Abdominal radiology Review article The peritoneum, mesenteries

Transcription

Eur. Radiol. 8, 886±900 (1998) Ó Springer-Verlag 1998
European
Radiology
Abdominal radiology
Review article
The peritoneum, mesenteries and omenta:
normal anatomy and pathological processes
J. C. Healy1, R. H. Reznek2
1
2
Department of Radiology, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, UK
Department of Radiology, St. Bartholomew's Hospital, West Smithfield, London EC1A 7BE, UK
Received 16 October 1997; Revision received 16 December 1997; Accepted 9 January 1998
Abstract. The peritoneum is the largest and most
complexly arranged serous membrane in the body.
The potential peritoneal spaces, the peritoneal reflections forming peritoneal ligaments, mesenteries,
omenta and the natural flow of peritoneal fluid determine the route of spread of intraperitoneal fluid and,
consequently, disease processes within the abdominal
cavity. The peritoneal ligaments, mesenteries and
omenta also serve as boundaries for disease processes
and conduits for disease spread. The peritoneal cavity
and its reflections are frequently involved by infectious, inflammatory, neoplastic and traumatic processes. Before the introduction of cross-sectional imaging, the peritoneum and its reflections could only
be imaged with difficulty, often requiring invasive
techniques. Computed tomography and, to a lesser
extent, sonography and MR imaging allow the accurate examination of the complex anatomy of the peritoneal cavity, which is the key to understanding the
pathological processes affecting it. This article reviews the normal peritoneal anatomy and its disease
processes.
Key words: Abdomen, peritoneum ± Normal anatomy, pathology, CT, MRI-peritoneum
Introduction
The peritoneal cavity and its reflections, including its
mesenteries and omenta, are frequently involved by infectious, inflammatory, neoplastic and traumatic processes. Before the introduction of cross-sectional imaging, the peritoneum and its reflections could only be imaged with difficulty, often requiring invasive techniques.
Computed tomography and, to a lesser extent, sonography and MR imaging allow the accurate examination
of the complex anatomy of the peritoneal cavity, which
Correspondence to: J. C. Healy
is the key to understanding the pathological processes
affecting it. This article reviews the normal peritoneal
anatomy and its disease processes.
Normal anatomy
The peritoneum is the largest and most complexly arranged serous membrane in the body, which in the male
forms a closed sac, and in the female is penetrated by
the lateral ends of the Fallopian tubes. The peritoneal
cavity is a potential space between the parietal peritoneum, which lines the abdominal wall, and the visceral peritoneum, which envelopes the abdominal organs. It consists of a main region, termed the greater sac, and a diverticulum, the omental bursa or lesser sac, situated behind
the stomach. These two areas communicate via the epiploic foramen (foramen of Winslow). The free surface
of the peritoneum has a layer of flattened mesothelial
cells kept moist and smooth by a thin film of serous fluid.
The potential peritoneal spaces, the peritoneal reflections forming peritoneal ligaments, mesenteries,
omenta and the natural flow of peritoneal fluid determine the route of spread of intraperitoneal fluid and,
consequently, disease processes within the abdominal
cavity. This flow is directed by gravity to its most dependent sites. It is also directed in a cephalad direction by
the negative intra-abdominal pressure generated in the
upper abdomen by respiration [1]. The peritoneal ligaments, mesenteries and omenta serve as boundaries for
disease processes and also conduits for disease spread.
The anatomy of the peritoneum is described in detail,
dealing first with the peritoneal spaces (Fig. 1 a) and
then with the peritoneal reflections including the peritoneal ligaments, the mesenteries and the omenta (Figs.
1 b, 2). This anatomy is illustrated on axial CT in a patient with chronic renal failure on continuous ambulatory peritoneal dialysis (CAPD; Fig. 3). The peritoneal
space has been opacified using positive contrast medium
in this patient in an attempt to visualise inflammatory
adhesions.
J. C. Healy and R. H. Reznek: The peritoneum, mesenteries and omenta
Peritoneal spaces
The peritoneal cavity is divided into two main compartments by the transverse colon and its mesentery which
connects the colon to the posterior abdominal wall: (a)
the supramesocolic; and (b) the inframesocolic compartments (Fig. 1).
Supramesocolic compartment
The supramesocolic compartment can be divided into
right and left peritoneal spaces, which in turn are arbitarily divided into several subspaces, which are normally
in communication but often become separated by adhesions.
The right supramesocolic space has three subspaces:
1. The right subphrenic space, which extends over the
diaphragmatic surface of the right lobe of the liver to
the right coronary ligament posteroinferiorly and the
falciform ligament medially, which separates it from
the left subphrenic space (Fig. 3 a).
2. The right subhepatic space, which can be further divided into anterior and posterior compartments. The
anterior compartment is limited inferiorly by the transverse colon and its mesentery (Fig. 3 b). The posterior
compartment, also known as the hepatorenal fossa or
Morrison's pouch, extends posteriorly to the parietal
peritoneum overlying the right kidney (Fig. 3 b). Superiorly the subhepatic space is bounded by the inferior surface of the right lobe of the liver. Both the right subphrenic and right subhepatic spaces communicate freely
with the right paracolic gutter (Fig. 3 c).
3. The lesser sac extends behind the stomach, anterior to
the pancreas, communicating with the rest of the peritoneal cavity through a narrow inlet, the epiploic foramen
(foramen of Winslow). A prominent oblique fold of
peritoneum is raised on the posterior wall of the lesser
sac by the left gastric artery, dividing it into two major
recesses. The smaller superior recesss completely encloses the caudate lobe of the liver. It extends superiorly
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deep into the fissure for the ligamentum venosum and
lies adjacent to the right diaphragmatic crus. The larger
recess lies between the stomach and the visceral surface
of the spleen. It is bounded inferiorly by the transverse
colon and its mesentery but can extend for a variable
distance between the leaves of the greater omentum.
