DOI: 10.1148/rg.271065050
RadioGraphics 2007;27:129-143
© RSNA, 2007
The Perihepatic Space: Comprehensive Anatomy and CT Features of Pathologic Conditions1
Suk Kim, MD,
Tae Un Kim, MD,
Jun Woo Lee, MD,
Tae Hong Lee, MD,
Suck Hong Lee, MD,
Tae Yong Jeon, MD and
Ki Hyung Kim, MD
1 From the Departments of Diagnostic Radiology (S.K., T.U.K., J.W.L., T.H.L., S.H.L.), Surgery (T.Y.J.), and Obstetrics and Gynecology (K.H.K.), Pusan National University Hospital, 1-10 Ami-Dong, Seo-gu, Busan 602-739, Korea. Presented as an education exhibit at the 2005 RSNA Annual Meeting. Received March 30, 2006; revision requested May 24; final revision received August 9; accepted August 14. All authors have no financial relationships to disclose.
Address correspondence to J.W.L. (e-mail: junwlee{at}pusan.ac.kr).
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Abstract
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The liver is covered by visceral peritoneum except at the bare area, bed of the gallbladder, and porta hepatis. The investing peritoneum becomes contiguous with the adjacent structures such as the diaphragmatic peritoneum, lesser omentum, and ligamentum teres. An inflammatory process or tumors involving the perihepatic space are usually affected by intraperitoneal flow dynamics, which depend on the anatomy of the recess as well as gravity and negative subdiaphragmatic pressure. Pathologic conditions that occur in the perihepatic space include abnormal air, fatty masses, conditions producing fluid attenuation at computed tomography (CT), and soft-tissue masses. Enhancement of the hepatic capsule indicates inflammation, as is seen in Fitz-Hugh–Curtis syndrome. The perihepatic ligaments may be invaded by various conditions by means of direct invasion, subperitoneal extension, or extension along the lymphatic vessels. Knowledge of the normal anatomy of the perihepatic space together with the clinical history and characteristic features at CT can assist the radiologist in making the correct diagnosis.
© RSNA, 2007
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LEARNING OBJECTIVES FOR TEST 5
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After reading this article and taking the test, the reader will be able to:- Describe the normal anatomy of the perihepatic ligaments and their relationships to the other peritoneal folds.
- Identify the various pathologic conditions that involve the perihepatic spaces and ligaments on CT scans.
- Discuss intraperitoneal flow dynamics.
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Introduction
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There is usually a small amount of serous fluid, approximately 50–100 mL, in the peritoneum (1). The distribution of the peritoneal fluid is determined by the mesenteric reflections, the peritoneal recesses, the action of gravity, and hydrostatic pressure. The hydrostatic pressure under the diaphragm is normally subatmospheric, and it further decreases during inspiration. This is explained by the lateral movement of the ribs during inspiration, which enlarges the space in the upper abdomen more than it is decreased by the descent of the diaphragm (2).
The changes in the intraperitoneal hydrostatic pressure and the anatomic arrangement of the peritoneal recesses result in transcelomic migration of fluid toward the undersurface of the diaphragm. The distribution of fluid plays a significant role in the spread of inflammation and metastatic disease in the peritoneal cavity (3). Therefore, perihepatic abscess, perihepatitis, or seeded perihepatic metastases are not uncommon. The perihepatic ligaments may be invaded by various conditions by means of direct invasion, subperitoneal extension, or extension along the lymphatics.
In this article, we describe the anatomy and the pathologic features of the perihepatic structures. Specific topics discussed are conditions producing air attenuation, conditions producing fat attenuation, perihepatic fluid collections, perihepatic infections, peritoneal tumors, and the subperitoneum.
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Anatomic Considerations
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The liver is covered by visceral peritoneum except at the bare area, bed of the gallbladder, and porta hepatis. The investing peritoneum becomes contiguous with the adjacent structures such as the diaphragmatic peritoneum, lesser omentum, and ligamentum teres.
The falciform ligament is a double fold of peritoneum that connects the liver with the anterior abdominal wall and the diaphragm. As the falciform ligament approaches the diaphragm, it separates to surround the bare area of the liver. The left layer of the falciform ligament becomes the superior layer of the left coronary ligament, which is continuous with the left triangular ligament. To the right, it is continuous with the superior layer of the right coronary ligament, which travels downward to form the right triangular ligament. The inferior layer of the right triangular ligament meets the right leaf of the lesser omentum after passing in front of the groove for the inferior vena cava and then travels a half-circle course in front of the caudate lobe. The inferior layer of the left triangular ligament is continuous with the left leaf of the lesser omentum (4). The perihepatic spaces are divided into subgroups by these perihepatic ligaments (Fig 1).
