65  T_h e peritoneum, mesentery, greater omentum a

ACKNOWLEDGEMENTS
ACKNOWLEDGEMENTS
The author would like to acknowledge the artistic support of Dara Walsh, who generated all digital images and videos. He would also like to acknowledge Mr Kevin Byrnes for his work on the development of  the mesentery and abdominal digestive system.

ANATOMY OF THE MESENTERY AND PERITONEUM
ANATOMY OF THE MESENTERY AND PERITONEUM
All abdominal digestive organs develop in or on the mesentery and then remain directly connected to it ( Figure 65.3 ). In the adult setting, these collectively comprise a discrete anatomical unit, the mesenteric domain ( Figure 65.4 ). All genitourinary organs develop on and remain on the musculoskeletal main - frame of  the abdomen. In the adult, these are collectively termed the non-mesenteric domain. Thus, the adult abdomen comprises two discrete anatomical compartments: the mesen - 65.2 ). teric and non-mesenteric domains ( Figure 65.5 ) ( When development is complete, the mesentery and con - joined digestive organs (intestine, pancreas, spleen and liver) have taken shape and adherence to the posterior abdominal wall is nearly complete. The dorsal mesogastrium, meso - duodenum, right and left mesocolon and mesorectum are anchored to the subjacent abdominal wall (or pelvic sidewall) ( Figure 65.4 ). The small intestinal region of  mesentery , trans verse mesocolon and lateral mesosigmoidal mesentery are not adherent and thus are mobile. Adhesion of  the mesentery to the abdominal wall anchors the mesenteric to the non-mesenteric domain, maintained by peritoneal reflection at the periphery of  the mesenteric domain ( 65.1 and 65.3 ). At the periphery , the peritoneal reflection bridges the surface lining of  the mesenteric and non-mesenteric domains ( Figure 65.6 ). The peritoneum thus comprises visceral peritoneum (corresponding to the surface lining of the mesenteric domain), parietal peritoneum (corresponding reflection joining both. Peritonitis refers to inflammation of any region (see Peritonitis ). The surface contours generated by the organisation of  the domains and the peritoneum explains the sacs, recesses, fos - sae and pouches in which abnormal fluid collections arise in 65.3 ). On completion of  development, the the abdomen ( free (non-adherent) surface of  each organ of  the mesenteric domain is peritonealised. The opposing adherent surface is not peritonealised. In the male, the peritoneal cavity is normally closed. In the female, the peritoneal cavity is open to the environment at the fimbrial entrance to the fallopian tubes. In both sexes (but more frequently in the male) a peritoneal tube (processus vaginalis) can persist at the deep inguinal ring and predispose to inguinal hernia formation. The interface between adherent regions of  the mesenteric and non-mesenteric domains is termed the retroperitoneal space ( 65.4 ). The retroperitoneal space normally contains connective tissue fascia. The space (and fascia) continues into the thorax superiorly and into the pelvis inferiorly . The retro - peritoneum is deep to the retroperitoneal space. It includes the kidneys, ureters, gonadal vessels, lumbosacral plexus and the musculoskeletal frame of  the posterior abdominal wall. The arterial inflow to the mesenteric domain is limited to - the coeliac trunk and superior and inferior mesenteric arter - ies. The venous drainage of  the mesenteric domain occurs via the hepatic veins at the junction of  these and the inferior vena cava. In between the arterial inflow and venous drainage, the vasculature of  the abdominal digestive org ans is entirely intramesenteric and aligned with the mesenteric regional anatomy ( 65.5 ). The limited routes of  arterial inflow and venous drainage have significant implications when these are a ff ected by pathology (discussed in Vascular abnormalities of the mesentery ).
Duodenum
Pancreas
Mesentery
Figure 65.3
The right lateral aspect of the mesentery during develop
ment. The mesentery has been sectioned to expose the developing
stomach (red), pancreas (light blue) and major blood vessels.
(a)
(b)
Dorsal
Upper region
mesogastrium
Left
Right
mesocolon
mesocolon
Figure 65.4
The mesentery.
(a–d)
The adult mesentery (and mesenteric domain) as seen from anterior
and left anterolateral
(d)
perspectives.
(c)
(d)
Greater
omentum
Lower
region
Mesoileum and
mesojejunum
(mid-region)
Mesorectum
(a)
, posterior
(b)
, right posterolateral
(c)
A knowledge of  the anatomical relationships between the mesenteric and non-mesenteric domains provides the student of  abdominal surgery with a roadmap by which to perform safe and optimal abdominal surgery . The above description is termed the mesenteric model of  abdominal anatomy . It is a model that matches observations during development with clinical observations in vivo and with radiological depictions of  the abdomen. It provides the anatomical context on which surgical diseases of  the abdomen and pelvis arise. Given this, it is rapidly substituting the peritoneal model in reference ana tomical texts.
The abdomen
Figure 65.5
The mesenteric and non-mesenteric domains of the
abdomen.
(a)
Intact abdomen.
(b)
Mesenteric domain (top) and
non-mesenteric domain (bottom).

