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96 Pathology of the mesentery
locally, have high rates of recurrence, but do not metasta-
size [78]. Genetic, endocrine, and trauma-related factors
are linked to their etiology. Desmoid tumors are associ-
ated with familial adenomatous polyposis, multiparity,
and postsurgical scars [79]. Mutations within genes cod-
ing for adenomatous polyposis coli and beta-catenin are
implicated [80]. Although they lack metastatic potential,
they progress locally and can ultimately compromise mes-
enteric vasculature or cause obstruction. ere are several
treatment modalities, but surgical excision remains the
mainstay [78]. Postoperative radiotherapy reduces the rate
of local recurrence [78].
Contained sigmoid perforation
Forceps in
perforated
diverticulum
Epiploicae
limiting
perforation
Mesosigmoid
(a)
Sigmoid mucosa
(b)
(c)
Figure 7.8 (a) Postoperative image of a colonic perforation contained within the appendices epiploicae of the
colon. (b) Postoperative image of the mesosigmoid demonstrating clear thickening and edema of the mesosigmoid.
(c)Postoperative image of mucosa in specimen from A and B, pointing to the perforation.
Secondary mesenteropathies 97
MESENTERIC CYSTS
A rare form of primary mesenteropathy, mesenteric cysts are
more likely to develop on the mesentery of the small bowel or
right colon [81] (Figure 7.9). While the etiology is unknown,
developmental abnormalities of mesenteric lymphatics may
play a role [82]. ey can present clinically in a broad range
of manners, including asymptomatic abdominal swelling,
chronic abdominal pain or as an acute abdomen secondary
to torsion, infection, or hemorrhage into the cyst itself [83].
SCLEROSING MESENTERITIS
Sclerosing mesenteritis includes a range of conditions
characterized by chronic inammation, brosis, and
(sometimes) necrosis of the mesenteric organ. Mesenteric
lipodystrophy, mesenteric panniculitis, and IgG4-related
sclerosing mesenteritis are included in this class of primary
mesenteric abnormality. Although its etiology remains
unknown, reports suggest links with aberrant autoimmu-
nity or previous abdominal surgery [84].
Mesenteric panniculitis is classically described as
a paraneoplastic phenomenon although it has been
observed in the absence of a background malignancy
[85,86]. Patients with MP may present with an abdomi-
nal mass, pain, nausea, vomiting, or altered bowel habit
[84]. Systemic manifestations including anorexia, weight
loss, or fever can be prominent [84]. Treatment is usually
based on immunosuppression with corticosteroids and
azathioprine, perhaps refl cting a primary immunologic
or inammatory basis [87].
IgG4-RELATED SCLEROSING
MESENTERITIS
IgG4-related sclerosing mesenteritis is an intra-abdominal
manifestation of IgG4-related disease. IgG4-related dis-
ease can aff ct virtually any organ and mesenteric lesions
are characterized by lymphoplasmacytic inltrate and
storiform brosis [88]. Obliterative phlebitis accompanies
plasma cell inltrations. Patients present with nonspecic
symptoms such as abdominal pain, and imaging reveals a
mesenteric mass [89]. Immunosuppression is the mainstay
of treatment. Glucocorticoids are the rst line of therapy
while refractory cases are treated with disease-modifying
antirheumatic drugs or rituximab [89].
MESENTERIC NEUROLOGIC PATHOLOGY
e intestine receives postganglionic sympathetic and
parasympathetic nerves that regulate myriad functions.
ese nerves are derived from three main ganglia at
the origins of the celiac trunk, the superior and inferior
mesenteric arteries. Apart from these assertions, there
is a dearth of information describing the relationship of
postganglionic nerves to the mesentery. Recent clarica-
tion of mesenteric structure indicates that postganglionic
nerves must enter and traverse the mesentery along with
major vessels. At the intersection between mesentery and
adjacent gastrointestinal tract, they penetrate the outer
layers of the latter and ultimately reach Meissner’s and
Auerbach’s plexus.
e enteric nervous system (ENS) regulates peristalsis,
secretion, absorption, local inammation, and immune
responses [90]. During embryogenesis of the ENS, the
mesentery acts as a conduit for enteric neural crest cells
migrating from midgut to hindgut regions. As a result, the
development of a mesentery in the rst instance is essential
for eff ctive innervation of the hindgut [91]. It has been sug-
gested that Hirschsprung’s disease arises from a failure of
transmesenteric migration of enteric neural crest cells [90].