The falciform ligament separates the left and right subphrenic spaces. Both perihepatic spaces are divided into the subphrenic space and the subhepatic space by the triangular ligament, and these spaces communicate freely (Fig 2). The lesser omentum forms the boundary between the right subhepatic space and the lesser sac, and the lesser sac is connected to the main peritoneal space by the foramen of Winslow.
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Figure 2a. Coronal reformatted computed tomographic (CT) scans (a obtained anterior to b) show the peritoneal spaces and ligaments. The images were obtained with intraperitoneal contrast material in a patient undergoing continuous ambulatory peritoneal dialysis. Lt = left, Rt = right.
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Figure 2b. Coronal reformatted computed tomographic (CT) scans (a obtained anterior to b) show the peritoneal spaces and ligaments. The images were obtained with intraperitoneal contrast material in a patient undergoing continuous ambulatory peritoneal dialysis. Lt = left, Rt = right.
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Conditions Producing Air Attenuation
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Pneumoperitoneum
A spontaneous pneumoperitoneum is often a result of perforation of an intraperitoneal hollow viscus, and this condition requires urgent surgical intervention. Perforation of a hollow viscus can be caused by such diverse conditions as peptic ulcer disease, a traumatic event, inflammation, neoplasms, and iatrogenic factors. Free intraperitoneal air can be seen anywhere in the peritoneal cavity, but it is often found anterior to the liver.
Pneumoperitoneum can rarely be seen with benign conditions such as ruptured pneumatosis intestinalis, downward tracking of pneumomediastinum, or leakage through a distended loop of bowel. Therefore, extraluminal air is not always a pathognomonic finding of bowel perforation (5).
CT is regarded as the standard of reference for detection and localization of a pneumoperitoneum, which are facilitated by the use of wide window settings. CT also has the advantage of depicting mural or extraluminal changes such as bowel wall thickening and fat stranding, which may help determine the origin of the free air (Fig 3) (6). However, CT is not always required when a pneumoperitoneum is suspected because of the cost and radiation burden of the procedure.
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Figure 3a. Free perihepatic air in a 67-year-old man with perforating sigmoid diverticulitis. (a) Axial contrast-enhanced CT scan (lung window) shows free air (arrowheads) in the perihepatic space. Free air is more easily identified by using lung window settings. (b) CT scan of the pelvis shows a thickened wall of the sigmoid colon (arrow) and mild pericolonic inflammatory fat stranding, findings that represent diverticulitis.
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Figure 3b. Free perihepatic air in a 67-year-old man with perforating sigmoid diverticulitis. (a) Axial contrast-enhanced CT scan (lung window) shows free air (arrowheads) in the perihepatic space. Free air is more easily identified by using lung window settings. (b) CT scan of the pelvis shows a thickened wall of the sigmoid colon (arrow) and mild pericolonic inflammatory fat stranding, findings that represent diverticulitis.
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Chilaiditi Syndrome
Chilaiditi syndrome is synonymous with symptomatic hepatodiaphragmatic interposition of the intestine. The prevalence of this syndrome has been reported to be 0.025%–0.28% of the general population (7). Increased colonic mobility, reduced liver volume, a lax suspensory ligament, phrenic nerve palsy, and even obesity may allow misplacement of a loop of bowel into the normal hepatic space. Subdiaphragmatic air within the bowel lumen may then be mistaken for pneumoperitoneum.
CT is useful to differentiate pneumoperitoneum from its mimics such as Chilaiditi syndrome or pneumoretroperitoneum (8). A wide spectrum of symptoms may exist, and these include emesis, abdominal pain, distention, and constipation. When treatment is required, it is usually conservative with bed rest and nasogastric decompression.
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Conditions Producing Fat Attenuation
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Ruptured Teratoma
Spontaneous rupture of cystic ovarian teratomas is a rare occurrence because of the thick capsule that is usually present. 
The two clinical presentations associated with the intraperitoneal rupture of benign cystic teratomas are acute peritonitis, which is caused by the sudden rupture of the tumor contents, and chronic granulomatous peritonitis, which results from a chronically leaking dermoid (9). The latter is the more common presentation.
