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86 Pathology of the mesentery
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 mesen-
tery (as well as other sources) that are of pathobiological
relevance.
It should be said that this is an emerging fi ld. 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 rep-
resents a considerable shift in current thinking, the data to
support it will be discussed in detail.
Both the etiology and pathobiology of Crohn’s dis-
ease 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 molec-
ular basis remain unknown [3]. The following section
explores data supporting the theory that Crohn’s dis-
ease 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 signi-
cant 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
Table 7.1 Mesenteropathies
Mesenteropathies
Primary Secondary Indeterminate
Subtypes
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
Secondary—dialysis Mesenteric cavitation syndrome
Epiploic appendagitis
Crohn’s disease (primary mesenteropathy) 87
predict the rate and severity of recurrence in Crohn’s dis-
ease (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 eff ct eyes, joints, skin, and other
systems [10]. Although mesenteric disease manifestations
are characteristic of Crohn’s disease, they are remark-
ably understudied. Fat wrapping and mesenteric thicken-
ing 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 eff cts of smoking in Crohn's disease. It suggests
that mesenteric events are of primary pathobiologic sig-
nicance 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. Th s 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. Th s is
referred to as axial polarity (Figure7.3) [7,8,14,15]. Although
the molecular basis for this observation is unknown, increas-
ing 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 dem-
onstrates a connective tissue continuity between it and adja-
cent intestinal tract [19]. When the mesentery and associated
intestine are examined in Crohn’s disease, similar mesenchy-
mal 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 instru-
ments such as Ingenuity
®
[21]. When this is completed for
mucosal gene expression in Crohn’s disease, emerging nd-
ings indicate that the diseases associated are linked with
vascular and metabolic disorders. In contrast, diseases asso-
ciated with abnormal mesenteric gene expression appear to
be more associated with mesenchymal and inammatory
disorders. us, it seems that the transcriptional environ-
ment 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
Mucosal ulceration
Mesenteric fat wrapping
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.
88 Pathology of the mesentery
Mesenteric disease manifestation in Crohn’s disease
Mild
Moderate
Severe
(a)
Normal
mucosa and
bowel wall
Ulcerated
mucosa
Ulcerated
mucosa
Regions
of fat
wrapping
(b)
Figure 7.2 (a) Mild, moderate, and severe mesenteric manifestations in Crohn’s disease. (b) With advancing mesenteric
manifestations, the mesentery thickens with the result that the adipovascular pedicles can no longer be distinguished from
adjacent avascular interpedicular areas. With advancing mesenteric manifestations fat wrapping extends over the serosal
surface to involve a greater amount of the circumference.
Crohn’s disease (primary mesenteropathy) 89
Fat wrapping and mucosal disease
Mesenteric fat wrapping
Mesenteric fat wrapping
Normal mesentery
Abnormal Mesentery
Abnorman mucosa
Normal mucosa
(b)
(a)
Figure 7.3 (a) Terminal ileum demonstrating a transition from mild to moderate and then severe fat wrapping inthe termi-
nal ileum. (b) Mucosa corresponding to the regions in (a). Aphthous ulceration is apparent in the region adjacent early fat
wrapping while conuent linear ulceration occurs in the region corresponding to the region of severe fat wrapping. In all
cases, ulceration is conned to the mesenteric pole of the mucosa (i.e., axial polarity).
90 Pathology of the mesentery
be identifi d radiologically, this involves exposure to radia-
tion [22]. e mesentery cannot presently be examined
endoscopically. Data are emerging indicating that circulat-
ing brocytes may have a biomarker potential in this con-
text (Figure7.4)[23].
Circulating brocytes and disease activity in
Crohn’s disease
Fibrocytes can be immunohistochemically identifi d in
the mesentery of patients with Crohn's disease (Figure7.4)
[8,24,25]. Emerging data indicate they cluster at the
interface between the intestinal serosa and the adjacent
mesentery. From these clusters, they may extend along
connective tissue ramications, into the longitudinal and
circular smooth muscle layers. Circulating brocyte levels
appear to correlate with the CDAI. ey decrease follow-
ing surgical resection and are signicantly reduced if the
patient undergoes fecal diversion via an ostomy. Although
circulating brocyte levels are increased in appendicitis
and diverticular disease, the increase in Crohn’s disease
appears greater than in either of these inammatory con-
ditions. Circulating brocyte levels appear to be related
to mesenteric disease scores, and thus may provide a
serologic biomarker of mesenteric progression in Crohn’s
disease.
