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necrotic liver tissue acting as a nidus. Abscess imaging is discussed in a later section; suffice it here to state that trauma-associated abscesses are readily identified by CT. The presence of gas bubbles is almost pathognomonic, although occasionally noninfected necrotic liver parenchyma secondary to ischemia has a similar appearance.
Blunt trauma is a rare cause of a major liver infarct.
Imaging
Computed tomography is the first imaging study performed in a hemodynamically stable patient suspected of blunt liver injury. A CT blunt trauma liver injury grading scale has been proposed based on CT findings (Table 7.3). Its initial function was to assess the value of CT in predicting outcome following blunt liver injury. It should be kept in mind that this CT grading scale employs different parameters than the liver injury classification scale devised by trauma surgeons; the latter is meant to help standardize surgical findings and outcomes. Also, although CT aids in establishing the scope of an initial insult and detects complications, whether a patient is explored or managed conservatively often continues to be based on clinical findings.
The most sensitive US finding in patients with liver trauma is intraabdominal free fluid; actual liver injury is detected less often. Mild parenchyma injury appears as a focal hyperechoic region.
Table 7.3. Computed tomography (CT)-based liver injury grading system
Grade Criteria
1Capsular avulsion Superficial laceration <1 cm
Subcapsular hematoma <1 cm
2Lacerations 1–3 cm deep Central/subcapsular hematoma 1–3 cm deep
3Lacerations >3 cm deep Central/subcapsular hematoma >3 cm deep
4Massive hematoma >10 cm Lobar tissue destruction/ischemia
5Bilobar tissue destruction/ischemia
Source: Adapted from Mirvis et al. (15).
ADVANCED IMAGING OF THE ABDOMEN
Is CT helpful in monitoring healing? In most patients routine follow-up CT does not influence subsequent treatment and often is not necessary; a need for follow-up CT should be based on the patient’s clinical course.
Hemorrhage/Hematoma
A hematoma is the most common liver injury. These hematomas range from subcapsular to intraparenchymal in location. Not all are due to trauma. Common nontraumatic causes of liver hemorrhage include bleeding from a hepatic neoplasm; bleeding also occurs with hemangiomas, focal nodular hyperplasia, an occasional metastasis, the HELLP syndrome (discussed later; see Liver in Pregnancy), and such infiltrative conditions as amyloidosis.
A subcapsular hematoma tends to compress the underlying liver parenchyma, thus differentiating it from intraperitoneal fluid. An appropriately located hematoma will obstruct the intrahepatic portion of the inferior vena cava and hepatic veins and result in Budd-Chiari syndrome (discussed in Chapter 17). At times a slow bleed and resultant liver hematoma manifests by anemia.
Contrast extravasation is detected by CT if bleeding is sufficiently brisk. This extravasated contrast–blood mixture has a higher attenuation than an old hematoma, and the two are readily differentiated. If needed, transcatheter embolization is an option for hemorrhage control.
Unenhanced blood has an attenuation value of 30HU or greater. Initially clotted blood has a CT density higher than nonclotted blood, and an acute hematoma is thus hyperdense compared to normal liver parenchyma. Some liver lacerations, however, result in a hypodense hematoma, presumably due to simultaneous leakage of bile. Postcontrast, a hematoma has a lower density than normally enhancing liver parenchyma.
Occasionally CT identifies regions of low attenuation parallel to the portal vein and its branches. Such periportal tracking of blood was initially believed to be a marker of significant liver injury, although currently most radiologists tend to ascribe periportal tracking to lymphatic distention and edema and discount its importance as a marker for significant trauma.
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Its use as a guide for management decisions is controversial; whether periportal tracking is present or not has no effect on the eventual success rate of nonoperative management or on the complication rate. Such tracking usually does not signify a laceration.
The sonographic appearance of a hematoma depends on its age. Initially a hematoma is mostly hyperechoic, with some having a complex, heterogeneous appearance. With time, a hypoechoic pattern predominates as a clot lyses and eventually the hematoma becomes anechoic. A similar US pattern is found with hematomas in other solid organs.
