progresses, splanchnic blood is shunted via portosystemic collateral vessels to the systemic circulation [24]. For simplicity, collateral vessels can be subdivided into those that drain into the superior vena cava (SVC) and those that drain into the inferior vena cava (IVC).

Collaterals draining into the SVC include:

Left gastric (or coronary) vein
Posterior and short gastric veins
Esophageal and paraesophageal varices

Collaterals draining to the IVC include:

Gastrorenal and splenorenal shunts
Paraumbilical vein and abdominal wall veins (including caput medusae)
Retroperitoneal shunts
Mesenteric varices (e.g., rectal varices) [22, 25]

The left gastric (coronary) vein is the most commonly visible varix in portal hypertension and is considered abnormal and indicative of portal hypertension when it measures larger than 5–6 mm in diameter. It originates from the splenic vein or portal vein and courses between the medial wall of the stomach and posterior surface of the left hepatic lobe. As may be expected, left gastric varices are often associated with esophageal and/or paraesophageal varices (Fig. 4.7) [26].

Fig. 4.7

Varix of the left gastric (coronary) vein. Dilated coronary vein (arrows) courses between the stomach and left hepatic lobe. There are associated (para) esophageal varices more cranially

Short gastric veins are normal veins that drain the gastric fundus and left side of the greater curvature and empty into the splenic vein. With portal hypertension, they form gastric varices, mostly near the fundus. The posterior gastric vein represents a potential venous drainage system between the left and short gastric veins and can connect to the SVC via esophageal varices or the IVC via the left renal vein [22].

Esophageal varices refer to those within the wall of the lower esophagus, while paraesophageal varices refer to those outside the wall (Fig. 4.8). These varices are mostly supplied by the left gastric vein, which splits into the anterior branch supplying esophageal varices, and posterior branch supplying paraesophageal varices. Along with gastric varices, these are the most common portosystemic pathways detected on cross-sectional imaging. Esophageal varices are clinically important, as they are the most common cause of upper gastrointestinal bleeding. Although endoscopy is important for diagnosis and often treatment of esophageal and gastric varices, CT and MR better depict the extent of collateralization [26].

Fig. 4.8

Paraesophageal varices. Multiple tortuous veins surround the distal esophagus secondary to portal hypertension. Splenomegaly is also present

Gastrorenal shunts form between the gastric and perigastric varices and drain into the left renal vein via the left inferior phrenic vein and adrenal vein. Splenorenal shunts can be separated into direct and indirect shunts. A direct splenorenal shunt is a direct communication between the splenic vein and left renal vein (Fig. 4.9). These can be large shunts that take a circuitous path and can cause significant enlargement of the left renal vein. Indirect splenorenal shunts represent communication of the splenic vein and left renal vein via the short and posterior gastric veins [22].

Fig. 4.9

Spontaneous splenorenal shunt. A prominent venous collateral (*) extends between the splenic vein (S) and the left renal vein (R), which is segmentally dilated to the level of the IVC

The paraumbilical veins are small veins within the ligamentum teres and falcifom ligament, adjacent to the closed off umbilical vein. Although it was initially postulated that the umbilical vein recanalizes, Lafortune et al. demonstrated that in fact the paraumbilical veins collateralize with the SVC (via the superior epigastric or internal thoracic veins) or with the IVC (via the inferior epigastric and external iliac veins) in the setting of portal hypertension [27]. Although a recanalized paraumbilical vein increases the predisposition to hepatic encephalopathy, it also tends to correlate with smaller esophageal and gastric varices, therefore, indicating a decreased risk for significant variceal gastrointestinal bleeding [28].

Sometimes the paraumbilical veins connect with subcutaneous abdominal wall veins creating the “caput medusae” pattern (Fig. 4.10) [29, 22]. Such abdominal wall collaterals are a potential source of bleeding during laparoscopic surgeries and their presence (discovered on physical examination or with imaging) will prompt surgeons to modify umbilical trocar placement [30].