Abdominal fluid collections
Abdominal fluid collections
Abdominal collections are subdivided into intraperitoneal and retroperitoneal collections. Retroperitoneal collections are further subdivided into those limited to the retroperitoneal space (e.g. in pancreatitis) and collections arising in relation to retroperitoneal organs such the kidney . The latter are collec tions of  the retroperitoneum. Collections of  the retroperitoneal space and retroperitoneum are considered in the final section of  the chapter.

Acute bacterial peritonitis
Acute bacterial peritonitis
Acute bacterial peritonitis most commonly arises from perforation of  a viscus of  the alimentary tract. Other routes of  infection can include the female genital tract and exoge nous contamination. Less common forms involve a primary ‘spontaneous’ peritonitis due to streptococcal, pneumococcal or Haemophilus infection.

Adhesions
Adhesions
Pathology - Adhesions are best classified with reference to their appear - ance. They are subdivided into peritoneal, areolar and dense adhesions. Peritoneal (sclerotic) adhesions - These are mesothelial adhesions between two mesothelial surfaces ( Figure 65.15a ). They reflect mesothelial prolif - eration, resemble peritoneum and are generally soft and non-vascular. They are similar in appearance (though not in consistency) to the peritoneal cocoon that occurs in mesenteric sclerosis. T hese can be band-like. They may occur following laparoscopic surgery , where they form a band linking a viscus to the inner surface of  a port site. Band adhesions can lead to Figure focal abdominal pain, internal herniation (through the window - created with surrounding related structures) or intestinal torsion around the band. Areolar adhesions These flimsy connective tissue adhesions are identical to the connective tissue that fills the retroperitoneal space between the mesentery and posterior abdominal wall ( Figure 65.15b ). Given this appearance they have been called ‘angel hairs’. They are generated in a process similar to that involved when - the mesentery adheres to the posterior abdominal wall.
Figure 65.14
Mesenteric sclerosis.
(a)
Coronal section of abdomen
on computed axial tomography demonstrating a sclerotic mass.
(b)
Postexcision mass in
(a)
. The intestine is contained in a sclerotic
capsule.
(c)
Appearance of the mass in
(b)
after division into halves.
The intestine is draped across the surface of a mesenteric tissue
mass.
(d)
Mesenteric panniculitis (misty mesentery).
(d)
The capacity to adhere is shared by all organs of  the mesenteric domain. This explains the anatomical relations between the liver, colon, spleen and mesentery on one side and the abdominal wall on the other. The capacity is retained to varying degrees among individuals and explains adhesion formation in the adult setting. Adhesion occurs following abdominal surgery when the intestine and mesentery adhere to the inside surface of  the anterior abdominal wall. The resultant anatomical arrangement is similar to that observed during development, except the anterior abdominal wall is involved. Postoperative adhesion formation occurs to varying degrees. At one end of  the spectrum, it may be entirely absent. At the other end, mesenteric, intestinal and other components of  the mesenteric domain may adhere over broad areas to the mally commences in the anterior abdominal wall. This nor midline and extends laterally towards the flanks, displacing the overlying peritoneum. The conformation of  the peritoneal cavity changes markedly . In the most extremes cases, the peri toneal cavity may be obliterated or limited to small pockets at the flanks. This generates considerable technical challenges during reoperative surgery . Dense adhesions These di ff er markedly in appearance from peritoneal or areolar adhesions. They can bridge the abdominal wall and intestine, or intestine and mesentery , and lead to fusion of  the bridged structures. Surgical division can be challenging. Sometimes it is not possible to separate conjoined organs without disrupting the integrity of  one of  them. Such dense adhesions arise mostly following severe intraperitoneal contamination (e.g. after perforation) at sites of  gross fibrin deposition and are highly variable in terms of  vascularity . Complications of adhesions The most common adhesion-related problem is small bowel obstruction (SBO). Adhesions are the most frequent cause of SBO in resource-rich countries and are responsible for 60–70% of  SBOs (see Chapter 74 ). Adhesions are also implicated as a major cause of  secondary infertility (see Chapter 87 relationship of  adhesions to chronic abdominal and pelvic pain is contentious. Unguided division of  adhesions has not been shown to reduce chronic abdominal pain although conscious pain mapping (laparoscopy under local anaesthesia) to direct lysis may improve success rates. A substantial industry has developed around the preven - tion of  adhesions. To date, no agent or mechanism has been identified that reliably reduces adhesion formation.
Figure 65.15
Adhesions.
(a)
Peritoneal (sclerotic) adhesions.
(b)
Areolar adhesions. (Reproduced
with permission from Coffey JC,
Lavery I, Sehgal R (eds).
Mesenteric
principles of gastrointestinal surgery:
basic and applied principles
. Boca
Raton: CRC Press, 2017: 333–42.)