At imaging, detection of discontinuity of the wall of the tumor is diagnostic for ruptured teratoma. Chronic granulomatous peritonitis demonstrates the unusual imaging findings of ascites, hazy omental infiltration, and an inflammatory mass involving the omentum. These findings simulate carcinomatous or tuberculous peritonitis. Visualization of the fatty implants within the peritoneal cavity may be diagnostic (Fig 4).
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Figure 4a. Ruptured teratoma in a 51-year-old woman with a palpable periumbilical mass. (a) Axial contrast-enhanced CT scan shows a floating fat droplet (arrowhead) with a fat-fluid level in the perihepatic space and ascites in the peritoneal space. The hazy omental infiltration is suggestive of chronic granulomatous peritonitis. (b) Axial contrast-enhanced CT scan of the pelvis shows an ovarian teratoma (*) with fat attenuation and foci of calcification. (Case courtesy of Y. W. Kim, MD, Pusan Baik Hospital, Busan, Korea.) a pneumoperitoneum is suspected because of the cost and radiation burden of the procedure.
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Figure 4b. Ruptured teratoma in a 51-year-old woman with a palpable periumbilical mass. (a) Axial contrast-enhanced CT scan shows a floating fat droplet (arrowhead) with a fat-fluid level in the perihepatic space and ascites in the peritoneal space. The hazy omental infiltration is suggestive of chronic granulomatous peritonitis. (b) Axial contrast-enhanced CT scan of the pelvis shows an ovarian teratoma (*) with fat attenuation and foci of calcification. (Case courtesy of Y. W. Kim, MD, Pusan Baik Hospital, Busan, Korea.)
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Lipoma and Liposarcoma
Liposarcoma may arise in any region of the body that contains fat. Liposarcomas are one of the most common malignant tumors in the retroperitoneum, whereas primary mesenteric and peritoneal liposarcomas are rare (10). Differentiation of liposarcoma from lipoma may be difficult with imaging or even at pathologic examination. A retroperitoneal fatty mass can be confused with a perihepatic mass.
Pseudolipoma
Pseudolipoma of the Glisson capsule is a rarely reported entity. It is thought to arise from a detached piece of colonic fat (an epiploic appendage) that undergoes degenerative changes and becomes covered by a fibrous capsule before lodging between the diaphragm and the superior aspect of the liver (11).
The pseudolipoma can grossly mimic a meta-static nodule as it protrudes from the surface of the liver. At CT, it appears as a well-circumscribed nodule on the liver surface with a center of fat or soft-tissue attenuation (Fig 5).
Juxtacaval Fat
Juxtacaval fat is a focal collection of fat that is typically observed medially and adjacent to the lumen of the inferior vena cava, near the hepatic venous confluence. Juxtacaval adipose tissue mimicking an intracaval fatty mass has been described as occurring as commonly as 0.5% of adults undergoing abdominal CT (Fig 6). This lesion can be a normal variant, which is more frequently seen in patients with cirrhosis (12).
Omental Infarct
Omental infarction is a relatively uncommon disorder that simulates common surgical emergencies such as cholecystitis, appendicitis, or diverticulitis. The etiology remains uncertain, but an anomalous arterial supply to the omentum, kinking of veins secondary to increased intraabdominal pressure, and postprandial vascular congestion have been proposed (13).
This condition usually occurs on the right side, but it may be seen on the left. The predilection has been attributed to an embryologic variant of the blood supply of the right portion of the omentum that predisposes it to venous thrombosis. CT demonstrates a heterogeneous fatty mass in the omentum that contains strands of soft-tissue attenuation (Fig 7).
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Figure 7. Omental infarct in a 27-year-old man. Axial contrast-enhanced CT scan shows a small, ovoid, fatty mass (arrowhead) surrounded by fat stranding around the falciform ligament.
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Intrahepatic Omental Packing
The omentum is often used as a packing material in hepatobiliary surgery. It appears as a fatty lesion of the liver in postoperative patients (Fig 8) (14).
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Figure 8. Omental packing in a 65-year-old woman who underwent surgery for hepatocellular carcinoma. Axial contrast-enhanced CT scan shows a metallic surgical clip (arrowhead) and a fat-containing masslike lesion (*), which is consistent with omentopexy due to hepatocellular carcinoma surgery.