Surgical retractors cause transient focal liver injury. Computed tomography in one patient revealed a focal, sharply marginated hypodense lesion, while MR identified a hypointense, poorly defined region on T1-weighted sequences that was heterogeneous and hyperintense on T2-weighted sequences (16).
Some traumatic liver hematomas are associated with pseudoaneurysms or arteriovenous fistulas; these should be detected by CTA and, if diagnosis is unclear, angiography.
Most subcapsular hematomas resolve within several months. Parenchymal hematomas, on the other hand, take considerably longer to resolve, probably because of their common admixture of bile.
Laceration/Rupture
Numerous nontraumatic disorders are associated with spontaneous liver rupture (Table 7.4).
Postcontrast CT reveals a liver laceration as an irregular linear or branching hypodense region surrounded by enhancing liver parenchyma (Fig. 7.6). Some of these linear lacerations mimic dilated bile ducts. Lacerations of the porta hepatis commonly involve bile ducts and major vessels. Extensive lacerations tend to radiate toward the periphery. A hemoperitoneum is common; the exception being with injury to the liver bare area (segment VII) when a hemoretroperitoneum can develop (17).
Biloma
Table 7.4. Conditions associated with spontaneous liver rupture
Infections
Typhoid
Malaria
Nonneoplastic tumors
Hemangioma
Peliosis hepatis
Focal nodular hyperplasia
Nodular regenerative hyperplasia
Angiomyolipoma
Neoplastic tumors
Hepatic adenoma
Hepatocellular carcinoma
Metastasis
Other
HELLP syndrome
Amyloid infiltration
Polyarteritis nodosa
Ehlers-Danlos syndrome
tion of contrast from the duct involved, thus establishing the diagnosis.
At times differentiation among a resolving hematoma, abscess, and biloma is difficult both by CT and US. Ultrasonography simply reveals an encapsulated fluid collection. In such a scenario either scintigraphy or percutaneous aspiration of fluid is necessary to establish the diagnosis.
Magnetic resonance imaging differentiates between a simple intrahepatic biloma and
Spontaneous perforation of an intrahepatic bile duct is uncommon.A cholangiogram,regardless of how it is performed, should reveal extravasa-
Figure 7.6. Liver laceration in a 25-year-old man (arrows). (Courtesy of Patrick Fultz, M.D., University of Rochester.)
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hematoma. A biloma is hypointense on T1weighted images and hyperintense on T2weighted images; a hematoma is hyperintense on both T1and T2-weighted images; in practice, blood and proteins modify the MR appearance of a biloma. Nevertheless, a differentiation is more than theoretical because most bilomas should be drained, but hematomas tend to resolve spontaneously.
Porta Hepatis Injury
Although injury to the porta hepatis region is rare, it is often lethal; intraoperative exsanguination is not an uncommon cause of death in these patients, and thus hemorrhage control is the first priority. Other associated injuries are common. Suspected bile duct injuries are identified by intraoperative cholangiography and repaired either primarily or an enteric anastomosis.
In stable patients with blunt liver injury undergoing both CT and hepatic angiography, CT was only 65% sensitive and 85% specific in detecting arterial injury (18); if in doubt, hepatic angiography is the gold standard in detecting arterial injury.
Infection/Inflammation
Abscess
Pyogenic
Clinical
A pyogenic liver abscesses is often associated with bile duct stones and duct obstruction. At times simply removing retained stones, stenting, and medical management are therapeutic.
A not uncommon etiology for multiple liver abscesses is sigmoid diverticulitis and hematogenous spread of infection to the liver. Most abdominal radiologists have encountered patients with not only multiple liver abscesses but also portal venous gas; Bacteroides fragilis, producing gas by fermentation, is one such responsible organism. Chlamydia trachomatis is a common organism found in Fitz-Hugh–Curtis syndrome. A rare liver abscess evolves with this infection. The specific diagnosis is often established by percutaneous aspiration.
ADVANCED IMAGING OF THE ABDOMEN
An uncommon association for a liver abscess is with a silent colon adenocarcinoma.
The most common clinical presentation in patients with a pyogenic hepatic abscess is fever and leukocytosis, and less often abdominal pain, hepatomegaly, and abnormal liver tests. Jaundice and marked elevation of alkaline phosphatase are common with a biliary tract abscess origin.