The left supramesocolic space has four arbitrary
communicating subspaces:
1. The left anterior perihepatic space bounded medially
by the falciform ligament, posteriorly by the liver surface and anteriorly by the diaphragm.
2. The left posterior perihepatic space, also called the
gastrohepatic reccess, follows the inferior surface of the
lateral segment of the left hepatic lobe.
3. The left anterior subphrenic space lies between the
anterior wall of the stomach and the left hemi-diaphragm, communicating inferiorly with the left anterior
perihepatic space.
4. The posterior subphrenic (perisplenic) space covers
the superior and inferolateral surfaces of the spleen
(Fig. 3 a).
The phrenicocolic ligament, extending from the
splenic flexure of the colon to the diaphragm, partially
a
Fig. 1. a Coronal view of posterior peritoneal
spaces. b Coronal view of peritoneal attachments
to the posterior abdominal wall
b
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b
a
c
d
Fig. 2. a Position of the sagittal sections through
the upper abdomen. b Sagittal section A±A
through the right lobe of the liver and right kidney. c Mid-sagittal section through the upper
abdomen B±B. d Sagittal section C±C through
the left lobe of the liver and less sac. e Sagittal
section D±D through the spleen and left kidney
e
a
b
c
d
e
f
Fig. 3a±f. Axial CT scans with intraperitoneal contrast in a patient
on continuous ambulatory peritoneal dialysis to show the peritoneal spaces and ligaments. a Axial CT with intraperitoneal contrast, at the level of the porta hepatis, demonstrating the right subphrenic space (small arrows), the falciform ligament (curved arrow), the left posterior subphrenic space (open arrow). b CT with
intraperitoneal contrast, at the level of the renal hilum, demonstrating Morrison's pouch (curved arrow). Fat is noted in the greater omentum (open arrow) and within the transverse mesocolon
(straight arrow). c CT with intraperitoneal contrast just above the
aortic bifurcation, demonstrating the right paracolic gutter
(straight arrows), left paracolic gutter (curved white arrows) and
right infracolic space (straight black arrow). Note is also made of
fat within the small bowel mesentery (curved black arrow). d CT
with intraperitoneal contrast just below the aortic bifurcation,
demonstrating the right paracolic gutter (white arrows) and left infracolic space (curved arrows). Note is also made of fat within the
root of the small bowel mesentery (straight black arrow). e CT
with intraperitoneal contrast at the level of the mid-sacroiliac
joints, showing fat within the sigmoid mesocolon (arrows). f CT
with intraperitoneal contrast at the level of the uterus and bladder,
demonstrating the paravesical (curved arrows), uterovesical
(straight arrow) and rectovesical (open arrow) spaces
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separates the perisplenic space from the rest of the peritoneal cavity. It forms a partial barrier to the spread of
fluid from the left paracolic gutter into the left subphrenic space, explaining why left subphrenic collections are less common than right-sided collections.
Inframesocolic compartment
The inframesocolic compartment is divided into two unequal spaces by the root of the small bowel mesentery,
as it runs from the duodenojejunal flexure in the left upper quadrant to the ileocaecal valve in the right lower
quadrant (Fig. 3 d):
1. The smaller right infracolic space is bounded inferiorly by the small bowel mesentery, extending from the
duodenojejunal flexure to the ileocaecal valve.
2. The larger left infracolic space is in free communication with the pelvis, except where it is bounded by the
sigmoid mesocolon (Fig. 3 d).
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The paracolic gutters are the peritoneal recesses on the
posterior abdominal wall lateral to the ascending and
descending colon. The right paracolic gutter is larger
than its counterpart on the left and is continuous superiorly with the right subhepatic and subphrenic spaces.
Both paracolic gutters are in continuity with the pelvic
peritoneal space.
Inferiorly the peritoneum is reflected over the fundus
of the bladder, the anterior and posterior surface of the
uterus in females, and on to the superior part of the rectum. The urinary bladder subdivides the pelvis into right
and left paravesical spaces. In men there is only one potential space for fluid collection posterior to the bladder,
the rectovesical pouch. In women there are two potential spaces posterior to the bladder, the uterovesical
pouch, and posterior to the uterus, the rectouterine
pouch (pouch of Douglas; Fig. 3 f).
Peritoneal reflections
In early fetal life as the abdominal cavity divides into the
retroperitoneum and peritoneum, the parietal peritoneum is reflected over the peritoneal organs to form a series
of supporting ligaments, mesenteries and omenta. Consequently, a natural connecting pathway for the extension of intra-abdominal disease is formed between the
retroperitoneum and structures enveloped by peritoneum, which has been termed the subperitoneal space.
The small bowel mesentery, sigmoid mesocolon and
greater omentum are frequently involved in disease processes, and can sometimes be identified in normals.
1. The small bowel mesentery is a broad fan-shaped fold
of peritoneum connecting the loops of jejunum and ileum to the posterior abdominal wall, extending obliquely
from the duodenojejunal flexure to the ileocaecal valve
(Fig. 3 d).
2. The sigmoid mesocolon is a fold of peritoneum which
attaches the sigmoid colon to the posterior pelvic wall
(Fig. 3 e).
3. The greater omentum is the largest peritoneal fold in
the abdomen. It descends from the stomach and proximal duodenum, passing inferiorly, anterior to the small
bowel, before turning superiorly again to insert into the
anterosuperior aspect of the transverse colon (Fig. 3 b).
Peritoneum: pathology
Fluid collections are by far the most common pathological peritoneal process imaged. Free fluid, or ascites,
within the abdomen may result from a variety of underlying conditions. Ascites may be exudative, secondary
to carcinomatosis, peritonitis and pancreatitis, or
transudative, secondary to hypoproteinaemia, congestive heart failure and cirrhosis. It may also be haemorrhagic or chylous in composition.
