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- •Preface
- •Acknowledgments
- •PART 1
- •1: History
- •2: Mesenteric and peritoneal anatomy
- •4: Histology of the mesentery
- •5: Toldt’s fascia
- •6: Mesenteric physiology
- •7: Pathology of the mesentery
- •9: Operative nomenclature
- •10: Teaching mesenteric principles
- •11: Gastroenterology
- •PART 2
- •12: Mesenteric-based colorectal surgery
- •13: Appearance of the mesentery during laparoscopic/robotic colorectal surgery
- •15: Instruments used during mesenteric-based colorectal surgery
- •16: General techniques in mesenteric-based colorectal surgery
- •17: Mesenteric component of sigmoid colectomy
- •18: Mesenteric component of rectal resection
- •19: Mesenteric component of right colectomy
- •22: Mesenteric considerations in small bowel resection
- •25: Mesenteric considerations in reoperative abdominal surgery
- •26: Future directions
- •Appendix A: Operative templates

78 Mesenteric physiology
Mesenteric lymphatics
l
(c) (d)
100 µm
(a) (b)
25 µm
100 µm
Surface
mesothelium
Submesothelia
connective
tissue
25 µm
Connective
tissue
septation
Lymphatic
vessels in
connective
tissue
Figure 6.7 Photomicrographs based on serial sections of mesentery. (a) Section stained with podoplanin (a lymphatic
and mesothelial surface marker) demonstrating lymphatic channels beneath the surface mesothelium of the mesentery. (b)Corresponding serial section stained with Masson’s trichrome highlight connective tissue. Correlating A and B,
the lymphatic channels identied occurred within the submesothelial connective tissue. (c) Podoplanin positive vessels
(i.e., lymphatics) within the connective tissue septations that spanned the mesentery and together generated the connective
tissue lattice. (d) Corresponding serial section stained with Masson’s trichrome to highlight connective tissue septations.
it is not unreasonable to suggest that cellular and molecular activities associated with the greater omentum should
be included in any discussion on mesenteric functionality.
Atthe least, this could provide important clues of function
and avenues for future research.
e omentum has appropriately been termed the “abdominal policeman,” as it adheres to areas of inammation and
prevents the diusion of pathologic processes throughout
the peritoneal cavity. In this manner, it can mechanically
seal perforations, localize inammation, limit the spread of
infection, and simultaneously prompt local revascularization and tissue regeneration [142–144].
e greater omentum contains adipocy tes, macrophages,
B cells, T cells, mast cells, and dendritic cells [145]. Lynch
etal. noted that while iNKT and CD1d+ cells amass in the
greater omentum, this phenomenon is reduced in obesity
and in patients with colorectal cancer [144]. us, it would
appear that the policeman activity of the greater omentum
extends beyond the simple mechanical and may also include
immune protection against the development of malignancy
[146]. Lysaght et al. aimed to characterize T lymphocytes
in visceral adiposity (using omentum) and peripheral blood
from 35 patients with esophageal adenocarcinoma. T cell
activation markers CD69 and CD107a were increased in

References 79
expression in omental CD4+ and CD8+ T cells, compared
with corresponding levels in peripheral blood. CD45RO
T cells were more prevalent in omentum compared with
peripheral venous blood. While the relevance of these ndings is under investigation, they indicate that the greater
omentum, like the mesentery, is likely to be far more active
than previously appreciated [146]. ese observations have
yet to be investigated in the context of the mesenteric component of visceral adiposity.
FUTURE STUDIES
From the earlier discussion, it can be seen that the mesentery does not act simply in a bystander manner providing
a scaold for the passage of blood vessels to and from the
intestine. It occupies a unique anatomic position between
the intestine and the body proper. e histologic, connective tissue, lymphatic, and immunologic continuity between
all three mean it is optimally placed to exert a key inuence over local and systemic homeostatic processes. It is
ideally placed to sample microbial environmental cues and
orchestrate appropriate systemic as well as local mucosal
responses. It is important to further investigate this regulatory hub, or signal box, and to characterize its role in normality and disease.
e mesentery is a highly active immunological, endocrine, and metabolic organ. Mesenteric mesothelium has
regenerative and pluripotential properties that are important in response to injury within the abdomen, but that may
be deranged in hernia or adhesion development. Future
studies should aim to investigate the regenerative capacity
of mesenteric mesothelium and the role that this may have
in abdominal pathology.
SUMMARY
Mesenteric physiology is an emerging eld. e recent
clarication of mesenteric anatomy from duodenojejunal
exure to mesorectal level provides an ideal platform to
better characterize the physiologic relevance of this organ
in general. Scientic and clinical communities are now
provided with exciting opportunities that will enhance our
understanding of its function in normality and hence its
role in disease processes.
