AJR 2005; 184:156-162
© American Roentgen Ray Society
Omental Infarction in Children: Color Doppler Sonography Correlated with Surgery and Pathology Findings
Matteo Baldisserotto1,
Deise Regina Maffazzoni2 and
Marcelo Dourado Dora3
1 Departamento de Radiologia, Hospital da Criança
Conceição, Ministério da Saúde–Brazil, Rua
Francisco Trein, 596, Porto Alegre, RS, CEP 91350-200, Brazil.
2 Departamento de Patologia, Hospital da Criança Conceição,
Ministério da Saúde, Porto Alegre, RS, 91350-200, Brazil.
3 Departamento de Pediatria, Hospital da Criança Conceição,
Ministério da Saúde, Porto Alegra, RS, 90035-030, Brazil.
Received February 15, 2004;
accepted after revision April 12, 2004.
Address correspondence to M. Baldisserotto
(matteo{at}via-rs.net).
Abstract
OBJECTIVE. The objective of our report is to describe color Doppler
sonography findings of omental infarction and correlate them with surgical and
pathology findings. Ten children underwent preoperative gray-scale and color
Doppler sonographic examinations; omental infarction was confirmed at
surgery.
CONCLUSION. Color Doppler sonography findings were reviewed and
correlated with surgical and pathology findings. Color Doppler sonography
features of idiopathic omental infarction differ from those of infarction
secondary to omental torsion.
Introduction
Omental infarction, sometimes idiopathic but more commonly associated with
omental torsion, is a rare cause of acute abdomen in adults and children
[1,
2]. According to Sweeney et al.
[1], approximately 0.1% of
children undergo laparotomy for suspected appendicitis that is diagnosed later
surgically as omental infarction associated with torsion. Our review of the
medical literature revealed that the first studies about omental torsion that
report sonography and CT findings are isolated case reports. In 1992, Puylaert
[3] described sonography and CT
findings of omental infarction for seven patients ranging in age from 10 to 77
years who were treated conservatively. More recently, three studies have
described sonography findings
[4] or sonography and CT
findings [5,
6] in relatively large samples
of children with omental infarction. In those studies, diagnoses were
confirmed surgically.
Although several studies have described sonography findings for omental
infarction in children and have correlated them with surgical and pathology
findings, our review of the literature did no yield any studies that report
color Doppler sonography findings and correlate them with surgical and
pathology findings. Therefore, the purpose of our study was to report 10 cases
of omental infarction in patients who underwent surgery. We describe clinical,
color Doppler sonography, and surgical and pathology findings of omental
infarction, and we correlate color Doppler findings with surgical and
pathology findings.
Subjects and Methods
This prospective study describes medical records of 10 pediatric patients
(eight boys and two girls) who were diagnosed with omental infarction at
surgery and by pathologic examination of specimens and who had undergone
gray-scale and color Doppler sonography examinations preoperatively. Patients
were seen in our institution from June 2001 to October 2003, and their ages
ranged from 5 to 11 years (mean age, 7.5 years). Lesion size, site,
echogenicity, form, and vascularization were evaluated. Gray-scale and color
Doppler sonography findings were correlated with surgical and pathology
findings. This study was approved by the ethics committee of the institution
where the investigation was conducted.
All patients underwent sonographic examination because of symptoms
suggestive of acute appendicitis with an atypical presentation. They presented
with intense diffuse abdominal pain in the right lower quadrant for more than
24 hr; five patients complained of pain for 3 or more days. A complete blood
count was performed for all patients. One patient had leukocytosis with a left
shift, two had a leukocyte count at the upper limit of the normal range, and
the other children had a normal blood count. Only one patient was febrile
(38.5°C) at presentation. No abdominal masses were palpable at physical
examination. All children's weights were between the 75th and 90th percentile
for their age.