Ascites. Imaging plays a significant role in assessing the
amount, aetiology and in assisting sampling or draining
of ascitic fluid. Sonography and CT are the primary imaging tools used, with MR imaging occasionally being
used to demonstrate peritoneal or ascitic fluid enhancement, especially in patients with compromised renal
function [2].
Sonography is extremely sensitive for detecting peritoneal fluid, identifying as little as 10 ml in the pouch
of Douglas in experimental studies [3]. Uncomplicated
ascites is typically echo free and mobile within the peritoneal cavity. However, more posterior structures and
collections may be obscured by bowel loops floating anteriorly. Ascites secondary to infection or malignant
neoplasm may contain low-level echoes due to pus, other cellular material or septa. It frequently becomes loculated by adhesions from bowel and peritoneal ligaments
tethered to the abdominal wall. The mesentery may be
thickened and bowel peristalsis may be diminished or
abolished.
Computed tomography provides more complete
evaluation of the peritoneal cavity than sonography. It
detects smaller amounts of ascites and allows visualisation of fluid behind loops of bowel, e. g. in the leaves of
the mesentery and lesser sac. The distribution of ascites
may suggest its aetiology; transudate ascites usually has
a smaller lesser than greater sac component, carcinomatosis has similar-sized collections in both sacs and pancreatitis gives large lesser sac collections which may extend into the greater omentum or even into the mediastinum [4].
On MRI most fluid has a low signal on T1-weighted
images and a very high signal on T2-weighted images.
Infective and malignant fluid often has a higher protein
content than transudate ascites and therefore may have
recognisably higher signal on T1-weighted images [5].
However, the MRI appearances are not specific and
needle aspiration, which can be guided by ultrasound
or CT, is needed to confirm the nature of the ascites.
Intraperitoneal haemorrhage may be secondary to
anticoagulation, a bleeding diathesis or visceral trauma.
On CT haemorrhage is usually of increased attenuation;
however, acute haemorrhage can have low attenuation,
similar to the attenuation of water [6]. Also increased
attenuation of peritoneal fluid may be seen in exudates
secondary to malignancy, in chylous ascites and with
urine leaks following intravenous contrast [7]. Additionally, simple peritoneal fluid can enhance on delayed
scans as a result of increased vascular±peritoneal permeability in disease [8]. Within several days of haemorrhage, clot lysis occurs and its attenuation decreases, approaching the density of water by 2±4 weeks. Haemorrhagic fluid may appear inhomogeneously dense on CT
due to irregular clot formation and resorption, and because of intermittent bleeding. On MR imaging, subacute and acute haemorrhage may be high signal on
T1-weighting and of varied signal intensity on T2weighting [9].
Chylous ascites due to the collection of lymphatic fluid can occur as a consequence of disruption to the lymphatic vessels by tumour or surgery. It may be indistinguishable from other ascitic fluid collections, but occasionally on CT the Hounsfield numbers may be negative
due to its high fat content or a fat fluid level may be
identified if the patient has been on bed rest [10].
Infection
Peritoneal cavity infection may be localized (peritoneal
abscess formation) or generalized (peritonitis). The response of the peritoneum to infection is consistent, producing oedema and inflammation, followed by a fibroblastic exudate forming adhesions between peritoneal
surfaces in an attempt to contain the infection.
Intraperitoneal abscess usually presents with nonspecific symptoms and signs. Prompt diagnosis depends on
understanding the dynamic anatomy of the peritoneal
spaces and the peritoneal reflections. The most common
site for abscess formation is the pouch of Douglas,
which is the most dependent site in the peritoneal cavity; infection preferentially ascends in the right paracolic
gutter into the right subphrenic and subhepatic spaces
[1].
Peritoneal abscess formation most frequently follows
surgery despite modern surgical techniques and antimicrobial therapy. It may also complicate appendicitis or
Crohn's disease in younger patients, and diverticulitis
in older patients (Fig. 4 a).
The sonographic appearances of both sterile and infected fluid collections are not specific and can overlap;
however, abscesses frequently have ill-defined walls,
low-level internal echoes and poorer through transmission than simple fluid collections. Gas within fluid collections, although inconsistently present, is highly suggestive of infection. Gas usually appears as an area of increased echogenicity with or without acoustic shadowing, depending on the amount present [11]. The principal limitations of ultrasound are related to its nonspecificity and technical limitations which preclude examination of all areas of the abdomen and pelvis. However, it
does benefit from being a rapid, inexpensive and readily
available technique. It is best suited for diagnosing abscesses in the right and left upper quadrants, especially
subphrenic collections, as imaging in the longitudinal
plane allows easy distinction between fluid above and
below the diaphragm. It is also very good at detecting
pelvic collections using the distended bladder as an
acoustic window.
Computed tomography, which is much less operator
dependent than ultrasound, is the most sensitive technique for the detection of intraperitoneal abscess as the
entire abdomen and pelvis can be surveyed [12]. The CT
appearances depend to some extent on the age of the abscess. In the earliest stages the abscess may appear as a
mass, representing the swollen tissues or viscera colonised by neutrophils and bacteria. As the process advances, its centre undergoes liquefactive necrosis, producing
a region of fluid attenuation, the margin of which enhances following intravenous contrast enhancement.
Approximately 40±50 % of abscesses contain air which
appears as dark bubbles on CT or produces an air/fluid
level [11]. Displacement of adjacent structures and thickening or obliteration of adjacent fat planes accompanies
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abscess formation. Most abscesses are round or oval in
shape on CT, but those adjacent to solid organs may be
lenticular or cresenteric in configuration.
The CT appearances may suggest the cause of the abscess:
1. Acute appendicitis can be diagnosed on unenhanced
CT by identification of the appendix, periappendiceal
inflammation and an appendix abscess with an associated appendicolith [13].
2. Acute diverticulitis is identified on CT by ill-defined
inflammation in the pericolic fat and sigmoid mesocolon, in association with colonic diverticula and thickening of the colonic wall [14].