The intervening liver capsule, subphrenic space, and diaphragm prevent spread of most intrahepatic abscesses into the thorax. An exception is an abscess involving the liver bare area; an occasional such abscess communicates with the mediastinum.
A liver abscess is a recognized complication of Crohn’s disease. Steroids and other therapy tend to mask the presence of these abscesses. Occasionally such an abscess is the initial presentation of Crohn’s disease.
Diabetes mellitus is a major predisposing factor for pyogenic liver abscesses even without a known infectious focus; gas within the abscess, detected with conventional radiography, CT, or US, is associated with a higher mortality than one without gas. Diabetes tends to predispose rupture of a pyogenic liver abscess. These patients have a high mortality even with prompt surgical cleansing of the abdominal cavity. Klebsiella pneumoniae is a common bacterium isolated.
Rarely, rupture of an infected gallbladder leads to a liver abscess. After percutaneous abscess drainage, contrast injected into the abscess cavity should reveal a fistulous communication with the gallbladder. A rare pyogenic liver abscess contains multiple stones and is caused by perforation of an adjacent necrotic gallbladder; these combined gallbladder and liver abscesses are notoriously difficult to evaluate adequately.
Imaging
Liver abscesses range from solitary to multiple; unilocular to multiloculated; large to small. In most instances imaging findings strongly suggest an abscess. It should be realized, however, that an occasional necrotic, or infected liver cancer presents as a hepatic abscess. These include primary liver cancer, gallbladder carcinoma, or even a metastasis. Imaging does not always differentiate a complex necrotic and
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cystic cancer from a liver abscess. Likewise, a pyogenic abscess appears similar to an amebic abscess.
Only an occasional hepatic abscess contains gas.
Computed tomography shows most intrahepatic abscesses as hypodense regions but with peripheral contrast enhancement. Nevertheless, the appearance of pyogenic abscesses varies from homogeneous and hypodense to a heterogeneous solid tumor. Some abscesses incite little surrounding inflammation; others induce considerable inflammation, and postcontrast they appear target-like, with the hypodense abscess surrounded by a hyperdense rim, which in turn is surrounded by a thin hypodense periphery thought to represent liver edema. Segmental hepatic enhancement during arte- rial-phase CT is common, presumably caused by decreased portal flow resulting from portal tract inflammation.
Ultrasonography shows approximately two thirds of pyogenic abscesses to be hypoechoic, with the rest inhomogeneous. Anechoic abscesses are uncommon. Approximately half have a smooth wall. With progression and necrosis, abscesses tend to become more hypoechoic. The abscess wall thickens with chronicity. Gas within an abscess is hyperechoic and reveals shadowing. Contrast aided phase inversion harmonic mode US reveals rim enhancement, arteries along abscess margins and internal septa, septal enhancement, absent circulation in fluid and arterial hypervascularity surrounding the abscess (19).
Magnetic resonance imaging appearance of a liver abscess is similar to other fluid-containing lesions. Most are hypointense on T1and hyperintense on T2-weighted images. Most abscesses tend to be better defined postcontrast and often show an immediate hyperintense enhancing rim, which persists in later phases, but the central portion, as expected, does not enhance. It should be kept in mind that many metastases also have rim enhancement. An absolute distinction between an abscess and a neoplasm is often not possible purely on MRI findings alone. An infected neoplasm complicates this issue further.
Indium 111 leukocyte scintigraphy readily detects most hepatic abscesses. An occasional abscess, however, results in a cold defect.
Normal hepatic uptake of gallium 67 makes interpretation of a Ga-67 abscess scan difficult;
a Tc-99m sulfur colloid scan performed in conjunction with Ga 67 scintigraphy is helpful for interpretation.
Therapy
Although some of the smaller abscesses can be treated medically, most require either percutaneous or surgical drainage, at which time diagnostic aspiration confirms the diagnosis. In many centers surgical drainage is reserved for abscesses that cannot be adequately drained percutaneously. Percutaneous drainage using a large-caliber drainage catheter is associated with few complications and has a high success rate. Both multiloculated and multiple abscesses are drained successfully. Previously considered a lethal disease, currently abscess cure rates up to 93% are typical with percutaneous drainage. The success rate is lower in patients with an underlying malignancy. Abscesses with a biliary fistula are also drainable percutaneously. Most of the underlying fistulas resolve unless distal bile duct obstruction is present.