All patients underwent preoperative sonographic examination; other imaging
examinations—radiography or CT—were not performed. An HDI-5000
scanner (Advanced Technology Laboratories) and curved 7-4–MHz and linear
12-5–MHz transducers were used for the sonographic studies. All
examinations were performed by one of four experienced pediatric radiologists
from our radiology department, all of whom have qualifications equivalent to
the certification of the American Board of Radiology. The sonographic
criterion for the diagnosis of omental infarction was the identification of
both a hyperechoic mass in the right abdomen and a normal appendix.
Although a diagnosis of omental infarction was suggested strongly by color
Doppler sonography findings in six cases in our study, our institution still
adopts the surgical procedure that prescribes the removal of infarcted tissue
[7]. Infarcted omental tissue
and appendix were removed from all patients at surgery. All surgical specimens
underwent pathologic examination.
Results
Omental infarction was diagnosed for all 10 patients at surgery and was
confirmed at pathologic examination of the surgical specimens; it was
idiopathic in eight patients and secondary to torsion in two. Sonography
findings suggested a diagnosis of omental infarction for the six patients
whose normal appendix was visualized. For the four patients whose appendix was
not identified, preoperative sonography findings were inconclusive.
Sonographic studies revealed a hyperechoic mass adjacent to the anterior
abdominal wall in all 10 patients. Mass diameters ranged from 2.0 to 6.2 cm.
The mass was in the right upper quadrant, anteromedial to the ascending colon,
in seven patients, and in the right iliac fossa in three patients. It was
triangular (Fig. 1A) in five
patients, amorphous in three, and ovoid in two. No cases of a mass in the
middle line or in the left abdomen were found.
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Fig. 1A. —7-year-old girl with abdominal pain for 1 week and
leukocytosis. Transverse gray-scale sonogram shows cakelike hyperechoic mass
in right upper quadrant (arrows) with poorly defined hypoechoic areas
(arrowheads).
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At gray-scale and color Doppler sonography, six of the eight cases of
omental infarction without torsion showed avascular, poorly defined hypoechoic
nodular areas within a hyperechoic mass surrounded by hyperemia (Figs.
1A,
1B, and
1C); the other two cases showed
avascular, poorly defined hypoechoic linear areas (Figs.
2A,
2B, and
2C). Gross examination of
specimens revealed small areas suggestive of infarction and necrosis
interspersed with omental parenchyma with edema and vascular congestion (Figs.
1D and
2D). These findings were
confirmed at microscopic examination.
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Fig. 2A. —8-year-old boy with abdominal pain for 3 days and leukocyte
count within normal range. Transverse gray-scale sonogram shows poorly defined
hyperechoic mass next to anterior abdominal wall in right upper abdominal
quadrant (arrows) that contains poorly defined linear hypoechoic
structure (arrowheads).
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Fig. 2B. —8-year-old boy with abdominal pain for 3 days and leukocyte
count within normal range. Transverse color Doppler sonogram shows a few
vessels inside mass (arrow) and absence of vessels in poorly defined
linear hypoechoic structure (arrowheads).
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Fig. 2C. —8-year-old boy with abdominal pain for 3 days and leukocyte
count within normal range. Cranial color Doppler sonogram shows large vessels
inside cranial region of hyperechoic tissue (arrows).
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Fig. 1D. —7-year-old girl with abdominal pain for 1 week and
leukocytosis. Photograph of gross pathologic specimen shows streaks of
necrosis and hemorrhage crossing omentum (arrows). Preserved tissue
can be visualized between areas of necrosis (arrowheads). Scale:
centimeters.
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Fig. 2D. —8-year-old boy with abdominal pain for 3 days and leukocyte
count within normal range. Photograph of gross pathologic specimen from
examination of omental tissue removed at surgery reveals that linear structure
corresponded to tissue with hemorrhage and necrosis (arrows) within
congested omental tissue (arrowheads).
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Microscopic examination also revealed that six of the eight patients with
infarction without torsion had arterial and venous congestion and the
remaining two had arterial thrombosis and venous congestion. The correlation
of sonography and gross pathology findings revealed that the distribution and
size of the hypoechoic areas within the mass closely conformed to the areas of
hemorrhagic infarction. The hyperechoic area corresponded to preserved omental
tissue with edema and vascular congestion.