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Perihepatic Fluid Collections
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Ascites is defined as an abnormal amount of intraperitoneal fluid. Ascites can be caused by cirrhosis in 75% of cases, peritoneal carcinomatosis in 10%, and cardiac failure in 5%. Accumulations of blood, urine, chyle, bile, or pancreatic juice are more unusual causes. Ascites usually demonstrates low attenuation values (0–20 HU), with no differences that might help establish its nature and etiology. Some specific ancillary findings such as cirrhosis and nodular peritoneal thickening may suggest the origin of the ascites (15).
High-attenuation ascites of more than 20 HU suggests hemoperitoneum (Fig 9). Acute intraperitoneal blood is of high attenuation (20–90 HU). The attenuation value falls within several days of the hemorrhage because of clot lysis. Other causes of high-attenuation ascites include tuberculous ascites or extravasated contrast material from the gastrointestinal tract or urinary tract (16). The ascitic fluid of tuberculous peritonitis typically has high attenuation values (20–45 HU) due to its high protein and cellular contents (17).
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Figure 9a. Hemoperitoneum in a 45-year-old man with hepatocellular carcinoma. (a) Nonenhanced CT scan shows an exophytic mass in the caudate lobe (arrowhead). Note the high-attenuation fluid (*) around the liver and spleen. (b) Coronal contrast-enhanced reformatted image shows leakage of contrast material (arrowhead) from the caudate lobe mass into the lesser sac. This appearance is suggestive of hemoperitoneum from rupture of a hepatocellular carcinoma. * = high-attenuation fluid.
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Figure 9b. Hemoperitoneum in a 45-year-old man with hepatocellular carcinoma. (a) Nonenhanced CT scan shows an exophytic mass in the caudate lobe (arrowhead). Note the high-attenuation fluid (*) around the liver and spleen. (b) Coronal contrast-enhanced reformatted image shows leakage of contrast material (arrowhead) from the caudate lobe mass into the lesser sac. This appearance is suggestive of hemoperitoneum from rupture of a hepatocellular carcinoma. * = high-attenuation fluid.
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Perihepatic Infections
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The infective processes involving the perihepatic space can be perihepatic abscess or peritonitis. An abscess involves the formation of an infected fluid collection that is encapsulated by fibrinous exudate, omentum, or the adjacent visceral organs. Peritonitis is defined as inflammation of the serosal membrane that lines the abdominal cavity and the organs contained therein. Perihepatitis—inflammation of the liver capsule—is a kind of localized peritonitis of the perihepatic space.
Perihepatic Abscess
The location of perihepatic abscesses is determined by the anatomy of the peritoneal recesses and the intraperitoneal pressure gradient. Perihepatic abscesses can occur in the right subhepatic space (Fig 10), right subphrenic space, lesser sac, and left subphrenic space.
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Figure 10a. Abscess due to "dropped" appendicoliths in a 46-year-old woman who underwent laparoscopic appendectomy 2 months earlier. (a) Axial contrast-enhanced CT scan shows calcification (arrowhead) in the Morison pouch, a finding that represents dropped appendicoliths. (b) Axial contrast-enhanced CT scan obtained cephalad to a shows a cystic mass with wall enhancement (*). This appearance is consistent with an abscess in the posterior right subhepatic space.
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Figure 10b. Abscess due to "dropped" appendicoliths in a 46-year-old woman who underwent laparoscopic appendectomy 2 months earlier. (a) Axial contrast-enhanced CT scan shows calcification (arrowhead) in the Morison pouch, a finding that represents dropped appendicoliths. (b) Axial contrast-enhanced CT scan obtained cephalad to a shows a cystic mass with wall enhancement (*). This appearance is consistent with an abscess in the posterior right subhepatic space.
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The frequency of subhepatic and subphrenic abscesses on the right side is two to three times greater than on the left side. The reason is that the major flow route from the pelvis is through the right paracolic gutter because of the shallow left paracolic gutter and the limited spreading caused by the phrenicocolic ligament (2).
The Morison pouch, the most dependent recess, is the most common site of perihepatic abscess. The infected material can extend around the inferior edge of the liver or laterally from the Morison pouch to the right subphrenic space.
Perihepatic Tuberculous Abscess.—
Perihepatic tuberculous abscesses may demonstrate a mildly enhancing, thin, smooth wall and several internal septa at CT. This condition also has a tendency to be located in the right perihepatic space with accompanying adjacent peritoneal smooth wall thickening, enhancement, and lymphadenopathy.