Biliary peritonitis
Biliary peritonitis
Biliary peritonitis is mostly seen after cholecystectomy and arises from slippage of  a clip o ff the cystic duct, drainage of  bile from an accessory cystic duct or perforation of  the common bile or hepatic duct (see Chapter 71 ). It can also arise after hepatectomy or duodenal surgery , although this is unusual if  a drain has been placed at the time of  surgery . Investigation follows the principles and steps described in Peritonitis . The natural course of  biliary peritonism varies depending on the volume of  contamination. In severe con - tamination the patient will be e xtremely unwell and urgent intervention is required. Localised collections can be treated by percutaneous inser - tion of  a drain followed by endoscopic retrograde pancreato - graphy (ERCP) to identify the source of  bile leak. ERCP enables placement of  a stent across the source of  the leak. Di ff use or high-volume contamination, or the presence of  multiple sepa - rate locules, normally mandates surgical explora tion with the aim being lavage and drainage.

Chronic mesenteric ischaemia
Chronic mesenteric ischaemia
Chronic mesenteric ischaemia is due to atherosclerotic narrowing at the origin of  any of  the three arterial trunks. Patients describe postprandial abdominal pain that can be severe, resulting in a fear of  eating with progressive weight loss. The diagnosis requires CT angiography . Radiological stent placement may be successful, but surgical endarterectomy of bypass repair may be required. Venous ischaemia The venous drainage of  the mesenteric domain is limited to the junction between the hepatic veins and the inferior vena cava. Narrowing or blockage of  the lumen at this junction occurs in Budd–Chiari syndrome. It has major clinical implications. Most venous drainage of  the mesenteric domain returns to the liver via the portal vein. Portal venous thrombosis impedes venous drainage of  all abdominal digestive organs unless an alternative drainage route opens (i.e. a portosystemic shunt) or is created (see Chapter 69 ) ( 65.5 ).

Chylous ascites
Chylous ascites
In some patients, the ascitic fluid appears milky because of  an excess of  chylomicrons (triglycerides). Most of  these cases are associated with malignancy (usually lymphoma). Other causes include cirrhosis, TB, filariasis, nephrotic syndrome, abdominal trauma (including surgery), constrictive pericarditis, sarcoidosis and congenital lymphatic abnormality . The prognosis is poor unless the underlying condition can be cured. In addition to other measures used to treat ascites, patients should be placed on a fat-free diet with medium-chain triglyceride supplements.

DEVELOPMENT OF THE MESENTERY AND PERITONEUM
DEVELOPMENT OF THE MESENTERY AND PERITONEUM
Early in development, the human abdomen comprises a wall and enclosed space (coelom). A partition (mesentery) subdivides the cavity into left- and right-sided spaces ( Figure 65.1 The mesentery comprises a cell body (mesodermal mesentery) lined on either side by a sheet of  mesothelial cells ( 65.2 ). At first the cell body is continuous with the posterior abdominal wall, and the mesothelial covering of  the mesentery is continuous with that lining the inner surface of  the posterior abdominal wall. Soon after this arrangement has developed, the cell body of  the mesentery separates from the posterior abdominal wall but remains in contact with it ( 65.1 surface mesothelium of  the mesentery remains in continuity with that of  the posterior abdominal wall ( Figure 65.2 The mesentery remains continuous throughout develop ment, following birth and into adult life ( 65.2 ). Early during development, the mid-region of  the mesentery forms a fold that subdivides the mesentery into upper (pre-fold), mid- (fold) and lower (post-fold) regions ( Figure 65.1 ). The upper region develops as a sack overlapping the mid-region. As it develops, the spleen, stomach and liver emerge. The mid-region fold has left and right sides (on either side of the midline). The mid-region nearest the posterior abdominal wall is termed the central zone ( Figure 65.1 ). The remainder of  the fold is termed the peripheral zone. Soon after the mid- region fold first emerges, the sides of  the periphery (but not of  the central zone) switch position relative to the superior mesenteric artery (SMA). After the switch, the original right side of  the mid-region commences on the right side centrally but continues peripherally on the left of  the SMA. The original left side commences peripherally on the right side of  the vessel then returns centrally on the left of  the SMA ( 65.1 ). Failure of  switch formation occurs in malrotation (see Rotational disorders ). During development of  the upper region of  the mes entery , the region of  the mesodermal mesentery that is nearest the posterior abdominal wall adheres to the wall ( This process progresses from the midline laterally to the left. Adhesion of  both displaces the mesothelial junction between the mesentery and the adjacent posterior abdominal wall ( Figure 65.2 ). At completion of development the posterior wall of  the upper region (the dorsal mesogastrium) is fully adherent ). to the abdominal wall of  the left upper quadrant (LUQ). The spleen is located at the lateral part of  the upper region sac, Figure in the LUQ. The original mesothelial junction remains as the peritoneal reflection linking the surface lining the mesenteric domain (in this case the spleen) with the surface lining of  the adjacent non-mesenteric domain (in this case the LUQ). During development of  the mid-region fold, the region of  the mesodermal mesentery that is nearest the posterior ). The abdominal wall (i.e. the central zone) progressively adheres to the posterior abdominal wall. With continued adhesion, ). the periphery of  the mid-region fold also adher es ( 65.2 - and 65.3 ). Adhesion occurs inferolaterally to the right, and from the central to peripheral zones. The mesothelial junction between the mid-region mesentery and abdominal wall is displaced in tandem, inferolaterally to the right. At completion of  development the mid-region fold is adherent to the posterior abdominal wall at the right mesocolon. The original mesothelial junction is at the periphery of  the fold and persists as a peritoneal reflection bridging the surface lining of  the mesenteric and non-mesenteric domains ( Figure 65.2 ) ( 65.3 ). Incomplete adhesion of  the mid-region fold is associated with increased mobility of  the ileocaecal region and volvulus (see Volvulus of the intestine and adjoining mesentery ). During development of  the lower region of  the mesentery , the part nearest the posterior abdominal wall progressively adheres to the wall ( 65.1 ). This proceeds from the mid - line laterally to the left. The overlying mesothelial junction is Figure displaced in tandem ( Figure 65.2 ). At completion of  develop - ment, the lower region has fully adhered at the left mesocolon, medial mesosigmoidal and mesorectal levels. The lateral part - of  the mesosigmoid remains mobile. The mesothelial junction remains as a peritoneal reflection bridging the surface lin - 65.1 ). ing of  the mesenteric and adjacent non-mesenteric domain
Surgical conditions of the peritoneum, mesentery, greater
•
omentum and retroperitoneal space
( 65.3 ). Incomplete adhesion (and hence anchorage) of the lower region is associated with sigmoid volvulus (see Volvulus of the intestine and adjoining mesentery ).
R L
Central zone
(e)
(f)
Peripheral zone
Figure 65.1
Switching of the mid-region of the mesentery during development.
to switching of the sides of the mid-region fold.
(a, c, e)
Three-dimensional reconstructions of the mesentery before switching. The intestine
develops within the mesentery.
(b, d, f)
Three-dimensional reconstructions of the intestine. The mesentery has been removed to expose the
developing intestine.
(a1, c1, e1)
Digital reconstructions
of the developing mesentery after switching of the sides of the mid-region fold. The
mesentery is coloured yellow.
(b1, d1, f1)
Three-dimensional reconstructions of the intestine after the mid-region switch. The mesentery has
been removed to expose the developing intestine. Yellow, the mesentery; red, upper region of intestine; green, developing mid-region; blue,
lower region of the intestine. The superior mesenteric artery (blind-ending red tube) has been included for reference.
(a)
(b)
(c)
Posterior
abdominal wall
Mesentery
Fascia
(d)
(e)
(f)
Figure 65.2
(a-f)
Adhesion and displacement. Development of the
junction between the mesentery (*) and the posterior abdominal
wall. The peritoneal re
/f_l
ection (thick arrows) is displaced towards the
periphery during adhesion of the mesentery to the abdominal wall.
L R
Central zone
(e1)
(f1)
R
L
Peripheral zone
(a–f)
Digital reconstructions of the developing mesentery prior