In the two patients with omental infarction with torsion, sonography
revealed slightly different tubular hypoechoic structures within the
hyperechoic mass. In one patient, color Doppler sonography showed an
avascular, poorly defined tubular structure surrounded by hyperemic
hyperechoic tissue and by a large artery (Figs.
3A,
3B,
3C, and
3D). At surgery, this tubular
structure was found to be a narrow segment of greater omentum twisted on
itself several times (Fig.
3E). Gross and microscopic examinations of the twisted segment
revealed an area of intense infarction and necrosis surrounded by edematous
and congested tissue (Fig.
3F). Gross examination revealed a large artery with no signs of
thrombosis surrounding omental tissue. Microscopy revealed venous thrombosis
and arterial congestion.
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Fig. 3A. —7-year-old boy with abdominal pain for 2 days and leukocyte
count at upper limit of normal range. Longitudinal gray-scale sonogram shows
blind-ending hypoechoic tubular structure (arrowheads) within
hyperechoic mass (arrows).
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Fig. 3B. —7-year-old boy with abdominal pain for 2 days and leukocyte
count at upper limit of normal range. Transversal gray-scale sonogram shows
blind-ending hypoechoic tubular structure (arrowheads) within
hyperechoic mass (arrows).
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Fig. 3C. —7-year-old boy with abdominal pain for 2 days and leukocyte
count at upper limit of normal range. Longitudinal color Doppler sonogram
detects blood flow in artery (arrows) around hypoechoic avascular
structure (arrowheads).
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Fig. 3D. —7-year-old boy with abdominal pain for 2 days and leukocyte
count at upper limit of normal range. Transverse color Doppler sonogram shows
spiraling artery around hypoechoic structure (arrows). Pathologic
examination confirmed presence of large-diameter artery surrounding twisted
and infarcted omental tissue.
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Fig. 3E. —7-year-old boy with abdominal pain for 2 days and leukocyte
count at upper limit of normal range. Photograph of surgical specimen shows
central axis of omental torsion with signs suggestive of ischemia
(arrows).
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Fig. 3F. —7-year-old boy with abdominal pain for 2 days and leukocyte
count at upper limit of normal range. Photograph of gross pathologic specimen
shows central necrosis and hemorrhage (arrows) surrounded by
peripheral rim of well-preserved adipose tissue (arrowheads). Size
and form of infarcted tissue conform to color Doppler sonographic measurements
of avascular hypoechoic tubular structure. Scale: centimeters.
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In the second patient with omental infarction with torsion, the tubular
hypoechoic structure was large, well defined, and composed of layers of
omental tissue separated by small amounts of fluid (Figs.
4A and
4B). Color Doppler sonography
did not reveal any blood flow within this structure, but sonography did show
hyperemia of the adjacent hyperechoic tissue (Figs.
4C and
4D). Surgery confirmed omental
infarction secondary to torsion. Gross pathologic examination revealed folded
layers of omentum with significant infarction and necrosis that were
surrounded by adipose tissue with vascular congestion and edema
(Fig. 4E); these findings were
confirmed at microscopic examination. Microscopic examination revealed signs
of arterial thrombosis and venous congestion in omental tissue. A thin layer
of fibrous tissue separated the infarcted area from normal omental tissue,
which suggests that omental infarction secondary to torsion in this case might
have resulted from a chronic process. The correlation of sonography and gross
pathology findings in these two cases indicated that the avascular hypoechoic
structure corresponded to infarcted tissue: Pathologic measurements conformed
in size and form to sonography findings. The hyperemic hyperechoic area
corresponded to preserved congested omental tissue.
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Fig. 4A. —10-year-old girl with abdominal pain for 3 days and leukocyte
count at upper limit of normal range. Transverse gray-scale sonogram shows
blind-ending hypoechoic tubular structure composed of layers
(arrowheads) separated by small amount of fluid (F) within
hyperechoic mass (arrows). Sonographic appearance is difficult to
distinguish from that of nonperforative appendicitis.