Because absorption of inflammatory cells of the peritoneal cavity and pleural space through lymphatic channels is more extensive in the right subphrenic space than the left (18), it is easy to develop a secondary infection from pulmonary tuberculosis and peritoneal tuberculosis in the right perihepatic space.
Actinomycosis.—
Actinomycosis is an indolent, slowly progressive infection that is caused by anaerobic gram-positive bacteria, primarily of the genus Actinomyces, which colonize the mouth, colon, and vagina. Mucosal disruption can lead to infection at virtually any site in the body. The classic features include purulent foci surrounded by dense fibrosis that over time cross the natural boundaries into the contiguous structures with formation of fistulas and sinus tracts in some cases. Although fistulas and sinus tracts are not universally present, fistulization is common in the late stages of actinomycosis (19).
At CT, it may be seen as an infiltrative mass with unusual aggressiveness. Abundant granulation and dense fibrous tissues in the solid components of this mass may cause marked enhancement after infusion of contrast material (Fig 11). Small, rim-enhancing lesions are sometimes found in the solid portion of the mass. These lesions are thought to be small abscesses. Because of the size of the bacterium, the organism of actinomycosis usually does not spread via the lymphatic system. Also, despite the extensive inflammatory infiltration, the disease processes do not appear to spread into the whole peritoneal cavity. Furthermore, ascites is absent or minimal.
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Figure 11. Actinomycosis in a 37-year-old woman. The diagnosis was confirmed with sonographically guided percutaneous biopsy. Axial contrast-enhanced CT scan shows an inhomogeneously and avidly enhancing mass (arrowheads) with focal areas of low attenuation in the anterior right subhepatic space, findings suggestive of a small abscess.
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The presence of fistulas or sinus tracts and the lack of or minimal ascites and regional lymphadenopathy may help differentiate actinomycosis from malignant tumor (20,21).
Echinococcosis.—
Echinococcosis is a parasitic infection caused by the larval stage of the tapeworm Echinococcus. In humans, the two main forms are cystic hydatid disease, which is caused by E granulosus, and less frequently alveolar hydatid disease, which is caused by E multilocularis. A ruptured cyst may become infected and manifest as a perihepatic abscess (22).
Perihepatitis
Perihepatitis (hepatic capsular enhancement) is defined as inflammation of the peritoneal capsule of the liver. Perihepatitis is classically described as being associated with pelvic inflammatory disease, the so-called Fitz-Hugh–Curtis syndrome. Fitz-Hugh–Curtis syndrome is believed to result from the intraperitoneal spread of infection from the pelvic cavity. The typical symptoms include sudden onset of sharp right upper quadrant pain; thus, it is frequently confused with acute cholecystitis or pleurisy.
At dynamic CT, Fitz-Hugh–Curtis syndrome has been reported to manifest as intense enhancement along the anterior surface of the liver. The capsular enhancement seen on early-phase images may reflect increased blood flow at the inflamed hepatic capsule, whereas enhancement seen on the delayed images may reflect early capsular fibrosis (Figs 12, 13) (23,24).
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Figure 12a. Acute Fitz-Hugh–Curtis syndrome in a 31-year-old woman with right upper quadrant pain. (a) Arterial phase contrast-enhanced CT scan shows enhancement of the capsule of the left hepatic lobe (arrowhead). (b) Equilibrium phase contrast-enhanced CT scan shows disappearance of the hepatic capsular enhancement. The findings in a and b are suggestive of acute Fitz-Hugh–Curtis syndrome. (c) Axial contrast-enhanced CT scan of the pelvis shows a tubo-ovarian abscess (*) in the left adnexal region.
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Figure 12b. Acute Fitz-Hugh–Curtis syndrome in a 31-year-old woman with right upper quadrant pain. (a) Arterial phase contrast-enhanced CT scan shows enhancement of the capsule of the left hepatic lobe (arrowhead). (b) Equilibrium phase contrast-enhanced CT scan shows disappearance of the hepatic capsular enhancement. The findings in a and b are suggestive of acute Fitz-Hugh–Curtis syndrome. (c) Axial contrast-enhanced CT scan of the pelvis shows a tubo-ovarian abscess (*) in the left adnexal region.