Diffuse (generalised) peritonitis
Diffuse (generalised) peritonitis
This normally signifies the occurrence of  a life-threatening pathology . It means that regions (not just focal areas) of  the parietes (parietal peritoneum) are inflamed. It normally arises as a result of pressure-related perforation of a viscus (e.g. in the setting of  an obstructed colon), when large volumes of  blood abruptly enter the peritoneal cavity (ruptured aortic aneurysm) or when substantial volumes pour incessantly (albeit not under pressure) into the peritoneal cavity (e.g. perforated duodenal ulcer or anastomotic leak). The patient may describe acute or gradual onset abdomi nal pain of  considerable intensity . The pain may be localised at first and then become di ff use. The patient is gravely ill looking (Hippocratic facies) and usually lies as still as possible to mini mise fluid movement within the peritoneal cavity . The entirety Hippocrates of  Kos , Greek physician and surgeon, and by common consent ‘the father of  medicine’, was born on the island of  Kos, o ff Turkey , about 460 /uni00A0 and probably died in 375 /uni00A0 /b.sc/c.sc/e.sc . and feels board-like on palpation (‘board-like’ rigidity). In a thin patient, contraction of  the rectus abdominis muscles may be reflected in a scaphoid appearance of  the abdomen (see Chapter 63 ). A generalised ileus occurs and the abdomen may become distended. Vital signs are usually deranged. In advanced cases the patient is hypotensiv e, tachycardic and pyrexial. At first the - patient may seem confused, dr owsy and disoriented. If the underlying pathology is not corrected the patient will lose con - sciousness. Signs may be limited in obese patients or in patients on immunosuppressive medications. Investigation and treatment must be undertaken expedi - ently as the time available to salvage ma y be limited. Inves - tigations aim to identify the underlying cause and to guide p- treatment. An erect chest radiograph can be useful in identify - - ing subdiaphragmatic gas ( Figure 65.7 ). If  a patient is particu - larly unwell and a CT is not available, then a lateral decubitus radiograph serves the same purpose as an erect radiograph (provided the patient has been appropriately positioned for long enough for the gas to rise within the peritoneal cavity). tion, . Summary box 65.4 - Clinical features of peritonitis /uni25CF ). /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF m to Summary box 65.5 Management of peritonitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF - /b.sc/c.sc/e.sc
Abdominal pain, worse on movement, coughing and deep
respiration
Constitutional upset: anorexia, malaise, fever, lassitude
Gastrointestinal upset: nausea +/– vomiting
Pyrexia (may be absent)
Raised pulse rate
Tenderness +/– guarding/rigidity/rebound of abdominal wall
Pain/tenderness on rectal/vaginal examination (pelvic
peritonitis)
Absent or reduced bowel sounds
‘Septic shock’ (systemic in
/f_l
ammatory response syndrome
[SIRS] and multiorgan dysfunction syndrome [MODS]) in later
stages
General care of patient
Correction of
/f_l
uid and electrolyte imbalance
Insertion of nasogastric drainage tube and urinary catheter
Broad-spectrum antibiotic therapy
Analgesia
Vital system support
Surgical treatment of cause when appropriate
‘Source control’ by removal or exclusion of the cause
Peritoneal lavage +/– drainage
(b)
Figure 65.7
Intraperitoneal perforation.
(a)
Erect chest radiograph
demonstrating air under the diaphragm on the right side.
computed tomography image showing a segment of sigmoid divertic
ulosis with localised perforation (arrow).