3. Computed tomography also demonstrates marked
bowel wall thickening with mural stratification and often a target or double halo sign in Crohn's disease
(Fig. 4 b) [15].
The major advantage of CT over ultrasound is the ability to detect abscesses in the retroperitoneum and between bowel loops, which is independent of the patient's
body habitus. This makes CT more accurate than ultrasound in detecting abdominal and pelvic abscesses.
Both ultrasound and CT have significant roles to play
in needle aspiration and percutaneous drainage of abscesses, thus reducing the morbidity of re-operation.
Magnetic resonance imaging does not offer any benefit over ultrasound and CT for the diagnosis of intraperitoneal abscess. At present, MRI of the abdomen is degraded by respiratory and peristaltic bowel movement.
Also fluid in the bowel can be difficult to differentiate
from extraluminal collections as contrast opacification
of the bowel for MRI is not as effective as for CT [16].
Inflammation can become more generalised within
the peritoneum which is often the case with tuberculous
peritonitis, which, although rarely encountered in the
developed world, is increasing in association with
AIDS and with the increase in immigrant populations
(Fig. 5). Tuberculous peritonitis develops after rupture
of a caseous abdominal lymph node or due to secondary
spread to the intestinal tract. On CT the following signs
are highly suggestive of tuberculous peritonitis [17]: enlarged lymph nodes with central low density due to caseous necrosis, seen in up to 40 % of patients in the mesenteric and peripancreatic areas (Fig. 5 a), nodular thickening of the peritoneal surfaces (Fig. 5 b), associated ascites, which is characteristically of relatively high density due to its high protein content (Fig. 5 c), thickening
and nodularity within the small bowel mesenteric fat
(Fig. 5 d), and marked mesenteric lymphadenopathy.
Associated features of intra-abdominal tuberculosis
may also be present, such as thickening of the bowel
wall, particularly the terminal ileum, focal abnormalities in the liver or spleen due to granulomata (Fig. 4 a),
and occasionally adrenal pathology. Notably the chest
radiograph is abnormal in only 50 % of patients with tuberculous peritonitis.
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4a
4b
5a
5b
5c
5d
Fig. 4 a, b. Crohn's disease. a Post-contrast CT showing ªcobblestoneº mural thickening in the sigmoid colon (open arrows) in association with a large abscess with an enhancing margin (arrows).
b Axial post-contrast CT showing the ªcomb signº (straight white
arrows) in association with bowel wall thickening (straight black
arrows). Note also a loop of bowel demonstrating the ªdouble
halo signº (open arrow), with enhancing mucosa and low-attenuation submucosal oedema
6
Fig. 5a±d. Intra-abdominal tuberculosis. a CT with intravenous
contrast showing ring-enhancing, low-density lymph nodes at the
coeliac axis (white arrows). Note is also made of focal abnormalities within the spleen (black arrows). b CT showing nodular soft
tissue thickening in the greater omentum (arrows). c CT showing
high-density ascites (black arrows) and soft tissue thickening in
the mesenteric fat (white arrows). There is also inflammatory
thickening of the peri-renal fascia bilaterally (open arrows). d CT
showing marked thickening and nodularity within the small bowel
mesentery (arrows)
Fig. 6. Dynamic post-contrast CT following major abdominal trauma showing marked laceration of the spleen (solid arrow) and extravasation of intravenous contrast (open arrow). Note the low-attenuation ascites
Trauma
Computed tomography is essential in the diagnosis and
management planning of abdominal trauma, which has
significantly reduced the number of negative exploratory laparotomies [18]. Peritoneal fluid seen on CT after
trauma may represent blood, urine, third space fluid
losses or bowel contents [7].
Haemoperitoneum is seen in approximately two
thirds of all intraperitoneal solid-organ (hepatic or
splenic) injuries. It is not seen if the injury does not extend to the organ surface or if there is no capsular disruption. It is also seen in vascular injuries especially of
the pelvic vessels in association with skeletal fractures.
Following trauma the only sign of active haemorrhage on CT is focal or diffuse high-attenuation areas
( > 90 HU), representing extravasated intravascular
contrast mixed with blood (Fig. 6) [20].
Intraperitoneal bladder rupture is usually associated
with high-attenuation fluid collections as a consequence
of excreted IV contrast material. This extravasation is
best detected on delayed images [21].
In the absence of visceral or bony injury, large
amounts of free intraperitoneal fluid, free intraperitoneal air and intense bowel wall enhancement suggests
bowel rupture [22]. However, this is relatively rare, occurring in approximately 5 % of patients who have laparotomy for blunt abdominal trauma [19]. Bowel injury is
almost always associated with a large mesenteric haematoma.
Abdominal CT provides global evaluation of the abdomen and retroperitoneum and organ-specific information. However, it is a relatively expensive test which
requires transfer to the scanning suite. Diagnostic peritoneal lavage (DPL) is fast, comparatively inexpensive
and may be as sensitive as CT in screening for serious intraperitoneal injury [19]. Sonography is also a fast, accessible method for detecting haemoperitoneum, but it
suffers from being both operator and patient dependent,
resulting in a poorer sensivity than CT or DPL for detecting serious intraperitoneal trauma [23].
Peritoneal neoplasms
Metastatic disease is the most common malignant process involving the peritoneum, usually from intra-abdominal primary neoplasms, including the stomach, colon, ovary and pancreas.
Computed tomography is the best imaging procedure
for the evaluation of patients with known or suspected
peritoneal metastases. Prior to the advent of CT, peritoneal metastases were not radiographically detectable
until late in the disease, when they displaced adjacent
organs, caused intestinal obstruction or produced radiological signs due to massive ascites on plain films. Intraperitoneal positive contrast and pneumoperitoneum
with CT has been suggested to improve the detection
of small peritoneal metastases, but these techniques are
interventional and do not routinely opacify all the peritoneal recesses [24, 25].