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Figure 12c. Acute Fitz-Hugh–Curtis syndrome in a 31-year-old woman with right upper quadrant pain. (a) Arterial phase contrast-enhanced CT scan shows enhancement of the capsule of the left hepatic lobe (arrowhead). (b) Equilibrium phase contrast-enhanced CT scan shows disappearance of the hepatic capsular enhancement. The findings in a and b are suggestive of acute Fitz-Hugh–Curtis syndrome. (c) Axial contrast-enhanced CT scan of the pelvis shows a tubo-ovarian abscess (*) in the left adnexal region.
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Figure 13a. Chronic Fitz-Hugh–Curtis syndrome in a 30-year-old woman with right upper quadrant pain. (a) Arterial phase contrast-enhanced CT scan shows enhancement of the hepatic capsule (arrowhead). (b) Equilibrium phase contrast-enhanced CT scan shows persistence of the hepatic capsular enhancement (arrowhead). The findings in a and b are suggestive of chronic Fitz-Hugh–Curtis syndrome. (c) Laparoscopic image shows the classic "violin string" adhesions between the anterior liver capsule and the anterior abdominal wall or diaphragm.
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Figure 13b. Chronic Fitz-Hugh–Curtis syndrome in a 30-year-old woman with right upper quadrant pain. (a) Arterial phase contrast-enhanced CT scan shows enhancement of the hepatic capsule (arrowhead). (b) Equilibrium phase contrast-enhanced CT scan shows persistence of the hepatic capsular enhancement (arrowhead). The findings in a and b are suggestive of chronic Fitz-Hugh–Curtis syndrome. (c) Laparoscopic image shows the classic "violin string" adhesions between the anterior liver capsule and the anterior abdominal wall or diaphragm.
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Figure 13c. Chronic Fitz-Hugh–Curtis syndrome in a 30-year-old woman with right upper quadrant pain. (a) Arterial phase contrast-enhanced CT scan shows enhancement of the hepatic capsule (arrowhead). (b) Equilibrium phase contrast-enhanced CT scan shows persistence of the hepatic capsular enhancement (arrowhead). The findings in a and b are suggestive of chronic Fitz-Hugh–Curtis syndrome. (c) Laparoscopic image shows the classic "violin string" adhesions between the anterior liver capsule and the anterior abdominal wall or diaphragm.
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The diagnosis of Fitz-Hugh–Curtis syndrome may be confirmed by the presence of perihepatitis at laparoscopy and by isolation of Neisseria gonorrhoeae and Chlamydia trachomatis in a cervical smear or in fluid from the pelvic peritoneal cavity (25).
Similar capsular enhancement has been reported in a patient with perihepatitis associated with systemic lupus erythematosus (26). In our experience, contrast enhancement along the surface of the liver may occur in any of the other inflammatory conditions that cause perihepatitis, such as perforated cholecystitis, perforated hepatic abscess (Fig 14), tuberculous peritonitis (Fig 15), and direct exposure of the liver to radiation. Capsular enhancement may occur with peritoneal carcinomatosis. A milder degree of capsular enhancement combined with a plaquelike or nodular soft-tissue mass suggests carcinomatosis rather than perihepatitis, and this can be helpful in their differentiation (Fig 16). Some conditions such as a fatty liver or hepatocellular carcinoma treated with Lipiodol (iodized oil; Andre Guerbet, Aulnaysous-Bois, France) may simulate hepatic capsular enhancement (Fig 17) (24).
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Figure 14a. Perforation of a hepatic abscess in a 51-year-old woman. Axial contrast-enhanced CT scans show enhancement of the hepatic capsule (arrowhead in a) caused by perihepatitis, which was secondary to perforation of a hepatic abscess (* in b).
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Figure 14b. Perforation of a hepatic abscess in a 51-year-old woman. Axial contrast-enhanced CT scans show enhancement of the hepatic capsule (arrowhead in a) caused by perihepatitis, which was secondary to perforation of a hepatic abscess (* in b).
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Figure 15a. Peritoneal tuberculosis in a 34-year-old man. (a) Axial contrast-enhanced CT scan of the midabdomen shows enhancement of the hepatic capsule (arrow). (b) Axial contrast-enhanced CT scan of the lower abdomen shows thickening of the parietal peritoneum (arrowheads), nodularity of the mesenteric fat, and ascites.
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Figure 15b. Peritoneal tuberculosis in a 34-year-old man. (a) Axial contrast-enhanced CT scan of the midabdomen shows enhancement of the hepatic capsule (arrow). (b) Axial contrast-enhanced CT scan of the lower abdomen shows thickening of the parietal peritoneum (arrowheads), nodularity of the mesenteric fat, and ascites.