Circulating brocyte levels change following
intestinal resection in Crohn’sdisease
As mentioned earlier, circulating brocyte levels decrease
following surgical resection and are signicantly reduced in
patients undergoing fecal diversion via an ostomy (Figure7.4).
Two explanations can account for diffe ent ndings aer
resection or fecal diversion. e rst is that a key intestinal or
mesenteric cue is removed at the time of excisional surgery,
leading to reduced diffe entiation of circulating monocytes
into brocytes. A second explanation is that by performing
a mesenterectomy, the surgeon removes an additional source
of brocytes. Although brocytes are generally described
as derived from circulating monocytes (and hence from
bone marrow), a number of observations support composite
sources in Crohn’s disease. First, brocytes can be identifi d
in mesenteric mesothelium in Crohn’s disease. Second, cul-
ture of mesenteric mesothelium leads to the generation of
mesenteric-derived mesenchymal cells (MMCs). ese com-
prise of broblasts, activated broblasts, and brocy tes (Figure
7.5). Studies examining the cellular properties of MMCs show
that adhesion, proliferation, and migration correlate with the
CDA I [26–28].
Perhaps more signicantly, these cellular properties
also correlate with circulating brocyte levels [23,29,30].
Collating the earlier ndings, it is possible that mesenteric
mesothelium can transform and may offer an additional
source of mesenchymal cells.
Miscellaneous support for mesenteric
involvement
It is beyond the remit of the current chapter to list all data
supporting a role for the mesentery in Crohn’s disease. Some
additional points should be briey mentioned including
reference to appendicitis, mesenteric substance P, and CRP
production [31–33].
Appendicitis and Crohn’s disease
e incidence of appendicitis increases in Crohn’s dis-
ease. Prior appendicectomy is an independent risk fac-
tor for surgical recurrence (i.e., severe disease requiring
repeat operations) [8,34–36]. Interestingly, this relation-
ship was hinted at by Crohn etal. [37]. ey presciently
noted that, in cases of appendicitis in patients who devel-
oped Crohn’s disease, appendiceal inammation involved
the outer layers of the appendix (i.e., the inner layers were
not involved). is suggests that appendiceal inamma-
tion arose due to an exogenous (i.e., mesenteric-based)
rather than an endoluminal trigger (Figure 7.6). e term
“mesoappendicitis” had been coined in reference to this
phenomenon [33,38].
CRP production in Crohn’s disease
Investigators recently identifi d a direct linkage between
mesenteric production of CRP and systemic levels in Crohn’s
disease [32]. Th s was a groundbreaking observation as it
demonstrated how mesenteric events could eect systemic
disease manifestations. Interestingly, similar observations
have been made in several other conditions including meta-
bolic syndrome, atherosclerotic dyslipidemia, and type two
diabetes [39–44]. In each, visceral fat-related derived CRP
is a major determinant of systemic CRP levels.
Mesenteric production of substance P
inCrohn’s disease
e neuropeptide substance P is secreted from mesen-
teric adipocytes. It stimulates proliferation and reduces
apoptosis in preadipocytes, ndings that may be linked to
fat wrapping [45]. As fat wrapping correlates with trans-
mural inammation, muscular hypertrophy, brosis,
and stricture formation, mesenteric-derived substance
P may play a key signaling role in Crohn’s disease [18].
Mesenteric production of substance P is also linked to
symptoms in irritable bowel disease. It is noteworthy that
the symptoms of both IBS and Crohn’s disease overlap
considerably [46–48].
Summary
In summary, mesenteric disease manifestations closely fol-
low local mucosal and systemic manifestations in Crohn’s
Crohn’s disease (primary mesenteropathy) 91
Fibrocytes
tissue and circulation
Tissue fibrocytes
CD45
+
and SMA
+
near vessels
CD45
+
and SMA
+
Fibrocytes clustered
at intestinal surface
(i.e
., intersection with
mesentery)
8.00
7.00
6.00
5.00
4.00
Mean (SE) cFC level (%)
3.00
2.00
1.00
0.00
Controls Active CD
1.97
2.54
0
2
4
6
cfc
8
100 200
y=0.99+0.02*x
300
CDAI
CDAI
R=0.92
400
R
2
linear=
0.950
500
6.46
*P <0.001*P<0.001
Study cohort
Baseline CD
* Independent T test
Fibrocyte percentage in
circulating monocytes
Correlation between circulating
fibrocyte percentage and CDAI
(a)
(b)
(c) (d)
Figure 7.4 (a) Dual staining of human mesentery in Crohn’s disease with αSMA and CD45. Dual stained cells are
myobrocytes. These are numerous in diseased mesentery in Crohn’s disease. They are mostly observed either within or
nearby a capillary giving the impression that they are recruited to the mesentery. (b) Fibrocytes clustered at the intestinal
surface from which they extended into the outer longitudinal muscle layer along connective tissue septae. (c) Bar chart
depicting circulating brocyte levels in healthy control subjects, in active Crohn’s disease, and in quiescent Crohn’s
disease. (d) Correlation between circulating brocyte levels (y axis) and Crohn’s disease activity index (x axis). A strong
correlation was observed between both parameters.