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Sonography can demonstrate superficial peritoneal
and omental tumour nodules as small as 2±3 cm in patients with large amounts of ascites, but ultrasound does
not detect small peritoneal deposits if there is only minimal ascites [26]. Additionally, it does not identify centrally located tumour deposits as these are obscured by
bowel gas and by the increased acoustic impedance of
mesenteric fat.
Magnetic resonance imaging may offer superior
soft tissue contrast to CT in identifying peritoneal
metastases, but the spatial resolution of the technique, at present, is diminished by movement
artefact caused by bowel peristalsis and respiration [27,
28].
Metastatic neoplasms disseminate throughout the
peritoneum in four ways:
1. Direct spread along the peritoneal ligaments, mesenteries and omenta (Fig. 7a±c)
2. Seeding through the ascitic fluid (Fig. 7d±g)
3. Lymphatic extension
4. Embolic haematogenous spread (Fig. 7 m)
It must be stressed that none of these appearances are
specific for the malignancies mentioned and can be
mimicked by other metastatic tumours, primary peritoneal tumours such as mesothelioma, and inflammatory
conditions such as pancreatitis and tuberculous peritonitis. Also, many of the distinct patterns of metastatic
disease described often coexist.
Direct invasion from primary tumours to noncontiguous organs occurs along the peritoneal reflections and
is commonly seen with carcinoma of the stomach into
the left lobe of the liver via the lesser omentum
(Fig. 7 a). Computed tomography shows loss of the fat
plane between these two organs [29]. Direct spread
from retroperitoneal tumours, such as carcinoma of the
pancreas, into the liver can occur along the hepatoduodenal ligament [30]. Biliary and hepatic malignancies
can also spread in the reverse direction to the stomach
and pancreas via the lesser omentum and hepatoduodenal ligaments. Neoplasms of the colon, stomach and
pancreas often use the transverse mesocolon and greater omentum as conduits for spread. Direct invasion is
well demonstrated on CT as increased density or discrete soft tissue masses in the fat of the transverse mesocolon [31]. On CT early involvement of the greater
omentum produces increased density within the fat adjacent to the primary neoplasm (Fig. 7 k, l). Direct involvement of the small bowel mesentery is commonly
seen in carcinoid (Fig. 7 b, c), lymphoma, pancreatic,
breast and colonic metastases.
Intraperitoneal seeding of neoplasms depends on
the normal flow of fluid within the peritoneal cavity
allowing transcoelomic dissemination of malignant
cells [32]. The most common tumours to spread in
this fashion include ovarian cancer in females and malignancies of the gastrointestinal tract in males, especially cancer of the stomach, colon and pancreas. The
sites most commonly involved by peritoneal seeding
are:
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a
b
c
d
e
f
g
h
1. The pelvis, especially the pouch of Douglas (Fig. 7 d)
2. The right lower quadrant at the inferior junction of
the small bowel mesentery
3. The superior aspect of the sigmoid mesocolon
4. The right paracolic gutter
Spread of deposits to the right subhepatic and subphrenic spaces is also frequently seen, especially in ova-
Fig. 7 a±h
rian cancer (Fig. 7 e) [33]. On CT seeded metastases appear as nodular or plaque-like soft tissue masses in association with ascites. Intraperitoneal deposits as small as
5 mm can be identified, even in the presence of small
amounts of ascites [34]. Rounded or oval low-density
deposits on the surface of the liver are frequently seen
on CT in ovarian cancer [35]. It is presumed that these
deposits infiltrate the liver capsule following their depo-
i
j
k
l
m
sition on the liver surface. The parietal peritoneum may
be diffusely involved producing nodular thickening on
CT that often enhances [36].
Peritoneal calcification is also frequently seen on CT
with serous cystadenocarcinoma of the ovary (Fig. 7 h),
carcinoid tumour and rarely with gastric carcinoma [37].
A distinctive CT appearance is produced by
pseudomyxoma peritonei, resulting from the rupture of
a mucinous cystadenocarcinoma or cystadenoma of the
ovary or appendix (Fig. 7 i, j). The gelatinous nature of
the deposits produces a mantle of low-density material
over the surface of the liver, causing scalloping of its
margin, in association with cystic peritoneal collections.
The walls of the cystic collections may contain calcification. The pressure of the gelatinous material prevents
the bowel loops floating up towards the anterior abdominal wall, which may be a useful sign in differentiating
pseudomyxoma peritonei from ascites (Fig. 7 i) [38].
The small bowel mesentery and greater omentum are
frequently involved by intraperitoneal seeding of me-
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Fig. 7a±m. Metastatic peritoneal neoplasms. a Post contrast CT in
a patient with gastric carcinoma (solid arrow) directly invading the
lesser omentum (open arrow). b Axial post-contrast CT showing a
terminal ileum carcinoid tumour (solid arrow) extending into the
root of the small bowel mesentery. Note also small deposits within
the small bowel mesentery (open arrows). c Post-contrast axial
CT in the same patient with carcinoid tumour showing larger ill-defined nodules in the small bowel mesentery (solid arrows), surrounded by diffuse ill-defined mesenteric stranding (open arrow).
d Post-contrast CT in a patient with ovarian cancer showing ascites
within the pouch of Douglas, behind the uterus (U) and solid peritoneal deposits (curved arrows). e Axial post-contrast CT in patient with ovarian cancer showing ascites (white arrow) and multiple nodular and plaque-like peritoneal soft tissue masses (black arrows). f Axial post-contrast CT in a patient with metastatic renal
cancer (note the clips in the right renal bed; black arrow) showing
enhancing small peritoneal and serosal deposits (white arrows).