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Fig. 4B. —10-year-old girl with abdominal pain for 3 days and leukocyte
count at upper limit of normal range. Longitudinal gray-scale sonogram shows
hypoechoic tubular structure (arrowheads) surrounded by hyperechoic
tissue (arrows).
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Fig. 4C. —10-year-old girl with abdominal pain for 3 days and leukocyte
count at upper limit of normal range. Transverse color Doppler sonogram does
not detect blood flow in hypoechoic structure (arrows); sonogram
shows hyperemia of adjacent hyperechoic tissue (arrowheads).
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Fig. 4D. —10-year-old girl with abdominal pain for 3 days and leukocyte
count at upper limit of normal range. Longitudinal color Doppler sonogram
shows hypoechoic avascular structure corresponds to infarcted omentum
(arrows) surrounded by hyperechoic adipose tissue with adjacent
hyperemia (arrowheads).
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Fig. 4E. —10-year-old girl with abdominal pain for 3 days and leukocyte
count at upper limit of normal range. Photograph of gross pathologic specimen
shows folds of omentum forming necrotic and hemorrhagic layers in central
region (large arrows), surrounded by peripheral rim of well-preserved
adipose tissue (arrowheads). Folds are separated from preserved
peripheral tissue by thin streak of fibrosis (small arrows). Size and
form of folded infarcted omental tissue conformed to color Doppler sonographic
measurements of avascular hypoechoic tubular structure. Scale:
centimeters.
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A small amount of free intraabdominal fluid between bowel loops and in the
cul-desac was observed in all patients on sonography. At surgery, a small
amount of free serosanguineous fluid was found in the abdominal cavity. In
three patients, mesenteric lymph nodes, with their largest diameters ranging
from 1.0 to 1.5 cm, were adjacent to the hyperechoic lesion. Pathologic
examination of the lymph nodes revealed a nonspecific inflammatory process.
The appendix was removed from all patients, and pathologic examination of the
specimens did not reveal any significant changes.
Discussion
Omental infarction is a rare entity, particularly among children, and its
pediatric prevalence is difficult to calculate accurately because of the small
number of cases reported in literature. MacLean
[2] reviewed 165 cases of
primary omental torsion and found that only 15% of the patients were children.
This disease affects adult men and boys more frequently, but to date no
explanation has been found for this fact. Clinically, omental infarction often
mimics acute appendicitis because patients usually present with acute onset of
right lower quadrant pain, and approximately 50% report nausea, vomiting,
bowel disorders, dysuria, and fever
[7].
Although its pathogenesis is still unknown, omental infarction has been
shown to occur with or without torsion
[8]. Idiopathic omental
infarction is associated with predisposing factors, such as kinking of veins
caused by the patient's position or vascular congestion after a large meal,
which may lead to thrombosis and infarction of the omentum
[7]. In omental torsion, the
omentum twists gradually, compromising venous and arterial blood flow and
resulting in omental infarction and necrosis. Omental torsion may be primary
or secondary; secondary torsion is the more frequent presentation
[9]. Pathogenesis of primary
omental torsion is assigned to pure volvulus of the free edge of the omentum
[7]. Some predisposing factors
have been reported, such as a bifid omentum, a tonguelike portion of omentum,
and obesity [8]. Secondary
torsion may be caused by attachment of part of the omentum to acquired lesions
(hernias, cysts, tumors, previous surgical scars) or may be associated with a
primary congenital defect in the attachment of the omental portion to the
cecum, ascending colon, or both
[7].
The characteristic gross pathology findings of omental infarction are an
edematous, reddish blue to black portion of the greater omentum hanging free
by an elongated, narrow segment that has twisted around its own axis several
times [10]. When omental
infarction is idiopathic, gross pathologic examination reveals the presence of
an omental mass with areas of hemorrhagic infarction. The earliest microscopic
finding is hemorrhagic infarction; later, varying degrees of inflammatory
infiltrate are seen. The most advanced stage is characterized by the presence
of a fibroblastic reaction
[1].