Incomplete mesenteric migration of neural crest cells is linked
to multiple endocrine neoplasia, neuroblastoma, conotrun-
cal heart defects, and Waardenburg syndrome [92]. A delay
in ENS maturation may be responsible for the deranged
motility seen following surgical correction of gastroschisis
[93]. e later is associated failure of development of the
interstitial cells of Cajal, cells analogous to cardiac pace-
maker cells.
Although rare, terminal ileal mesenteric schwannomas
have been reported, pointing to a distribution of neural tis-
sue within the mesentery [94].
SECONDARY MESENTEROPATHIES
ese are abnormalities that arise outside the mesentery but
which can progress to involve the mesentery through either
direct or systemic spread.
Mesentery
Mesenteric cyst
Mesenteric
cyst
Figure 7.9 Intraoperative image of a mesenteric cyst on
the medial aspect of the mesosigmoid. The cyst con-
tained clear uid and had a smooth inner surface. It was
an incidental nding at surgery.
98 Pathology of the mesentery
APPENDICITIS
Although appendicitis is not a primary mesenteropa-
thy (i.e., a disease arising primarily from the mesen-
tery), a discussion of the retrocecal appendix is relevant.
Heretofore, this entity was not well accounted for. is in
itself is surprising as in most instances the appendix tip
occupies a retrocecal location. e reason for this is ana-
tomic and lies in the fact that the mesoappendix extends
from the undersurface of the mesentery [95]. At the junc-
tion of the ileum and cecum, the mesentery tapers toward
an apex. It is from the undersurface of this apex that the
mesoappendix extends to bridge the gap between it and
the appendix. As the mesoappendix is retromesenteric, so
too is the appendix.
e retromesenteric or retrocecal position of the appen-
dix partially explains the variability in how appendicitis
may present (Figure 7.10). If the appendix is positioned
posterior to the cecum, then inammation there is more
likely to be walled off by adjacent structures and not lead to
overt symptoms. If the mesoappendix is lengthy, then the
appendix is more likely to lie free in the right iliac fossa.
Here, it comes into direct contact with the anterior abdomi-
nal wall leading to early peritonism. us, the position of
the mesoappendix may account for the lack of diagnostic
certainty that oen accompanies appendicitis or pain in the
right iliac fossa.
PHLEGMON
Phlegmon is a frequently encountered surgical problem
(Figure 7.11). A phlegmon is an inammatory complex
involving multiple segments of the intestinal tract and
associated mesentery. It results from ongoing inamma-
tion and is mostly seen with diverticular disease, Crohn’s
disease, or prolonged untreated appendicitis (Figure 7.11).
It is important to discuss it in this chapter as the mesentery
is frequently, if not invariably involved. As a general rule,
surgeons avoid operating on a phlegmon unless compelled
to do so. Within the abdomen (as with most body cavities),
inamed surfaces tend to adhere to each other. e degree
of adhesion varies from minor to dense. With dense adhe-
sions, separation of components of a phlegmon can lead to
further mesenteric damage and devascularization. If the
surgeon is not comprehensively familiar with mesenteric
anatomy then he/she will struggle to identify and safely
separate phlegmon components.
MESENTERIC ADENITIS
Mesenteric adenitis may represent a secondary mesenter-
opathy as the primary abnormality is a systemic viremia.
Mesenteric adenitis is associated with right iliac fossa pain
similar to that seen in appendicitis. e etiology of the pain
is unknown thus oen making the two conditions indis-
tinguishable thereby necessitating surgical exploration
under general anesthesia. Eff rts on preventing potentially
Anti-mesenteric
border
Fat wrapping
Fat wrapping
Figure 7.11 Phlegmon involving inamed terminal ileum,
with adherent small bowel loops. There is fat wrapping of
the terminal ileum.