g Axial post-contrast CT in the same patient as f showing enhancing serosal deposits along the small bowel (solid arrows) and enhancing deposits within the greater omentum (open arrows), surrounded by ascites. h Axial post-contrast CT in a patient with ovarian cancer showing calcified peritoneal metastases (arrows). i Axial post-contrast CT showing pseudomyxoma peritonei as a consequence of rupture of a mucinous cystadenocarcinoma of the appendix. Note the low-density gelatinous deposits (white arrows)
producing scalloping of the liver margin (black arrows). j Axial
post-contrast CT in the same patient as in i showing that the small
bowel loops do not float anteriorly in the presence of the gelatinous material, which is a useful sign in differentiating pseudomyxoma peritonei from ascites. k Axial post-contrast CT in a patient
with colonic adenocarcinoma showing minimal disease in the
greater omentum (arrows). l Axial post-contrast CT in the same
patient as 6 months later showing marked greater omental ªcakelikeº metastatic deposits (arrows). m Axial CT in a patient with
malignant melanoma showing multiple embolic peritoneal metastases (arrows)
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a
b
c
d
tastases. Four patterns of involvement are described on
CT (Fig. 7 k, l) [39]: (a) round masses; (b) ªcake-likeº
masses; (c) ill-defined masses; and (d) stellate masses.
Metastatic deposits to the ovaries from gastric or colonic primary tumours in association with ascites and
other peritoneal deposits are a well-recognised entity.
These tumours, known as ªKrukenbergº tumours, are
presumed to be a consequence of transcoelomic spread
and are clearly visualised on CT [40].
Lymphatic spread is the primary route of metastasis
for lymphoma. Approximately 50 % of patients with
non-Hodgkin's lymphoma have enlarged mesenteric
lymph nodes at presentation. These nodes may be confluent producing large mass lesions in the mesentery.
Characteristically, these nodal masses surround and encase vessels, particularly the superior mesenteric vessels. It is important to note, however, that enlargement
of mesenteric lymph nodes can be due to inflammatory
causes such as Crohn's disease, Whipple's disease and
tuberculosis. Under these conditions individual lymph
nodes generally remain more discrete and rarely become a conglomerate mass.
Embolic metastases from both intra-abdominal and
extra-abdominal primary tumours spread via the mesenteric arteries to deposit on the anti-mesenteric border
of the bowel in the smallest arterial branches, where
they grow into mural nodules. The most common tumours that metastasise embolically to bowel and the
peritoneal reflections are melanoma as well as breast
and lung cancer. These metastases often occur several
years after treatment of the primary neoplasm. Occasionally, bowel obstruction or intussuception, as a consequence of embolic metastases, may be the first mani-
Fig. 8a±d. Primary neoplasms of
the peritoneum. a Axial CT in a
patient with malignant mesothelioma of the peritoneum showing ascites and plaque-like peritoneal
thickening (black arrows). Note
also the bilateral pleural plaques
(white arrows). b Axial post-contrast CT showing a relatively welldifferentiated liposarcoma (arrows)
arising from the perinephric fat,
which is a characteristic site. c Axial post-contrast CT showing a highgrade liposarcoma containing an
enhancing mass (solid arrow), enhancing septae (open arrows) and
ill-defined enhancement of the fatty
tissue (arrowheads). d Axial postcontrast CT showing a myxoid liposarcoma with a large lobulated
area of low-density material centrally (solid arrows) which appears
cystic on CT, surrounded by more
characteristic fatty material (open
arrows)
festation of an occult malignancy. On CT, embolic metastases may produce thickening of the bowel wall,
which is often asymmetrical with associated ulceration,
and thickening of the adjacent bowel wall [41]. They
may also appear as well-defined round masses within
the peritoneal fat (Fig. 7 m). Embolic metastases to the
stomach from breast cancer produces marked gastric
wall thickening with almost complete obliteration of its
lumen, an appearance that is indistinguishable from primary schirrous gastric carcinoma or lymphoma [42].
Primary neoplasms of the peritoneum are rare and
are usually of mesenchymal origin. Mesothelioma arises
in the serosal lining of the pleura, peritoneum and pericardium associated with asbestos exposure. Peritoneal
involvement may occur alone or in combination with
pleural involvement (Fig. 8 a). On CT there is marked
thickening of the peritoneum, mesentery and omentum,
which may show an irregular or nodular appearance.
Peritoneal calcification (which may be seen on plain
films) and associated ascites are seen on CT. The
amount of ascites may be disproportionately small in relation to the peritoneal disease when compared with
other peritoneal neoplasms. The mesenteric involvement may produce a stellate appearance due to thickening of perivascular bundles [43, 44]. These appearances,
however, are not specific for mesothelioma and may be
indistinguishable from metastases, lymphoma or tuberculous peritonitis. The diagnosis is strongly suggested if
there is concomitant thickening and calcification of the
pleura in a patient with a history of asbestos exposure.
Lipomatous tumours occasionally involve the peritoneal cavity and have typical CT and MRI appearances.
Benign lipomas are well defined and composed entirely
of low-attenuation fat on CT. On MR imaging these tumours are of high signal on T1-weighted scans. A welldifferentiated liposarcoma may be largely lipomatous
and well marginated on CT and MR imaging, but in contradistinction to lipoma there are irregular, nodular areas that enhance following intravenous contrast. Highgrade subtypes of liposarcoma may present as a nonspecific soft tissue mass or a heterogeneous mass with
both soft tissue and fatty components (Fig. 8 b, c). Myxoid liposarcoma may appear cystic on CT due to the
presence gelatinous material (Fig. 8 d) [45, 46].
The mesenteries and omenta
Computed tomography, with appropriate bowel contrast opacification, is the best modality for identification
of mesenteric and omental abnormalities. Pathological
conditions infiltrating the normal mesenteric and omental fat increase its attenuation, obscure the mesenteric
vessels and distort the associated bowel loops.
Currently, MRI is less valuable for detecting and
characterising mesenteric pathology because respiratory and peristaltic bowel movements degrade the images.