FURTHER READING
FURTHER READING
Byrnes KG, McDermott K, Co ff ey JC (eds). Mesenteric organogenesis. Semin Cell Dev Biol 2019; 92 : 1–138. Co ff ey JC, Dockery P . Peritoneum, mesentery and peritoneal cavity . In: Standring S (ed.). Gray’s anatomy: the anatomical basis of  clinical prac - tice , 42nd edn. Elsevier Limited, 2021: 1150–60. - Co ff ey JC, Lavery I, Sehgal R (eds). Mesenteric principles of  gastrointes - tinal surgery: basic and applied principles . Boca Raton: CRC Press, 2017. de Bakker BS, de Jong KH, Hagoort J et al . An interactive three- dimensional digital atlas and quantitative database of human development. Science 2016; 354 (6315): aag0053. Ha CWY , Martin A, Sepich-Poore GD et al . Translocation of  viable gut microbiota to mesenteric adipose drives formation of  creeping fat in humans. Cell 2020; 183 (3): 666–83. Sadler TW . Langman’s medical embryology , 14th edn. Lippincott Williams & Wilkins, 2019. - World Gastroenterology Organisation. WGO practice guideline – digestive tract tuberculosis , 2021. Available from https://www . worldgastroenterology .org/guidelines/digestive-tract-tuberculosis.

Familial Mediterranean fever
Familial Mediterranean fever
Familial Mediterranean fever (FMF; synonym familial paroxysmal polyserositis) is an autosomal recessive inherited autoinflammatory syndrome characterised by episodic di ff use abdominal pain and tenderness, mild pyrexia and joint pain. - Symptoms are usually mild and resolve within 24–72 hours. Rarely pericardial or meningeal inflammation may occur. Amyloidosis is a long-term complication. FMF is associated with mutations in the MEFV (Mediterra - nean fever) gene most frequently found in Arab, Armenian and - Jewish populations. MEFV encodes the protein pyrin, which is expressed in neutrophils and is thought to regulate interleu - - kin-1B (a proinflammatory cytokine) release. Symptoms often present in childhood and may be misdiag - nosed as appendicitis. Treatment of  an acute episode is symp - tomatic. Colchicine can be used to reduce the frequency and severity of attacks and to prevent development of amyloidosis .
(b)

History
History
In ileocaecal volvulus the patient often describes a longstand ing history of  intermittent, colicky abdominal pain associated with distension and vomiting. In between episodes (when the volvulus has detorted) the patient is entirely asymptomatic and repeated CT and endoscopic examinations are normal. The clinical pictur e is similar to that of  irritable bowel syndrome. Sigmoid volvulus occurs mainly in the elderly as the intes tine and mesentery continue to lengthen throughout life.

INTRAPERITONEAL ABSCESS FORMATION
INTRAPERITONEAL ABSCESS FORMATION
An intraperitoneal abscess is a collection of  pus in the peritoneal cavity ( Figure 65.10 ). It normally arises secondary to another - pathology . Inflammation of  any viscus, if  unresolved, will lead to hypersecretion of  peritoneal fluid. The nature of  the fluid progresses to frank pus unless adsorbed or drained. Hence, - abscess formation commonly accompanies inflammation of  an abdominal viscus and is usually labelled either according to location (subphrenic, intrapelvic) or with reference to nearby organs (periappendiceal, paracolic, subhepatic). - Intraperitoneal abscess formation is associated with a spectrum of symptoms and signs. At one end, patients may be asymptomatic or may feel somewhat unwell, anorectic, fatigued, with failure to maintain or gain weight. At the oppo - - site end, patients may have significant abdominal symptoms and signs (nausea, vomiting, abdominal pain, diarrhoea) and - be extremely unwell. A swinging pyrexia is strongly suggestive of  intraperitoneal abscess for mation. Summary box 65.8 Clinical features of an abdominal/pelvic abscess /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF
Figure 65.9
Computed tomography axial scan of the abdomen show
ing gross ascites.
Symptoms
Malaise, lethargy – failure to recover from surgery as expected
Anorexia and weight loss
Sweats +/– rigors
Abdominal/pelvic pain
Symptoms from local irritation, e.g. shoulder tip/hiccoughs
(subphrenic), diarrhoea and mucus (pelvic), nausea and
vomiting (any upper abdominal)
Signs
Increased temperature and pulse +/– swinging pyrexia
Localised abdominal tenderness +/– mass (including on pelvic
examination)
Figure 65.10
Intraperitoneal abscesses.
(a)
and
(b)
Subphrenic and subhepatic abscesses seen on computed tomography (CT) scanning.
(c)
Pelvic abscess seen on CT scanning.