The major complication of percutaneous drainage is bleeding, at times massive. An occasional patient develops an empyema due to pleural puncture. Mortality associated with percutaneous abscess drainage is less than 10%.
Common dogma holds that simple percutaneous needle aspiration is not a viable therapeutic option for a pyogenic liver abscess. Yet, percutaneous needle aspiration and systemic antibiotics can be successful in healing most abscesses, realizing that about half of these abscesses require two or more sessions (20). Large gauge trocar needles and US guidance, and complete pus removal are necessary.
Currently surgical drainage or liver resection are reserved for complex abscesses, those without a safe percutaneous access route, and failed percutaneous drainages.
Amebic
Clinical
Amebic liver abscesses have a wide geographic variation. Men predominate by a ratio of about 10 : 1. In nonendemic regions a high proportion of amebiasis is found in AIDS patients.
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The diagnosis is usually suspected from serologic testing. Fever, abdominal pain, and hepatomegaly are common presentations.
Independent mortality risk factors include an elevated bilirubin level, the presence of encephalopathy, the size of the abscess cavity, hypoalbuminemia, and the number of abscesses present; mortality is independent of the duration of symptoms.
Imaging
In general, imaging cannot differentiate an amebic abscess from a pyogenic abscess, and the imaging findings described above for pyogenic abscesses also apply to amebic abscesses.
Some patients develop a right pleural effusion, right basal atelectasis, a perihepatic fluid collection, or simply elevation of right hemidiaphragm. These findings occur with intraabdominal abscesses and do not necessarily imply intrathoracic abscess spread. Nevertheless, a rare liver amebic abscess evolves into a hepatopulmonary fistula or a hepatocolic fistula, or even spreads into the mediastinum and pericardium.
In patients resistant to medical therapy, abscess communication with the bile ducts should be suspected. These patients tend to be jaundiced. A minority of amebic liver abscesses are associated with focal intrahepatic bile duct dilation, presumably secondary to obstruction.
Amebic liver abscesses range from solitary to multiple. Single abscesses tend to be more common in tropical amebiasis. A right lobe location predominates. On precontrast CT these abscesses range from isoto hyperdense. Mother cysts tends to be hyperdense compared to daughter cysts. Secondary bacterial infection further increases the mother cyst or daughter cyst CT density. Most abscess walls enhance postcontrast. Internal septations develop in some.
Ultrasonography reveals most to have a smooth wall and a homogeneous, hypoechoic US appearance. Because of retained necrotic debris and blood, some abscesses appear solid and contain hypoor hyperechoic internal echoes. They are surrounded by a hyperechoic wall, which in turn is surrounded by a thin peripheral halo. Some are multiseptate.
An occasional amebic liver abscess is imaged by triple-phase bone scintigraphy.
ADVANCED IMAGING OF THE ABDOMEN
Therapy
Medical therapy of an amebic abscess is highly successful; only those not responding to medical therapy or clinically appear to be at risk of impending rupture require drainage. Nevertheless, especially with a larger abscess, faster recovery is often achieved if drug therapy is combined with image-guided percutaneous aspiration.About a third or so of these abscesses yield no Entamoeba histolytica. If the material obtained initially is nondiagnostic, the final aspirate should be examined because it is most often diagnostic. The aspirate usually is rather viscous, and aspiration through a large-bore catheter is helpful. Abscesses tend to recur if no drain is left in place.
Presence of a biliary fistula does not influence the cure rate for percutaneous drainage. Most biliary fistulas close spontaneously. Likewise, even with a ruptured amebic abscess percutaneous catheter drainage of extrahepatic collections appears safe and effective.
Hydatid Cyst
Clinical
Infection with Echinococcus granulosus, or hydatid disease, is uncommon in Northwestern Europe and North America but is endemic in the Mediterranean basin and several regions of East Africa. Dogs, ruminants, and humans constitute the infestation cycle. Most common ruminants involved are sheep and goats, although apparently camels also have a role in parts of Africa; the highest prevalence in humans is in the Turkana district of Kenya. Hydatid disease exists in cattle in West and Southern Africa but human infestation here is rare.