Mesenteric oedema
Mesenteric oedema may be a consequence of many pathologies, including hypoalbuminaemia, cirrhosis, nephrosis, heart failure, tricuspid disease, constrictive
pericarditis, portal hypertension, portal vein thrombosis, mesenteric artery and vein thrombosis, vasculitis,
Budd-Chiari syndrome, inferior vena cava obstruction
and trauma [47]. Some of these conditions, such as heart
failure and portal hypertension, are frequently encountered clinically and can sometimes present difficulty in
differential diagnosis with other frequent conditions
such as peritoneal carcinomatosis.
On CT, mesenteric oedema increases the density of
the mesenteric fat from ±100 to ±160, which is similar
to the density of subcutaneous fat, to values of ±40 to
±60 [47]. In addition, the mesenteric arteries and veins
are not clearly visualised as they course to the bowel
walls. It may also be associated with ascites.
If the mesenteric oedema is secondary to a systemic
disease, such as heart failure, it is accompanied by a generalised increased density in the retroperitoneal and
subcutaneous fat secondary to generalised oedema. In
cirrhosis, where mesenteric oedema is secondary to portal hypertension, CT may also demonstrate serpiginous
varices in the retroperitoneum, greater and lesser omentum, and mesentery [48].
Mesenetric oedema secondary to arterial or venous
thrombosis tends to be more focal in nature but can
sometimes be diffuse. Superior mesenteric vein
thrombosis is the cause of intestinal ischaemia in
5±15 % of cases [49]. The typical appearances of
chronic superior mesenteric vein thrombosis are enlargement of the vein, with a central low density surrounded by a higher-density wall. The thrombus may
897
be of high attenuation in the acute state [50]. If bowel infarction is present, CT will show intramural bowel gas and gas within the portal and mesenteric veins
[51]. Computed tomography is also of great value in
establishing an underlying local cause of venous
thrombosis such as pancreatic cancer, pancreatitis or
Crohn's disease.
Crohn's disease
Crohn's disease is identified on CT as bowel wall thickening of 1±2 cm in over 80 % of cases [15]. Computed
tomography also identifies extramural abnormalities in
the mesentery, including abscess formation, phlegmon,
fibro-fatty proliferation and enlarged mesenteric lymph
nodes [52]. Fibrofatty proliferation, also known as
creeping fat of the mesentery, is the most common cause
of separation of bowel loops on small bowel series in patients with Crohn's disease. On CT the sharp interface
between bowel and mesentery is lost and the attenuation is increased due to the influx of inflammatory cells
and fluid. The mesentery is often hypervascular, with
vascular dilatation, and wide spacing of the vasa recta,
which is known as the ªcomb signº (Fig. 4 b) [53]. A
phlegmon is an ill-defined inflammatory mass in the mesentery or omentum which may resolve completely or
progress to an abscess. On CT it produces a loss of definition of surrounding organs and a smudgy or streaky
appearance of the adjacent fat [54]. Computed tomography, with adequate bowel contrast, can also demonstrate the course of fistulae and sinus tracts. Demonstrating these changes in the mesentery on CT may
help in distinguishing between causes of inflammatory
bowel disease, as mesenteric complications do not occur
in ulcerative colitis.
Mesenteric desmoid tumour
Mesenteric desmoid tumours (aggressive fibromatosis)
are infiltrating fibroblastic proliferations which do not
show the features of an inflammatory response or neoplasia [55]. They occur in 9±18 % of patients with familial adenomatous polyposis [56]. In this condition,
desmoid tumours arise either in musculoskeletal sites
or in the mesentery. Unlike muscular desmoids which
seldom cause symptoms, mesenteric desmoids are potentially life threatening. On CT the earliest changes
are an ill-defined loss of clarity of the normal mesenteric fat, which with time acquires a ªwhorledº appearance as linear soft tissue is interleaved with fat. This
retractile mesenteritis results in tethering, angulation
and then encasement of bowel. Finally, this desmoplastic response results in an irregular mass-like lesion often encasing loops of bowel, which is also well demonstrated on barium follow-through examination
(Fig. 9 a). Depending on the stage of development,
these masses vary in size between 2 and 20 cm. Up to
50 % of the masses will be 10 cm or larger at the time
of presentation. The infiltrative nature of desmoids
898
9a
9b
9c
9d
9e
10
Fig. 9a±e. Mesenteric desmoid tumour. a Axial CT showing an illdefined mesenteric desmoid tumour (arrows) encasing a loop of
small centrally (black arrow). b Axial T1-weighted MRI, at the
same level as the CT scan in a showing an ill-defined mesenteric
desmoid of low signal intensity (black arrows), encasing a loop of
bowel containing low-signal contrast (white arrows). c Axial T2weighted MRI in the same patient showing the ill-defined mesenteric desmoid (arrows), which is predominantly of low signal intensity with several areas of intermediate signal intensity. d Axial T2weighted images in a patient with a desmoid tumour showing low
signal ªwhorledº appearance (curved black arrow) surrounded by
areas of high signal (arrows). e Axial T2-weighted MRI in the
same patient as d 6 months later showing that the mass in the right
iliac fossa has grown markedly in size (arrows)
Fig. 10. Axial post-contrast CT in a patient who was found to have
an incidental omental cyst (arrows)
commonly results in obstruction of, or damage to, local
bowel loops and vascular structures, as well as the urinary tract [57].
On MRI, desmoid tumours generally have low signal
on T1- and T2-weighted scans due to their largely fi-
brous component (Fig. 9 b, c). however; those desmoids
with high signal on T2 have a tendency for rapid growth
(Fig. 9 d, e) [58].