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7
Pathology of the mesentery
J. CALVIN COFFEY, JONATHON RODDY, MIRANDA KIERNAN, AND SHAHEEL M. SAHEBALLY
Aim 85
Introduction 85
Primary mesenteropathies 86
Crohn’s disease (primary mesenteropathy) 86
Mesenteric manifestations in Crohn’sdisease 86
Mesenteric manifestations correlate with local and
systemic disease manifestations inCrohn’s disease 87
Mesenteric and mucosal abnormalities directly
correlate in Crohn’s disease 87
Mesenteric and intestinal mesenchymal abnormalities
overlap 87
Mesenteric and mucosal transcriptional proles 87
Fibrocytes are a biomarker in Crohn’s disease 87
Circulating brocytes and disease activity in Crohn’s
disease 90
Circulating brocyte levels change following intestinal
resection in Crohn’sdisease 90
Miscellaneous support for mesenteric involvement 90
Appendicitis and Crohn’s disease 90
CRP production in Crohn’s disease 90
Mesenteric production of substance P inCrohn’s
disease 90
Summary 90
Non- (i.e., mal) rotation 92
Anatomy 92
Clinical implications of non (i.e., mal) rotation 93
Molecular basis of non (i.e., mal) rotation 93
Volvulus 93
Epiploic appendagitis 95
Mesenteric ischemia 95
Internal herniation 95
Desmoid tumor 95
Mesenteric cysts 97
Sclerosing mesenteritis 97
IgG4-related sclerosing mesenteritis 97
Mesenteric neurologic pathology 97
Secondary mesenteropathies 97
Appendicitis 98
Phlegmon 98
Mesenteric adenitis 98
Lymphoma 99
Peritoneal carcinomatosis 99
Neuroendocrine tumors 100
Castleman’s disease 101
Mesenteric lymph node cavitation syndrome 101
Indeterminate mesenteropathies 101
Adhesion formation 101
Congenital adhesion formation 101
Diabetes and metabolic syndrome 103
Irritable bowel syndrome 103
Future directions 103
Summary 104
References 104
The problem, when solved, will be simple.
On wall of General Motors
Research Laboratory
AIM
e rst aim is to dene the concept of a mesenteropathy
and describe a classication system for these. A second aim
is to describe the mesenteric and peritoneal manifestations
of mesenteropathy subtypes.
INTRODUCTION
e functional and anatomical distinctiveness of the mesentery has generated increasing interest in mesenteric
diseases. In keeping with this, a range of pathologies can
be identied that are readily and directly associated with
the mesentery. Several more are increasingly associated
through recent experimental ndings. As with diseases of
other organs, the mesentery appears to be vulnerable to a
range of pathologies including inammatory, vascular, connective tissue, and neoplastic.
85

86 Pathology of the mesentery
Table 7.1 Mesenteropathies
Primary Secondary Indeterminate
Crohn’s disease Mesenteric adenitis Adhesions
Ischemia Appendicitis Diabetes mellitus
Mal or nonrotation Phlegmon Atherosclerosis
Volvulus Metastatic disease Metabolic syndrome
Internal herniation Desmoid tumors Irritable bowel syndrome
Cysts Peritoneal carcinomatosis
Schwannoma Castleman’s disease
Sclerosing mesenteritis Primary—IG4 Lymphoma
Epiploic appendagitis
Mesenteropathies
Subtypes
Secondary—dialysis Mesenteric cavitation syndrome
A mesenteropathy is an abnormality of the mesentery.
A primary mesenteropathy is one that arises primarily
within the mesentery and can spread to involve adjacent
structures (i.e., the intestine) (Table 7.1). A secondary
mesenteropathy is one where the primary abnormality
originates outside the mesentery but which secondarily
involves the mesentery. Indeterminate mesenteropathies
are conditions that receive contributions from the mesentery (as well as other sources) that are of pathobiological
relevance.
It should be said that this is an emerging eld. Disease
entities are positioned in the earlier classication system
according to the weight of supportive data available. is is
not meant to be denitive or exhaustive and aims to provide
a platform from which abnormalities of the mesentery can
be investigated in a systematic manner.
PRIMARY MESENTEROPATHIES
ese are abnormalities that arise primarily within the
mesentery but can progress to involve local or systemic
organs.
CROHN’S DISEASE (PRIMARY
MESENTEROPATHY)
Recent ndings challenge the classic notion that Crohn’s
disease arises from the mucosa of the intestine. It is feasible
that Crohn’s disease represents a true primary mesenteropa-
thy, that is, a disease arising in the mesentery. As this represents a considerable shi in current thinking, the data to
support it will be discussed in detail.
Both the etiology and pathobiology of Crohn’s disease remain under investigation. Surgical excision rates
are unchanged despite the emergence of new treatment
regimens [1]. As a result, investigators are turning to
alternative hypotheses to explain this disease. The most
widely held theory is that Crohn’s is an inflammatory
and fibrotic disorder originating in the gastrointestinal
tract and progressing transmurally to the mesentery [2].