The mesoappendix and retrocecal appendix
Mesoappendix
Undersurface of
mobilized small
intestinal mesentery
Undersurface of
right mesocolon
Ascendin
g
colon
Figure 7.10 Appendix and mesoappendix. The mesoap-
pendix is arising from the undersurface of the junction
between small intestinal mesentery and right mesocolon
and had a retrocecal position. As a result, the appendix
only became apparent after mobilization of the mesoco-
lon and mesentery.
Peritoneal carcinomatosis 99
harmful surgical exploration center on the development
of molecular biomarkers including fecal calprotectin and
procalcitonin and cellular biomarkers including brocytes
[96 –98].
It is not known why symptoms in mesenteric adeni-
tis primarily aff ct the right iliac fossa. It is known that
the condition is associated with a pronounced mesenteric
lymphadenopathy in that region (Figure 7.12). However, a
similar lymphadenopathy occurs throughout the mesen-
tery and probably reects a systemic process. As described
in previous chapters, the small intestinal mesentery and
right mesocolon are continuous structures. is anatomic
property generates a mesenteric and lymphatic watershed
with an apex in the right iliac fossa, that is, at the junction
between the terminal ileum and cecum. It is feasible that the
substantive nature of the mesentery here inuences local-
ization of symptoms to the right side.
LYMPH OMA
e most common primary neoplasm of the mesentery is
diuse large B cell lymphoma [99]. Median age at presen-
tation is 70years and oen results from rapid enlargement
of a lymph node complex. One-third present with stage IV
disease, one-third have B symptoms (including fever, night
sweats, and weight loss), and half of all patients have an
elevated serum lactate dehydrogenase [100]. Mesenteric
lymphoma (ML) is usually asymptomatic in early stages dur-
ing which lymphatic expansion can be considerable [101]
(Figure7.13). Tumors can extend around mesenteric vascu-
lature to shackle vessels, but without causing ischemia [102].
Symptoms include abdominal pain, development of a pal-
pable mass, and postprandial fullness [102]. Computerized
axial tomographic (CT) imaging, coupled with biopsy, is
usually required for diagnosis. At CT, the “sandwich sign”
is specific for ML [103]. e presence of a soft- issue mass
with an air-uid level, combined with rarity of MLs, has led
to misdiagnosis as intra-abdominal abscesses [104].
PERITONEAL CARCINOMATOSIS
Peritoneal carcinomatosis is diuse intraperitoneal malig-
nancy arising in association with solid organ malignancies
such as ovarian, gastric, or colorectal. e mechanism by
which intraperitoneal spread occurs is unknown. e iden-
tication of free and viable malignant cells on peritoneal
uid cytology suggests the distribution may relate to ow.
However, this theory alone cannot explain why foci of neo-
plastic disease develop in multiple locations, oen separated
by substantial anatomic boundaries (i.e., pelvis, hemidia-
phragm, omentum, and intestinal tract) (Figure 7.14). If the
ow theory were correct, then one might expect to observe
a carpeting of malignancy, rather than the diuse punctate
pattern that is usually observed.
Recent histologic observations related to the mesen-
tery may shed light on the mechanism of spread in peri-
toneal carcinomatosis. Minute lymphatic vessels occur
within the mesenteric connective tissue lattice [105]. In
the submesothelial component of this lattice, these ves-
sels are intimately juxtaposed with surface mesothelium.
As the mesenteric connective tissue lattice is continuous
with that of the intes tinal tract, it is feasible that this pro-
vides a histologic platform for spread onto the intestinal
surface. is lymphatic-based theory is partly supported
by the experimental observations of Boni etal. [106]. ey
injected a human colon cancer cell line in two locations in
Lymph-
adenopath
y
Mesenteric and epiploical lymphadenopathy
Right
mesocolic
fat
C
oalescent
mesocolic
lymph-
adenopth
y
Cecum
Appendices
epiploicae
fat
Figure 7.12 Intraoperative image taken at laparoscopy.
The patient underwent a laparoscopic exploration for
investigation of right iliac fossa pain. There was extensive
mesocolic lymphadenopathy. Lymphadenopathy was also
evident in the appendices epiploicae overlying the cecum
and colon.