The most common sites of involvement are the liver and lungs, the right lobe more often than the left, adjacent to Glisson’s capsule. Echinococcal cysts are slow growing and often take years to reach a large size.
Cysts contain two layers. The outer pericyst, composed of an avascular layer, is a host response to infestation. An inner endocyst, about 2mm in thickness,is produced by the parasite and normally is adjacent to the pericyst, except when ruptured.
Although some cysts rupture spontaneously, especially when large, unrelated trauma is a not uncommon cause of cyst rupture. In a contained rupture only the endocyst ruptures, with the
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pericyst remaining intact. Some cysts rupture into an adjacent bile duct or directly into the peritoneal cavity, subphrenic space, or, rarely, into the gastrointestinal tract. Communication with a gas-containing viscus leads to a gas-fluid level within the cyst. Occasional cysts have transdiaphragmatic spread to the thorax. Rupture into a blood vessel, such as a hepatic vein, is rare.
Jaundice is usually due to cyst rupture into bile ducts and intrabiliary spread of the hydatid content. The resultant obstruction is generally treated by endoscopic sphincterotomy and removal of the obstructing intrabiliary daughter cysts. Occasionally, a hydatid cyst obstructs the bile ducts close to the liver hilum simply by compression, and jaundice develops even without a biliary communication. Likewise, a hydatid cyst close to the liver hilum can lead to cavernous portal vein transformation.
In some patients hydatid cyst content in the bile ducts induces a hypersensitivity reaction, even to the point of anaphylaxis. A ruptured cyst is one cause of a relapsing generalized anaphylactic reaction, including life-threatening laryngospasm. An occasional one results in an eosinophilic cholecystitis.
The less common echinococcal infection with
Echinococcus multilocularis is encountered in colder climates. Liver screening with US is practiced in some endemic regions, and screening appears to contribute to early detection.
A local form of aggressive hydatid disease is found in Central and South American neotropical zones. The infectious agent is Echinococcus vogelii, paca, and other wild rodents are intermediate hosts, and the bush dog the final host. The liver is most often involved, with metacestodes spreading into the peritoneal cavity and eventually invading other abdominal and thoracic organs. Infected patients most often present with hard, round tumors in or adjacent to the liver, hepatomegaly, increased abdominal girth, pain, and cachexia; liver involvement progresses to portal hypertension. Imaging reveals a polycystic liver disease pattern. Extensive involvement leads to numerous cysts in the liver, pancreas, spleen, and peritoneal cavity. Cyst calcifications are common.
Imaging
Type 1: Simple unilocular cyst. Believed to be an early stage in hydatid cyst formation, these cysts are water dense on CT and anechoic on US. Cyst wall and septal enhancement is seen with CT and MR contrast, thus differentiating this entity from simple cysts.
Type 2: Cyst containing daughter cysts. Round or irregular daughter cysts are surrounded by a higher density fluid in the mother cyst.
Type 3: Dead cysts containing extensive calcifications.
Type 4: Complex cysts. These consist of superinfected cysts or ones that have ruptured. In a contained rupture imaging identifies endocyst separation from the surrounding pericyst. Bacterial superinfection implies the presence of cyst rupture.
Curvilinear cyst rim calcifications are common with Echinococcus granulosus infections, and a cystic pattern is detected in about half.
The CT appearance varies, although a hydatid cyst tends to have an oval and sharply defined outline. Precontrast, cysts are mostly inhomogeneous and of low density; postcontrast enhancement is inhomogeneous (Figs. 7.7 and 7.8). The sonographic appearance ranges from an anechoic cyst, mural nodules, and visualization of the endocyst, to a complex multicystic structure.
Debris either tends to be displaced toward the center of the primary cyst or is located in
An imaging classification of hydatid cysts consists of the following:
Figure 7.7. Hydatid cyst. CT also identifies a soft-tissue component within the cyst (arrow). (Courtesy of Algidas Basevicius, M.D., Kaunas Medical University, Kaunas, Lithuania.)