In our series, there were more boys than girls, at an 8:2 ratio, which is
similar to ratios reported in literature. Our patients were above the average
weight for their age, and obesity might have been a predisposing factor.
Omental infarction occurred without torsion in eight patients and with torsion
in two. This ratio differed from that reported by Schlesinger et al.
[4], who found that omental
infarction was secondary to torsion in seven and without torsion in two of the
nine patients that they studied. In a study conducted by Helmrath et al.
[5], no distinction between
infarction with or without torsion could be made at surgery. In a study
performed by Grattan-Smith et al.
[6], the mechanism of omental
infarction was not mentioned.
The identification of an ovoid or cakelike hyperechoic mass adherent to the
peritoneum and located in the umbilical region or anterolaterally to the right
half of the colon has been described as suggestive of omental infarction.
Puylaert [3] and Schlesinger et
al. [4] described hypoechoic
areas within the hyperechoic mass, but their studies did not define the nature
of those findings. Schlesinger et al. reported nine cases of omental
infarction; they identified a homogeneous hyperechoic lesion in four cases, a
complex mass in three, a hypoechoic tubular structure in one, and no
detectable changes in one. Grattan-Smith et al.
[6] performed sonographic and
CT examinations in nine of 13 children with omental infarction: two children
underwent sonography; four, sonography and CT; and three, CT only. Sonography
detected a hyperechoic mass in the right abdomen in only three cases. Helmrath
et al. [5] reported 18 cases of
omental infarction; 14 patients in their series underwent sonographic
examination. The authors reported that in 10 of these 14 patients, omental
infarction was visualized on sonography as a hypoechoic mass. This finding
differs from those reported by Schlesinger et al. and Grattan-Smith et al.,
who reported cases in which sonography findings were interpreted as suggestive
of appendicitis.
We observed two characteristic appearances on gray-scale and color Doppler
sonography that conformed to pathology findings. The more frequent appearance,
seen in the eight cases of infarction without torsion, was a hyperechoic mass
containing poorly defined nodular or linear hypoechoic areas with few vessels
within the mass and hyperemia in the peripheral area. Gray-scale sonography
images were similar to those observed by Puylaert
[3] in some of his patients.
Gross pathologic examination of surgical specimens of idiopathic infarction
revealed small areas of necrotic tissue within the omental mass. The
correlation of sonography and color Doppler sonography findings revealed that
the distribution and size of areas of hemorrhagic infarction conformed to the
distribution and size of the hypoechoic areas within the hyperechoic mass.
The other characteristic appearance, observed in two cases, was a hyperemic
hyperechoic mass containing an avascular hypoechoic tubular structure.
Gray-scale sonography findings were similar to those observed by Schlesinger
et al. [4] in three of their
cases—that is, the sonographic appearance mimicked appendicitis. Surgery
confirmed omental torsion in these two patients in our series. The correlation
of gross pathologic and sonography findings showed that the avascular
hypoechoic tubular structure corresponded to the twisted and infarcted omental
tissue. In one of these cases, visualization of an artery around the tubular
structure was important in defining the mechanism of infarction. To date, the
identification of a spiraling artery on CT has been reported in only one case
of left-sided omental torsion
[11]. The extension and degree
of hemorrhagic infarction were greater in these two patients than in the
patients with idiopathic infarction.
Although observed in a small number of cases, which is a limitation of this
study, pathologic and color Doppler sonography features of idiopathic omental
infarction and omental infarction secondary to omental torsion were
different.
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A. C. van Breda Vriesman, J. B. C. M. Puylaert, and M. Baldisserotto
Omental Infarction: A Self-Limiting Disease
Am. J. Roentgenol.,
July 1, 2005;
185(1):
280 - 281.
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Abstract
Introduction