Right
mesocolon
Toldt’s fascia
Mass in
right
mesocolon
Figure 7.13 Axial computerized tomography slice dem-
onstrating lymphatic mass in the right mesocolon. The
patient underwent an ileocolic resection and was found to
have lymphoma on histology.
100 Pathology of the mesentery
a rat model. Injection in the rst location (i.e., the inter-
mesenteric border of the intestine) was followed by a pat-
tern of spread similar to peritoneal carcinomatosis, with
minimal mesenteric nodal spread. In contrast, when the
cells were injected into intestine near the intestinal hilum,
nodal spread was more prominent and peritoneal carci-
nomatosis less frequent [106].
NEUROENDOCRINE TUMORS
Neuroendocrine tumors (including carcinoid tumors) are
well-diffe entiated secretory tumors derived from entero-
chroman cells of the intestinal tract [107]. ey are cur-
rently classifi d based on embryonic origin. Although
primary mesenteric neuroendocrine tumors are rare, sec-
ondary mesenteric metastatic deposits are not an uncom-
mon nding in neuroendocrine tumors of midgut origin
(Figure 7.15a and b) [108]. Primary mesenteric neuroen-
docrine tumors may be explained by defective or incom-
plete mesenteric migration of neural crest cells. Release
of vasoactive substances and neuropeptides, most notably
serotonin, into the systemic circulation is responsible for
the clinical carcinoid syndrome: diarrhea, facial ushing,
bronchoconstriction, and right-sided valvular disease
[109]. Kinking of the mesentery secondary to prominent
mesenteric brosis and desmoplasia may lead to small
bowel obstruction. While carcinoid syndrome mostly
Carcinoid and metastatic deposit
Intestinal
carcinoid
Intestinal
carcinoid
Metastatic
lymph node
associated
with
ileal carcinoid
Figure 7.15a
(a)
(b)
Figure 7.15 (a) Intraoperative image of terminal ileal carcinoid. (b) Mesenteric lymphatic metastasis (postmesenterectomy)
in the same patient as in (a).
Peritoneal carcinomatosis
Terminal ileum
Serosal
metastatic
deposit
Figure 7.14 Peritoneal carcinomatosis on the surface of
the small bowel.
Congenital adhesion formation 101
occurs aer metastatic hepatic invasion, there are reports
of systemic symptoms without liver involvement [110].
e mesenteric connective tissue complex may serve as a
conduit between the mesenteric and systemic vasculature
and could partly explain this phenomenon.
CASTLEMAN’S DISEASE
Castleman’s disease is a benign lymphoproliferative disor-
der that can aff ct any part of the body containing lym-
phoid tissue [111]. e disease can be localized or systemic
and is histologically divided into hyaline-vascular type or
plasma cell type [111]. In 70% of cases, the mediastinum
is aff cted, while less than 10% occur intra-abdominally
[112]. e etiology is unknown, with current theories
focusing on a chronic inammatory reaction against an
unknown antigen or defect in immunoregulation of B
lymphocytes [113]. As the mesenteric organ is rich in lym-
phatics, it is not surprising that it may be involved in intra-
abdominal disease.
Mesenteric lymphoproliferation can be substantial as
reected in a report of a mass occupying the entire mesorec-
tum with mesosigmoid inltration [114]. Although mostly
localized and asymptomatic, disseminated Castleman’s
disease is associated with a systemic inammatory-like
response manifesting with fever, splenomegaly, and leuko-
cytosis [112]. Diagnosis is made following resection, which
is usually curative with localized disease [114]. Compression
of local structures and radiologic similarities with lym-
phoma, tuberculosis, sarcoidosis, and retroperitoneal sar-
coma create a challenge in diagnosis [115].