92 Pathology of the mesentery
disease. ey are hallmarked by pronounced histologic
changes and by a transcriptomic environment that sup-
ports brosis, inammation, mesothelial proliferation, and
transformation. e classic model of Crohn’s disease holds
that inammation commences at the mucosa and spreads
outward (becoming transmural) and thereaer aff cts the
adjacent mesentery. erefore, it is feasible, given the above,
that an alternative model may be involved and that mesen-
teric events could potentially play an earlier role than previ-
ously thought.
NON- (i.e., MAL) ROTATION
Non- or malrotation is a primary mesenteropathy.
Anatomy
Nonrotation and incomplete xation are usually described
as complex areas of pathology. However, they are readily
understood when one considers the intestine and mesentery
are continuous entities in the adult, just as they were in the
embryo. In patients with nonrotation, the typical ndings are
as follows: e second part of the duodenum extends verti-
cally into the right ank rather than crossing the abdominal
aorta. In tandem with the intestine, the mesentery adopts a
similar vertical orientation in the right ank (Figure 7.7a). As
a result, the entire small intestinal gastromesenteric complex
is located in the right ank (Figure 7.7b). In all cases of non-
rotation and nonxation, the le mesocolon, mesosigmoid,
Cytokeratin CD45+Col l Vimentin+Col l ˜SM A ˜SM A+Cytokeratin
Panel showing di˜erent cell types
Figure 7.5 Panel demonstrating different mesenchymal cell types that are generated following the exvivo culture of mes-
enteric mesothelium.
Volvulus 93
and mesorectum occur in their usual anatomic positions
(Figure 7.7b). is constant anatomic nding is most likely
related to an anchorage eff ct exerted by the bony pelvis on
the rectum and mesorectum. As these are secured in place,
the mesosigmoid and left esocolon are similarly secured.
Given the above, the right colon and mesocolon must
occupy a central position (Figure 7.7b). Although the cecum
is interposed between the small bowel and right colon, vari-
ations in the attachment of the ileocecal mesenteric conu-
ence mean that it can be variably positioned (and similarly
so can the appendix) (Figure 7.7c). Occult malrotation is not
infrequently observed in appendicitis, where the appendix
is located in an abnormal location such as the left or right
upper quadrant. e right mesocolon is typically shortened,
and as in normality it is contiguous with the small bowel
mesentery and with the transverse mesocolon.
In summary in nonrotation, the small bowel mesentery,
right, transverse, and left mesentery adopt a concertina-like
conformation from the right to the midline and thereaer
to the left ide of the peritoneal cavity (Figure 7.7).
Clinical implications of non (i.e., mal) rotation
e term “malrotation” is really a misnomer and should be
changed to nonrotation, as in most cases, there is a complete
absence of rotation of the mesentery. e condition is the
commonest cause of emergency abdominal presentation in
rst year of life. It may be compatible with life, however, as
many cases are discovered incidentally in adults undergo-
ing radiologic investigation. Fatalities arise when the small
intestinal mesentery t wists (i.e., torsion) around the superior
mesenteric artery root region. It is likely that in those cases
with nonrotation who survive into adulthood, the small
intestinal mesentery has partially attached to the retroperi-
toneum. is prevents a complete rotation on the superior
mesenteric vascular pedicle. Occasionally in adults, these
adhesions lead to acute or subacute obstruction although
this is rare (Figure 7.7d).