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Figure 16a. Peritoneal carcinomatosis in a 53-year-old man with stomach cancer. (a) Axial contrast-enhanced CT scan shows subtly thickened parietal peritoneum with mild enhancement (arrow), thickening of the falciform ligament (arrowhead), and ascites. (b) Axial contrast-enhanced CT scan obtained at a lower level shows stomach cancer and an omental cake (*).
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Figure 16b. Peritoneal carcinomatosis in a 53-year-old man with stomach cancer. (a) Axial contrast-enhanced CT scan shows subtly thickened parietal peritoneum with mild enhancement (arrow), thickening of the falciform ligament (arrowhead), and ascites. (b) Axial contrast-enhanced CT scan obtained at a lower level shows stomach cancer and an omental cake (*).
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Figure 17. Fatty liver in a 44-year-old man. Axial contrast-enhanced CT scan shows linear high attenuation along the hepatic surface (arrow), a finding that represents pseudoenhancement. The diaphragm has high attenuation relative to the decreased attenuation of the fatty liver and thus mimics an enhanced hepatic capsule.
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Peritoneal Tumors
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Peritoneal Carcinomatosis
Peritoneal carcinomatosis is malignant seeding of the peritoneum, and this is the most common peritoneal malignancy. It most commonly arises from the ovary, colon, stomach, and pancreas. There is usually a great deal of ascites, which is often loculated. It can appear as smooth or nodular peritoneal thickening and enhancement (Fig 18). Implants on the liver and the splenic surfaces are frequently seen and result in scalloping of the surface by the masses (27). Sites of tumor implantation are the intersegmental fissure, superior recess of the lesser sac, subphrenic space, and Morison pouch. Calcified peritoneal carcinomatosis may occur in serous ovarian adenocarcinoma, colon cancer, and gastric cancer (Fig 19).
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Figure 18. Peritoneal carcinomatosis in a 61-year-old woman with a history of ovarian cancer. Coronal reformatted image from abdominal CT performed with intravenous contrast material shows thickening of the right hemidiaphragm by tumor plaque (arrowheads), omental implants (*), and ascites.
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Figure 19a. Peritoneal carcinomatosis secondary to serous cystadenocarcinoma of both ovaries in a 73-year-old woman. (a) Axial contrast-enhanced CT scan shows sheetlike calcified tumor plaque (arrowheads) along the right lobe of the liver. (b) Axial contrast-enhanced CT scan shows multiple calcified masses (*) in the pelvic cavity.
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Figure 19b. Peritoneal carcinomatosis secondary to serous cystadenocarcinoma of both ovaries in a 73-year-old woman. (a) Axial contrast-enhanced CT scan shows sheetlike calcified tumor plaque (arrowheads) along the right lobe of the liver. (b) Axial contrast-enhanced CT scan shows multiple calcified masses (*) in the pelvic cavity.
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It is difficult to differentiate peritoneal carcinomatosis from other peritoneal disorders such as primary serous papillary carcinoma of the peritoneum, malignant peritoneal mesothelioma, and tuberculous peritonitis. Although the radiologic features of tuberculous peritonitis resemble those of peritoneal carcinomatosis, a noteworthy difference exists. Peritoneal thickening with tuberculous peritonitis is diffusely smooth (Fig 15), unlike the irregular peritoneal studding that is characteristic of peritoneal carcinomatosis.
Pseudomyxoma Peritonei
Pseudomyxoma peritonei is characterized by the gradual accumulation of large volumes of gelatinous ascites in the peritoneal cavity, which comes from ruptured mucin-producing tumors of the ovary or appendix.
The diagnostic CT criteria for pseudomyxoma peritonei are scalloping of the visceral surfaces (particularly the liver), septated ascites or ascites with attenuation slightly higher than that of water, and hypoattenuating peritoneal implants that may cause extrinsic pressure on the bowel loops (Fig 20). Pseudomyxoma peritonei is not characterized by hematogenous or lymphatic metastases, so the presence of lymphadenopathy should bring the diagnosis of pseudomyxoma peritonei into question (28).
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Figure 20. Pseudomyxoma peritonei due to rupture of an appendiceal mucocele in a 73-year-old man. Coronal contrast-enhanced reformatted CT scan shows multiple septated, low-attenuation masses (*) throughout the peritoneal space. Small cystlike masses create impressions on the hepatic surface (arrowheads).