Although transmural mesenchymal abnormalities are
hallmarks of Crohn’s disease, their cellular and molecular basis remain unknown [3]. The following section
explores data supporting the theory that Crohn’s disease is a primary mesenteropathy (i.e., the “outside-in
hypothesis”).
Mesenteric manifestations
inCrohn’sdisease
Mesenteric abnormalities in Crohn’s disease include fat
wrapping and mesenteric thickening. Fat wrapping is
unique to Crohn’s disease and represents the advancement
of mesenteric fat over the intestinal surface. Mesenteric
thickening is also a prominent feature and creates signicant technical diculties for surgeons [4–8].
A direct correlation occurs between fat wrapping and
increased risk of future surgery for recurrent disease
(Figure 7.1) [5,6,8,9]. In patients in whom fat wrapping
extends over 50% of the intestinal circumference, the
time to surgical recurrence is reduced. In a multivariate
analysis examining the predictive role of smoking and
other factors, fat wrapping remains the single strongest
predictor of surgical recurrence. ese points reinforce
the concept that increasing levels of mesenteric disease

Crohn’s disease (primary mesenteropathy) 87
Mesenteric fat wrapping
Mucosal ulceration
Mesenteric fat wrapping
Figure 7.1 Mesenteric and mucosal Crohn's disease as
observed following an ileocolic resection in a patient with
stricturing Crohn's disease.
predict the rate and severity of recurrence in Crohn’s disease (Figure 7.1). ey support the suggestion that mesen-
teric-based events are of importance in the pathobiology
of Crohn’s disease.
Mesenteric manifestations correlate with
local and systemic disease manifestations
inCrohn’s disease
In inammatory bowel disease, disease manifestations
outside the intestinal tract (i.e., extraintestinal disease
manifestations) can eect eyes, joints, skin, and other
systems [10]. Although mesenteric disease manifestations
are characteristic of Crohn’s disease, they are remarkably understudied. Fat wrapping and mesenteric thickening may be conceptually combined to generate a scoring
mechanism that allows the quantitation of mesenteric
disease, and its correlation with other disease activity
scoring systems (Figure 7.2). Emerging data indicate that
the mesenteric disease scores correlate with the Crohn’s
disease activity index (CDAI), as well as with increasing
levels of mucosal disease. Data suggests that smoking
leads to a signicant deterioration in mesenteric disease
scores. is is highly relevant as smoking is known to
worsen Crohn’s disease and increases the risk of disease
recurrence requiring surgery [8,11–13]. is combination
of ndings suggests that the mesentery is sensitive to the
negative eects of smoking in Crohn's disease. It suggests
that mesenteric events are of primary pathobiologic signicance in this condition (Figure 7.2).
Mesenteric and mucosal abnormalities
directly correlate in Crohn’s disease
Examination of postoperative specimens in Crohn's disease
demonstrates a zone at which the mesentery changes from
normal to abnormal. is is a short zone at which mucosal
disease appears to commence. A sharp demarcation separates
normal and abnormal mucosa. Mucosal ulceration in Crohn’s
disease invariably commences adjacent the mesentery and
not at the opposing antimesenteric side of the mucosa. is is
referred to as axial polarity (Figure7.3) [7,8,14,15]. Although
the molecular basis for this observation is unknown, increasing evidence points to involvement of mesentery-derived
cytokines such as TNF-α. Mesenteric adipocytes are major
sources of TNF-α [16,17]. TNF-α upregulates expression of
brogenic and mitogenic genes, prolongs inammation, and
increases expression of other inammatory cytokines.
Mesenteric and intestinal mesenchymal
abnormalities overlap
Recent investigation of the histology of the mesentery demonstrates a connective tissue continuity between it and adjacent intestinal tract [19]. When the mesentery and associated
intestine are examined in Crohn’s disease, similar mesenchymal abnormalities occur in both. ese include adipocyte
hyperplasia, increases in connective tissue, and brocytosis.
An overlap occurs at the interface between the mesentery and
intestine (i.e., the intestinal hilum) and mayexplain the trans-
mural features of mesenchymal abnormalities in Crohn’s.
Mesenteric and mucosal transcriptional
proles
It is now feasible, using in silico techniques, to compare
mucosal and mesenteric gene expression in Crohn’s disease
[20]. In addition, abnormalities in gene expression can be
linked to disease processes through network linkage instruments such as Ingenuity® [21]. When this is completed for
mucosal gene expression in Crohn’s disease, emerging ndings indicate that the diseases associated are linked with
vascular and metabolic disorders. In contrast, diseases associated with abnormal mesenteric gene expression appear to
be more associated with mesenchymal and inammatory
disorders. us, it seems that the transcriptional environment within the mesentery, but not in the mucosa, supports
the mesenchymal hallmarks of Crohn’s disease.
Fibrocytes are a biomarker in Crohn’s
disease
Given the above, quantitation of mesenteric manifestations
would be useful in terms of tailoring treatment in patients
with Crohn’s disease. While mesenteric manifestations can
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