Molecular basis of non (i.e., mal) rotation
In normality, Toldt’s fascia and peritoneal reections nor-
mally attach the mesentery to the retroperitoneum [49]. In
nonrotation, fascia and peritoneal reection attach the right
mesocolon to the retroperitoneum, nearer the midline, and
not on the right side of the abdominal cavity. e small bowel
mesentery comes to lie on the right side. Despite this how-
ever, it remains continuous with the right mesocolon. us,
the cellular and molecular processes responsible for attach-
ment (i.e., fascia and generation of the peritoneal reection)
remain intact. Given this, it appears that the fundamental
abnormality is lack of rotation (rather than an abnormal or
"mal" rotation). At present, it is not known whether this has
a primarily a mechanical, cellular, or molecular basis.
VOLVULUS
Volvulus, like nonrotation, is a primary mesenteropathy.
Volvulus involves twisting of a segment of intestine and
mesentery on its mesenteric attachment.
e general literature abounds in reports of “anomalous”
persistence of the right and left mesocolon, and the man-
ner in which this predisposes to volvulus formation [50–57].
Some descriptions, such as the following, are colorful albeit
incorrect;
… the mesocolon is as anomalous as a cleft
palate.[58]
As we now acknowledge persistence of the mesocolon
intoadulthood, this is no longer regarded as a pathogenic
anoma ly [19,59,60].
True anomalies do arise such as nonrotation (described
earlier). Variations in the degree to which the right meso-
colic and mesosigmoidal regions attach to the posterior
abdominal wall are far more frequent. ese are also true
mesenteric anomalies and if suffici t, predispose to vol-
vulus formation. In some individuals, there is minimal
attachment of the small intestinal mesentery and right
mesocolon to the retroperitoneum. Minor degrees of
nonattachment or fix tion are associated with technical
Inflamed adherent
appendix
Appendix and mesoappendix in Crohn’s disease
Inflammed adherent
mesoappendix
Figure 7.6 Appendiceal and mesoappendiceal inamma-
tion in Crohn’s disease. Both are secondarily inamed due
to the inammation in the adjacent mesentery.
94 Pathology of the mesentery
diculty in traversing the colon during colonoscopy and
probably increase the likelihood of loop formation.
Volvulus is frequently observed on the left side when it
involves an elongated sigmoid and mesosigmoid. Volvulus
here is an excellent example of the two factors that are key
in its development. First, most cases of volvulus are associ-
ated with an abnormally lengthy sigmoid. If the sigmoid is
lengthy, then the adjacent mesosigmoid will also be lengthy.
Second, the region of the mesosigmoid attached to the ret-
roperitoneum is frequently narrower than one would ordi-
narily expect. us, the diffe ential in length between the
attached and the intestinal region of the mesosigmoid con-
tributes to its torsion around the zone of attachment. e
greater the diffe ential, the greater the risk of torsion.
A similar mechanical phenomenon occurs at the ileo-
cecal region when the terminal ileum and cecum have not
Malrotation (non-rotation)
Normal gastromesenteric
confirmation
Gastromesenteric confirmation
in mal(non)rotation
(a)
(b)
Mesoappendix
Ladd’s bands
Appendix
Ladd’s bands leading to
obstruction in mal(non)rotation
Appendix/mesoappendix
in mal(non)rotation(c) (d)
Fig u re 7.7 2.5D illustrations taken from 3D digital sculpture demonstrating (a) normal small bowel and mesentery and
(b)small bowel and mesentery in non- or malrotation. In the latter, the gastromesenteric complex of the small bowel is
positioned to the right of the midline. (c) Mesoappendix and appendix in mal- (non) rotation. (d) Adhesions observed in
the setting of nonrotation. The adhesions pulled the third part of the duodenum toward the mesentery. The resultant
angulation led to a partial obstruction that required adhesiolysis.
Desmoid tumor 95
attached to the retroperitoneum. In this setting, the apex of
the mesenteric attachment is again narrow and predisposes
to torsion around it. Although the transverse colon and
mesocolon are mobile, volvulus here is much less frequent.
is is due to the attachment of the mesenteric and splenic
components of the exures on either side of the middle colic
adipovascular pedicle.
EPIPLOIC APPENDAGITIS
Appendices epiploicae are variously sized and shaped adi-
pose collections attached to the colon. Although some sug-
gest they derive from tenia coli on the antimesenteric side
of the colon, their distribution would not appear to sup-
port this [61]. In thin individuals, they are minimal, while
in adipose patients they are widespread and may carpet
the colonic surface. In these circumstances, they appear to
coalesce with the mesentery and can be dicult to diffe en-
tiate from the latter. Given these similarities, it is suggested
they may represent an ectopic form of mesentery. at
being so, then their inammation or infarction is a primary
mesenteropathy.
ey have paired arteries and one draining vein [62].