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Subperitoneum
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The liver is covered by a connective tissue capsule called the Glisson capsule, an extension of the peritoneum, except for the bare area, which is attached to the diaphragm (29). The Glisson capsule extends as a septum into the liver. The portal triad and lymphatics follow this connective tissue pathway throughout the liver. The hepatic veins traverse a route separate from the connective tissue scaffolding.
Anatomically, the part of the Glisson capsule that surrounds the intrahepatic portion of the hepatic portal system is called the Glisson sheath. The Glisson capsule or sheath continues into the subperitoneal space of the gastrohepatic and hepatoduodenal ligaments. The anatomic continuity of the subperitoneal space provides for the spread of disease not only between the intraperitoneal structures, but also between the extraperitoneal and intraperitoneal sites (Fig 21).
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Figure 21. Glisson capsule and Glisson sheath. The Glisson capsule covers the hepatic surface as an extension of the peritoneum, except for the bare area, which is attached to the diaphragm. The Glisson sheath is defined as the part of the Glisson capsule that surrounds the intrahepatic portion of the hepatic portal system. The Glisson capsule or sheath continues into the subperitoneal space of the gastrohepatic and hepatoduodenal ligaments in one direction. It also continues into the subperitoneal space of the ligamentum teres and falciform ligament in the other direction (long curved arrows).
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For example, the Cullen sign is a result of the subperitoneal spread of disease. According to the original description, the Cullen sign is associated with ectopic pregnancy. However, it is more commonly seen with acute severe pancreatitis. The Cullen sign in pancreatitis is secondary to the tracking of liberated pancreatic enzymes to the anterior abdominal wall from the inflamed hepatoduodenal ligament and across the falciform ligament (30). Air (Fig 22), inflammation (Fig 23), tumor, or proliferative disease (Fig 24) can extend along the subperitoneum.
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Figure 22a. Emphysematous cholecystitis in a 61-year-old man. (a) Axial contrast-enhanced CT scan shows gas originating from perforation of the gallbladder (arrows). (b) Axial contrast-enhanced CT scan shows that the gas has diffused along the hepatoduodenal ligament to the Glisson sheath (arrow).
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Figure 22b. Emphysematous cholecystitis in a 61-year-old man. (a) Axial contrast-enhanced CT scan shows gas originating from perforation of the gallbladder (arrows). (b) Axial contrast-enhanced CT scan shows that the gas has diffused along the hepatoduodenal ligament to the Glisson sheath (arrow).
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Figure 23a. Spread of pancreatitis along the Glisson sheath in a 41-year-old man. Axial contrast-enhanced CT scans show the inflammatory changes of pancreatitis extending upward along the portal vein (arrow) to the ligamentum teres (arrowhead in a). A peripancreatic fluid collection (* in b) is also seen.
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Figure 23b. Spread of pancreatitis along the Glisson sheath in a 41-year-old man. Axial contrast-enhanced CT scans show the inflammatory changes of pancreatitis extending upward along the portal vein (arrow) to the ligamentum teres (arrowhead in a). A peripancreatic fluid collection (* in b) is also seen.
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Figure 24a. Extramedullary hematopoiesis in a patient with known chronic myelogenous leukemia. Axial contrast-enhanced CT scans (a obtained at a higher level than b) show a hypoattenuating mass around the portal vein (arrows), ascites, and splenomegaly. The mass demonstrates subperitoneal spread through the Glisson sheath.
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Figure 24b. Extramedullary hematopoiesis in a patient with known chronic myelogenous leukemia. Axial contrast-enhanced CT scans (a obtained at a higher level than b) show a hypoattenuating mass around the portal vein (arrows), ascites, and splenomegaly. The mass demonstrates subperitoneal spread through the Glisson sheath.
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Conclusions
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A variety of pathologic conditions may occur in the perihepatic space, and they can have potentially overlapping radiologic features. Knowledge of the normal anatomy of the perihepatic space is required to appropriately interpret the anatomic location, size, and shape of the lesions and their involvement with the adjacent structures. Although CT findings are nonspecific for distinguishing between the many pathologic diseases of the perihepatic space, this knowledge together with the clinical history and certain details seen at CT can assist the radiologist in making the correct diagnosis.
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Acknowledgments
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We thank Sang Wook Kwak for his assistance in preparing the manuscript.
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References
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Abstract
LEARNING OBJECTIVES FOR TEST...