MESENTERIC LYMPH NODE CAVITATION
SYNDROME
As the name suggests, mesenteric lymph node cavitation
syndrome is associated with necrosis of mesenteric lymph
nodes. It has been linked with celiac disease [116]. While
the etiology and pathobiology are poorly understood, it is
suggested that excessive prolonged exposure to intestinal
antigens leads to lymphocyte depletion, involution, and
cavitation of mesenteric lymph nodes [116]. Radiological
investigation reveals a mesenteric lesion with features
similar to that observed in enteropathy-associated T-cell
lymphoma, Whipple disease, Mycobacterium tuberculo-
sis infection, or necrotic metastasis [117]. Introduction of
a gluten-free diet produces rapid improvement in lymph
node size and clinical symptoms [118]. Despite this, the
prognosis is poor due to infection, cachexia, and electrolyte
derangements [119].
INDETERMINATE MESENTEROPATHIES
ese are abnormalities that receive pathobiologic contri-
butions from the mesentery but also from other organs.
ADHESION FORMATION
Recognition of the fact that (1) mesothelium can trans-
form into a mesenchymal cell type and (2) a submesothe-
lial connective tissue layer occurs immediately beneath
the surface mesenteric mesothelium prompt investigation
of mesenteric mesothelium in adhesion formation. e
etiology of this process has not been formally conrmed,
and it remains problematic with few, if any, eff ctive pre-
ventative strategies available. ere is a striking similar-
ity between adhesions that occur in the postoperative
setting and the fascia interposed between the mesocolon
and underlying retroperitoneum (i.e., Toldt’s fascia) [120].
is prompts the suggestion that a single cellular process
may be common to both. is suggestion is relevant, as
the cellular source responsible for adhesion formation has
remained elusive.
CONGENITAL ADHESION FORMATION
Congenital adhesions are rarely problematic except in the
context of nonrotation. In the latter, congenital adhesions
can form between the second part of the duodenum and
the lateral parietal peritoneum. Here, they are called Ladd’s
bands and can cause an acute intestinal angulation and lead
to intestinal obstruction.
In the normal abdomen, congenital adhesions form
in several locations (see Chapter 2). ey tend to occur
wherever parietal and visceral peritoneum come into
prolonged and undisturbed contact. An example occurs
along the lateral aspect of the mesosigmoid. Here, the vis-
ceral peritoneum at the lateral aspect of the mesosigmoid
comes into direct contact with parietal peritoneum of
the left iliac fossa (Figure 7.16a and b). A further example
occurs at the splenic exure where the colon itself comes
into direct contact with the parietal peritoneum of the le
upper quadrant (Figure7.16c). Adhesions can also occur
at the duodenojejunal exure, which is attached to the ret-
roperitoneum (Figure 7.16d). ese adhesions bridge the
space between the fourth part of the duodenum and adja-
cent left or transverse mesocolon. ey do not contribute,
as has been proposed, to the paraduodenal fossae (Figure
7.16e). e latter arises between two closely positioned
peritoneal folds (and not reections) where the duodenum
sharply changes angulation to continue as the jejunum
(Figure 7.16e).
Perhaps the most surgically relevant of “normal” adhe-
sions occur between the under surface of the greater
omentum and upper surface of the transverse mesocolon.
Here, adhesions can be focal or extensive. eir eff ct is
to obliterate the lesser sac creating multiple chambers or
spaces underneath the greater omentum (Figure 7.17).
ese adhesions are of surgical relevance as they must be
divided to gain access to the lesser sac proper. ey may
also confer a barrier role restricting disease processes to
the lesser sac.
102 Pathology of the mesentery
Congenital adhesions
Congenital adhesions
at lateral aspect
of descending colon
(c)
Mesenteric
root region
3
rd
part of
duodenum
Para-duodenal
recess/fossa(d) (e)
Congenital adhesions
at lateral aspect
of mesosigmoid
(a) (b)
Figure 7.16 (a) Intraoperative and laparoscopic view of congenital adhesions between parietal peritoneum of left iliac fossa
and the lateral aspect of the mesosigmoid. (b) Cadaveric image demonstrating congenital adhesions at the lateral aspect
of the mesosigmoid. (c) Intraoperative appearance of adhesions just distal to the splenic exure. (d) Cadaveric view of
adhesions between the fourth part of the duodenum and adjacent structures. (e) Cadaveric example of the peritoneal folds
(not reections) that generate the paraduodenal fossa. Folds occur where the peritoneal reection doubles back on itself.