Intraperitoneal collections
Intraperitoneal collections
Ascites Peritoneal fluid is constantly secreted and absorbed. Accumu lation of  peritoneal fluid, termed ascites, occurs when there is excess production or reduced absorption. Production of large volumes of  a protein-rich fluid occurs in peritonitis and car cinomatosis peritonei. Reduced absorption occurs when capillary pressure is increased as a result of  generalised water retention, cardiac failure, constrictive pericarditis or vena cava obstruction. Capillary pressure is also raised selectively in the portal venous system in the Budd–Chiari syndrome, hepatic cirrhosis or extrahepatic portal venous obstruction. Plasma colloid osmotic pressure may be lowered in patients with reduced nutritional intake, diminished intestinal absorption, abnormal protein losses or defective protein synthesis, such as occurs in cirrhosis. Peritoneal lymphatic drainage may be impaired, resulting in the accumulation of  protein-rich fluid. Harry H LeVeen , 1915–1997, Professor of  Surgery , University of  South Carolina, Columbia, SC, USA. George Budd , 1808–1882, Professor of  Medicine, King’s College Hospital, London, UK. Hans Chiari , 1851–1916, Professor of  Pathological Anatomy , Strasbourg, Germany (Strasbourg was returned to France in 1918 at the end of  the First World War). Caput Medusa (head of  Medusa) , in Greek mythology depicted as having venomous snakes instead of  hair. Friedel Pick , 1867–1926, physician, Prague, the former Czechoslovakia, described this disease in 1896. Joe Vincent Meigs , 1892–1963, Professor of  Gynecology , Harvard University Medical School, Boston, MA, USA. due to portal venous hypertension secondary to fibrosis of  the intrahepatic venous bed. In the Budd–Chiari syndrome (see Chapter 69 ), thrombosis of  hepatic veins leads to obstruction of  venous outflow fr om the liver and hence from the mesen - teric domain in general. Alternative routes of  venous drainage may open up. One such route involves the vestigial umbilical vein at the base of  the falcif orm ligament. V enous drainage via this route may reach the systemic venous drainage at the umbi - licus. This is termed a portosystemic shunt and has a charac - teristic clinical appearance (involving veins) at the umbilicus (caput medusae). Congestive heart failure increases pressure in the vena cava and resistance to the venous outflow from the liver. In this set - ting, ascitic fluid is light yellow and has a low specific gravity and low protein concentration (<25 /uni00A0 g/L). In constrictive peri - carditis there is a diminished capacity of  the right heart. This leads to simultaneous peritoneal and pleural e ff usions due to engorgement of  the venae cavae (Pick’s disease). Ascites occurring in peritoneal metastases is due to e xces - sive exudation of  fluid and lymphatic blockage. T he fluid is dark yellow and frequently blood stained. The specific grav - ity and protein content (>25 /uni00A0 g/L) are high. Rarely , ascites and pleural e ff usion are associa ted with solid fibromas of  the ovary (Meigs’ syndrome). These e ff usions disappear when the tumour is excised. - Summary box 65.7 Causes of ascites /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF Ascites normally becomes clinically recognisable when greater than 1.5 litres of  fluid is apparent (although greater volumes may be required in obese patients). The abdomen is distended evenly with fullness of  the flanks, which are dull to percussion. Usually , shifting dullness is present but, when there is a very large accumulation of  fluid, this sign is absent. In such cases, flicking the abdominal wall produces a characteristic
Transudates (protein <25
/uni00A0
g/L)
Exudates (protein >25
/uni00A0
g/L)
Low plasma protein
Peritoneal malignancy
concentrations
Tuberculous peritonitis
Malnutrition
Budd–Chiari syndrome
(hepatic vein occlusion or
Nephrotic syndrome
thrombosis)
Protein-losing
enteropathy
Pancreatic ascites
High central venous pressure
Chylous ascites
Congestive cardiac failure
Meigs’ syndrome
Portal hypertension
Portal vein thrombosis
Cirrhosis
reliable clinical sign. In women, ascites must be di ff erentiated from an enormous ovarian cyst. Investigations The aims are identification of  ascites and determination of  the underlying cause. Liver function tests (LFTs), cardiac function, ultrasonography and/or CT scanning ( Figure 65.9 ) may help diagnose aetiology , e.g. carcinomatosis or liver disease. Ascitic aspiration or tap under imaging guidance helps minimise the risk of  visceral injury . It can be both diagnostic and therapeutic. After the bladder has been emptied, puncture of  the peritoneum is carried out under local anaesthetic using a moderately sized trocar and cannula. A peritoneal drain may be inserted at the time. In cases where the e ff usion is caused b y cardiac failure, fluid must be evacuated slowly . Fluid is sent for microscopy/cytology , culture, including mycobacteria (see Tuber culus peritonitis above), and analysis of  protein content and amylase. Unless other measures are taken the fluid soon accumulates and repeated tappings remove valuable protein. Management Management aims to address any reversible primary pathol ogy (following which the ascites resolves) or symptom-based management of the ascites itself. If portal venous pressure is raised, it may be possible to lower it by tr eatment of  the primary condition or by transjugular intrahepatic portosys temic shunt or transjugular intrahepatic portosystemic stent shunting (commonly abbreviated as TIPS or TIPSS). Dietary sodium restriction to 200 /uni00A0 mg/day may be helpful, but diuretics are usually required (combination of  spironolac tone and furosemide). For patients failing to respond to such measures, therapeutic needle paracentesis can be performed. Serial large volume paracentesis (4–6 /uni00A0 L/day and up to 8 litres in one session) can be performed safely with colloid replace ment and can be perf ormed in patients with cirrhosis and deranged clotting. Guidelines recommend albumin replace ment after paracentesis to reduce complications. It may also be possible to leave an indwelling external drain f or smaller volume home paracentesis.