Mesenteric/omental cysts
Mesenteric and omental cysts can be lymphatic hamartomas, lined by mesothelial cells with serous or chylous fluid within them, or enterogeneous cysts, derived
from a sequestered intestinal diverticulum [59]. The radiological appearance is the same irrespective of the aetiology. They appear as centrally placed soft tissue masses displacing adjacent bowel around them on the plain
abdominal film. On ultrasound they are well-defined,
echo-free fluid collections in the central abdomen. On
CT they are well-defined, single (occasionally multiple)
fluid-filled structures found most commonly in the small
bowel mesentery (Fig. 10). Occasionally, if there is a significant amount of chylous fluid present, there may be a
fat±water fluid level within them [60]. On MRI mesen-
teric cysts show the typical signal characteristics of fluid,
namely low signal intensity on T1-weighted images and
very high signal intensity on T2-weighted images.
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Book review
Hashemi, R. H., Bradley, Jr. W. G.: MRI: The Basics. London: Williams and Wilkins, 1997. 307 pp., 443 illustrations, (ISBN 0-68318240-4), £ 40.00.
This book ist not a mere introduction to the topic; instead, it aims
at a more in-depth approach through a comprehensive, step-bystep exploration of the physical principles underlying the MR phenomenon and MR image acquisition and processing. The authors
should be commended for their efforts to make this textbook readable and understandable. The chapters are kept short, essential information is singled out and numerous illustrations (over 400 in total) help visualize the concepts. The book is intended for radiologists and radiology residents as well as for radiology technologists.
The level of this work makes it equally suitable to provide a sound
basis for scientists and technologists in the field. Almost all MRimaging-related topics requiring some background are covered in
the 27 chapters spread over Part I, devoted to Basic Concepts,
and Part II, covering Fast Scanning.
For those wishing to refresh their elementary calculus skills, the
first chapter reviews the basic mathematical concepts used in this
text on MR imaging. The basic principles of NMR (magnetic
fields, spin, precession, RF pulses, relaxation) are introduced in
the following chapter and are discussed in more details in the subsequent chapters on radio frequency pulses, relaxation times T1,
T2 and T2*, and on TR, TE and contrast media. The authors should
be given credit for the (almost) consistent use of subscripts in the
relaxation time symbols. Chapters 7 and 8 introduce the pulse sequences and the concepts of saturation, inversion recovery and
spin echo. Chapter 8 is the unavoidable section on the Fourier
Transform required for the understanding of the subsequent discussions on image reconstruction and RF pulse bandwidth. Chapter 10 deals with slice selection and 11 with spatial encoding, in
which the authors take the reader in the (usual) step-by-step approach of frequency and phase encoding of a small (3 3) array
of pixels. The ªsignal processingº chapter, unlike its title, discusses
signal acquisition parameters such as sampling time and duration,
the Nyquist theorem and aliasing, bandwidth, etc. Two chapters
are devoted to the properties of k-space and the relations between
FOV, gradient strength and bandwidth. Chapter 17 integrates all
previous concepts on image acquisition in the relationships be-
55. Mackenzie DH (1972) The fibromatoses: a clinico-pathological
concept. Br Med J 4: 277±281
56. Farmer KCR, Hawley PR, Phillips RKS (1994) Desmoid disease. In: Phillips RKS, Spigelman AD, Thompson JPS (eds)
Familial adenomatous polyposis and other polyposis syndromes. Edward Arnold, London, pp 133±136
57. Brooks AP, Reznek RH, Nugent K, Farmer KCR, Thompson
JPS, Phillips RKS (1994) CT appearances of desmoid tumours
in familial adenomatous polyposis: further observations. Clin
Radiol 49: 601±607
58. Healy JC, Reznek RH, Clark SK, Phillips RKS, Armstrong P
(1997) Appearances of desmoid tumours in familial adenomatous polyposis. AJR 169: 465±472
59. Hjermstad BH, Sobin LH (1987) Mesenteric and omental cysts:
histologic classification with imaging correlation. Radiology
164: 327
60. Sivit C (1996) CT scan of mesentery±omentum peritoneum.
Radiol Clin North Am 34 (4): 863±884
European
Radiology
tween signal-to-noise ratio, the ultimate image-quality index and
the various image-acquisition parameters. The first part closes on
a concise survey of MR image artefacts and their corresponding remedies, supported by appropriate photographic material, which
unfortunately is of medium quality. The remaining one third of
the book is dedicated to Part II on fast scanning. Chapter 19 covers
fast spin echo and its numerous variants including a discussion of
the corresponding trade-offs and disadvantages. The next two
chapters present the basic principles and various techniques of gradient-echo sequences, including the related S/N, contrast and artefacts issues. Echo-planar imaging (EPI) is the subject of a (too
short) separate chapter, describing the main features of this increasingly used type of sequence. The discussion of fast sequences
concludes with a summary of recent and advanced image acquisition software features such as fractional k-space, fractional echo,
rectangular FOV, oversampling, spatial and spectral saturation.
Tissue suppression techniques (STIR, FLAIR, magnetization
transfer and presaturation) have been grouped under a common
heading. Chapter 25 and 26 are devoted to a discussion of the basics of flow phenomena and their application to MR angiography.
The concluding section is a brief discussion of the new technology
of high performance, i. e. high-amplitude-, short-rise-time gradients, required for any fast imaging sequence.
This brief overview should convince the potential reader of the
extent of topics covered by this excellent book. Both content and
presentation have been designed to ease the access to a thorough
understanding of the physical concepts. Self-study is facilitated
and encouraged through the summaries of key points, the numerous examples and the questions at the end of each chapter (answers provided at the end of the book). A quite exhaustive index
is provided; unfortunately, some frequently used acronyms, such
as STIR or FLAIR, are not listed as such. Overall, the limited
mathematics and the abundant illustration offered by this book
make it a suitable choice at an affordable price for a more advanced study of the imaging concepts and parameters, their relationships and their ultimate impact on image contrast, quality and
speed of acquisition, the key issues in daily MR imaging.
P. Van Hecke, Leuven

Abdominal radiology Review article The peritoneum, mesenteries

Transcription

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