Future directions 103
DIABETES AND METABOLIC SYNDROME
e association between increased adipose tissue and diabe-
tes is well established [121]. Mesenteric, visceral, and subcu-
taneous adipose tissue are distinct fatty compartments with
diffe ing activities. Mesenteric release of glycerol contributes
to the development of insulin resistance in diabetes. Within
the mesentery, a balance occurs in leptin and adiponectin
gene expression. Derangements in this balance have been
associated with the pathogenesis of diabetes [122]. Mesenteric
chemerin, a novel soluble protein, is increased in rat models of
impaired glucose tolerance and type 2 diabetes [123].
e liver is directly exposed to mesenteric chemokines
(including free fatty acids) and cytokines released directly
into the portal venous system [124]. As per the “portal
hypothesis,” direct hepatic exposure to increases in free
fatty acids contributes to impaired glucose tolerance, hyper-
insulinemia, and hypertriglyceridemia seen in metabolic
syndrome [125].
IRRITABLE BOWEL SYNDROME
Irritable bowel syndrome (IBS) may also be included in
the category of indeterminate mesenteropathy. Mesenteric
adipocyte-derived substance P has been linked to IBS. In
IBS, visceral hypersensitivity to multiple stimuli is medi-
ated by mast cells [126]. ese are signicantly increased
in the terminal ileum, ascending colon, and rectum of
patients with diarrhea-predominant IBS, where they lie
in close proximity to enteric nerves [127]. While mast cell
counts do not directly correlate with symptomatology,
substance P levels do and are increased in patients with IBS
diarrhea predominant subtype (IBS-D). Vasoactive intes-
tinal peptide levels are also raised in women with IBS-D
[128]. It is feasible that increased mesenteric-derived sub-
stance P leads to mast cell hyperstimulation that, in turn,
is followed by release of inammatory mediators, diarrhea,
and abdominal pain [31].
FUTURE DIRECTIONS
e recent characterization of mesenteric structure has
greatly enhanced interpretation of it. In keeping with this,
there have been dramatic improvements in understanding
of the associated histology and lymphangiology. is in
turn provides a platform by which abnormality (disease)
could be diffe entiated from normality, with the result that
we are increasingly recognizing new roles for the mesentery
in a wide variety of disease processes (including metabolic
syndrome, diabetes mellitus, atherosclerosis). Mesenteric
derangements may have an earlier role in Crohn’s disease
than previously thought. is represents an excellent exam-
ple of how advances in understanding of normal histol-
ogy have advanced understanding of disease processes. In
Crohn’s disease, the connective tissue continuity between
mesentery and adjacent intestinal tract provides a platform
along which inammation and mesenchymal abnormalities
progress.
We are now provided with opportunities to refresh
our approaches to numerous intra- and extra-abdominal
diseases, based on an improved and crystallized knowl-
edge of structure. is has already translated to improve-
ments in the radiologic interpretation of intra-abdominal
diseases and provided novel targets for disease modi-
cation. An excellent example of this is the mesenteric
mesothelium that, through increased proliferation and
mesenchymal transformation, may contribute to mes-
enchymal pools in Crohn’s disease and adhesion forma-
tion. e scientic and clinical communities are poised
to make signicant advances in numerous diseases that
to date have evaded explanation in terms of etiology and
pathogenesis.
Greater omentum and transverse mesocolon
Greater omentum
Adhesions to transverse
colon and mesocolon
Figure 7.17 Cadaveric demonstration of adhesions between
undersurface of greater omentum and upper surface of
transverse mesocolon. These adhesions are visualized
after division of the peritoneal reection between both
structures. Omento-mesocolic adhesions create multiple
pseudo-chambers and can mislead the surgeon into think-
ing that he or she has entered the lesser sac.
104 Pathology of the mesentery
SUMMARY
Data are emerging supporting the suggestion that the human
mesenteric organ is subject to the same pathologic vulner-
abilities as other organs. In keeping with this, abnormalities
may be classifi d into primary, secondary, and indeterminate
mesenteropathies. Primary mesenteropathies arise in the
mesentery. Secondary mesenteropathies spread to involve
the mesentery through either direct or systemic spread.
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