Introduction
Introduction
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Investigation
Investigation
The modern diagnosis of  an abscess is radiological using CT ( Figure 65.10 ). CT imaging can also guide treatment by drain placement or aspiration. Ultrasound is a useful (though non-specific) modality for use in select populations (e.g. paedi atric or pregnant patients). Serial imaging is used to monitor treatment e ffi cacy or disease progression. Radiolabelled white cell scanning may occasionally prove helpful if  an abscess is suspected but has not been identified by the above means. Investigation
There is often a leukocytosis of  10 /uni00A0 000–12 /uni00A0 000/ /uni03BC L (10–12 9 ×/uni00A0 10 /L) or more on the first day of  the attack, but this falls on the second day . Ultrasonography may be helpful in di ff eren tiating this from appendicitis. Sometimes a CT or exploratory laparoscopy is required. Investigation
A plain film of  the abdomen is frequently diagnostic. CT is recommended when planning operative intervention.

Learning objectives
Learning objectives
To understand: The development and anatomy of the mesentery and • peritoneum

MESENTERIC ADENITIS AND THE MESENTERY IN CROHN’S D
MESENTERIC ADENITIS AND THE MESENTERY IN CROHN’S DISEASE
Ileocaecal mesenteric adenitis occurs in ileocolic Crohn’s disease and the mesentery is thickened, shortened and oedem atous with a tendency to bleed readily when handled. The vascular pedicles within the mesentery may not be apparent, thus great care is needed when dividing the mesentery as normal techniques may not be suitable. In Crohn’s disease , the mesentery can extend over adjoin ing intestine as ‘fat wrapping’ or ‘creeping fat’ ( Figure 65.12 These appear to be specific to Crohn’s disease. The mesentery changes from normal to abnormal at the mesenteric transition zone. Conventional sur gery for Crohn’s disease involves ampu tation of  the intestine at its intersection with adjoining mes entery . The mesentery is thus retained. Increasingly , surgeons are removing the mesentery adjoining the diseased intestine (see Chapter 75 ).

MESENTERIC ADENITIS
MESENTERIC ADENITIS
This is inflammation of  the lymph nodes of  the mesentery - ( Figure 65.11 ). It mostly occurs in the ileocaecal region because of  the volume of  lymphatic tissue. It is often the site of  viral - or infective lymphadenopathy ( Yersinia spp., Campylobacter spp., - Mycobacterium tuberculosis ) and may follow an upper respiratory tract infection with either a viral or bacterial pathogen. Mesen - teric adenitis caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is not uncommon. Swelling of ileocaecal lymph nodes results in capsular stretch and somatic pain in the right iliac fossa. The patient is frequently pyretic (often the temperature is mar kedly elevated) and may have enlarged cervical lymph nodes. During childhood, acute, non-specific mesenteric adenitis is a common condition. The typical history is one of short attacks of  central abdominal pain lasting from 10 to 30 min - utes, commonly associated with v omiting. The patient seldom looks ill. In more than half of  the cases the temperature is present, shifting tenderness is a valuable sign for di ff erentiating the condition from appendicitis. The neck, axillae and groins should be palpated for enlarged lymph nodes.

MESENTERIC HAEMATOMA
MESENTERIC HAEMATOMA
A mesenteric haematoma can follow abdominal compression in trauma (e.g. seat-belt syndrome) or during abdominal surgery , when the mesentery must be manipulated. The mesenteric stroma is mainly adipose and thus easily damaged. It bleeds readily if  disrupted. A haematoma may form and quickly enlarge to compress mesenteric veins. Mesenteric haematoma can sometimes occur during surgery for Crohn’s disease.