Anatomically, they are greatest number in the cecum and
sigmoid colon [63]. Torsion of their base or thrombosis
of a draining vein can lead to vascular compromise, isch-
emia, infarction, and inammation. e pain experienced
by the patient is somatic in nature and, not surprisingly,
can be mistaken for intestinal inammation in that region.
Cecal epiploic appendagitis may mimic appendicitis, while
sigmoid epiploic appendagitis may mimic diverticulitis
[64,65]. Epiploic appendagitis or infarction is thus a chal-
lenging diagnosis with a broad diffe ential.
While their function is unknown, there are several
hypotheses. ese include bacterial sampling, facilitation
of colonic absorption, and protection of colonic blood sup-
ply (i.e., when the main vasculature has collapsed [66]).
Although evidence to support these roles is limited, identi-
cation of lymph nodes within epiploicae may be considered
supportive.
Epiploicae can exert an important barrier or buffer
eff ct, restricting colonic perforation and inammation to
the zone immediately surrounding the colon. A number of
cases have been reported where an intestinal perforation
was contained by the fat of overlying appendices epiploicae.
Figure 7.8a and b illustrate perisigmoidal appendices epi-
ploicae that limited intraperitoneal contamination follow-
ing an underlying diverticular perforation.
MESENTERIC ISCHEMIA
As mesenteric ischemia is a vascular disorder of the mes-
entery, it falls into the category of primary mesenteropathy.
Occlusion of the vascular supply of the mesocolon results
in ischemia and necrosis of the bowel. ere are three
principal pathological causes: mesenteric arterial embolus
and thrombus, mesenteric venous thrombus, and nonoc-
clusive mesenteric ischemia [67]. is surgical emergency
requires prompt diagnosis and treatment. Development of
symptoms can be acute or chronic. Acutely, patients classi-
cally present with abdominal pain out of proportion with
clinical ndings. As the acute ischemic event progresses,
metabolic abnormalities occur that can progress to mul-
tiple organ dysfunction [68]. e nonspecic nature of
the acute presenting complaint, along with rapid progres-
sion of ischemia, contributes to a perioperative mortality
of 44%–90% [69]. When surgical intervention is initiated
within 12 hours of onset of symptoms, survival rates can
reach 72.3% [70]. e same study found that only 20% of
patients survived when surgery was delayed to between
24and 48 hours. In chronic mesenteric ischemia, the clini-
cal pattern oen resembles that of angina pectoris or clau-
dication. Following a meal, increased splanchnic blood
ow is insucient to meet the metabolic requirements of
the bowel producing mesenteric angina [71]. Sitophobia,
weight loss, and nausea and vomiting commonly occur [72].
Intervention generally requires bypass of a narrowed seg-
ment. Conservative management is described involving
anticoagulation with close monitoring. Resolution in these
contexts is likely due to the development of collateral vas-
culature. Endovascular repair (angioplasty and stenting)
are emerging treatment modalities [73].
INTERNAL HERNIATION
If this arises due to a defect in the mesentery then it falls
into the category of primary mesenteropathy. Any defect in
the continuity of the mesentery may lead to internal hernia-
tion of abdominal viscera. Internal hernias are a rare cause
of small bowel obstruction. Reported incidences vary from
0.5% to 5.8% [74]. Transmesenteric hernias account for 8%
of all internal hernias [75]. Defects in the mesentery can be
congenital or due to surgery, trauma, inammation, or cir-
culatory pathology [76]. irty-ve percent of transmesen-
teric hernias occur in pediatric populations aged between
3 and 10years [75]. e increased frequency of congenital
defects in attenuated or avascular regions of mesentery,
combined with their high prevalence in infants with atretic
bowel segments, points to an association with prenatal
intestinal ischemic events [75]. Mesenteric defects in adults
are more likely due to previous intra-abdominal surgery,
abdominal trauma, or intraperitoneal inammation [75].
Mortality rates are high at 50% [74]. e lack of a hernial
sac allows large amounts of bowel to herniate [75]. e size
of the defective aperture dictates the risk of strangulation,
ischemia, and necrosis [75].
DESMOID TUMOR
Desmoid tumors frequently develop in the mesentery and
should be considered as a primary mesenteropathy [77].
ese are benign, broblastic proliferations that invade