Mesenteric cysts
Mesenteric cysts
Cysts may occur in any region of  the mesentery ( Figure 65.16 ). They are most often observed in mesentery adjoining the small intestine (60%) or the colon (40%) and can be classified as follows: /uni25CF chylolymphatic; /uni25CF enterogenous; /uni25CF traumatic; /uni25CF hydatid. Chylolymphatic cysts Although mesenteric cysts are rare, this is the most common - variety , probably arising in congenitally misplaced lymphatic tissue that has no e ff erent communication with the lymphatic system (most frequently in the mesentery of  the ileum). The thin wall of  the cyst, which is composed of  connective tissue ). The
Mesentery
Mesenteric
cyst
Figure 65.16
Mesenteric cyst. (Reproduced with permission from
Coffey JC, Lavery I, Sehgal R (eds).
Mesenteric principles of gastro-
intestinal surgery: basic and applied principles.
Boca Raton: CRC
Press, 2017: 85–108.)
frequently , with chyle, varying in consistency from watered milk to cream. Occasionally , the cyst attains a large size. More often unilocular than multilocular, a chylolymphatic cyst is almost invariably solitary , although there is an extremely rare variety in which myriads of  cysts are found in various regions of the mesentery . A chylolymphatic cyst has a blood supply that is independent from that of  the adjacent intestine and, thus, enucleation is possible without the need for resection of the gut. Enterogenous cysts These are believed to be derived either from a diverticulum of  the mesenteric border of  the intestine that has become sequestrated from the intestinal canal during embryonic life or from a duplication of  the intestine (see Chapter 18 enterogenous cyst has a thicker wall than a chylolymphatic cyst and is lined by mucous membrane, which is sometimes ciliated. The content is mucinous and either colourless or yellowish brown as a result of  past haemorrhage. The muscle in the wall of  an enteric duplication cyst and the bowel with which it is in contact have a common blood supply; consequently , removal of  the cyst always entails resection of  the related portion of intestine.

Mesenteric sclerosis and panniculitis Mesenteric s
Mesenteric sclerosis and panniculitis Mesenteric sclerosis
This is also termed sclerosing encapsulating peritonitis or abdominal cocoon syndrome ( Figure 65.14 ). It occurs mostly in patients on long-term peritoneal dialysis. It is a disease of  the mesothelial component of  visceral peritoneum (i.e. peritoneum overlying organs of  the mesenteric domain). The mesothelium undergoes hypertrophy and the peritoneum becomes thickened. Underlying organs become encapsulated by a peritoneal ‘cocoon’. Mesenteric sclerosis may follow intra - peritoneal sepsis, when fibrin plaques accumulate along the hypertrophy . History and investigation The clinical picture is highly variable, as is the natural history of the condition among individuals. Mesenteric sclerosis can lead to obstruction of  the intestine. The diagnosis is normally made based on CT and intraoperative appearances and post operative surgical histology . Treatment Treatment is supportive and surgery is reserved for emergency cases only as surgical intervention may lead to further perito neal sclerosis. Mesenteric panniculitis This is inflammation of  the mesodermal mesentery (i.e. the mesenteric stroma). It is always present in Crohn’s disease (see Mesenteric adenitis and the mesentery in Crohn’s disease ). Often it is an incidental finding on cross-sectional imaging of  the abdomen by CT (‘misty mesentery’; 65.14 ). Although there are concerns over malignant poten tial, this is not supported by the general literature. It can arise secondary to inflammation in any digestive organ. It is associated with connective tissue disorders (including Weber– Christian disease). As with mesenteric sclerosis, treatment is normally medical and surger y is rarely required. Serial CT scanning is indicated to ensure resolution. Sclerosing mesenteritis Sclerotic (mesothelial) and inflammatory (mesodermal) abnor malities of  the mesentery may coexist. Although this can arise Frederick Parkes Weber , 1863–1962, physician, Mount V er non Hospital, London, UK. Henry Asbury Christian , 1876–1951, pathologist, Boston, MA, USA. pathology (i.e. immunoglobulin G4 [IgG4] disease, which is a systemic fibroinflammatory disease).
(a)
(b)
(c)

Mesenteric stretch during colonoscopy
Mesenteric stretch during colonoscopy
Development of  pain doing colonoscopy is frequently attributed to distension of  the colon and stretch of  the colon wall. In reality , substantial volumes of  gas would be required to insu ffl ate the colon to the degree at which the colon stretches. Pain during colonoscopy is common and arises mainly because of  stretch of  the adjoining mesentery . Looping of  the intestine is a frequent event during colonoscopy . The loop corresponds to a coil, which means that the mesentery adjoining the loop must form a spiral. It thus resembles the anatomical arrange - ment seen in volvulus. Attempts to advance the endoscope - beyond a coil will place both the intestine and mesentery central under stretch. Stretch of the mesentery leads to severe colicky abdominal pain, often accompanied by bradycardia. An understanding of  the anatomical basis of  loop formation enables the endoscopist to take appropriate preventative or corrective measures. -

Non-gastrointestinal causes of acute bacterial per
Non-gastrointestinal causes of acute bacterial peritonitis
Pelvic infection via the Fallopian tubes is responsible for a high proportion of  ‘non-gastrointestinal’ infections. The most Francis Glisson , 1597–1677, Regius Professor of  Medicine, Cambridge, UK. Fitz-Hugh–Curtis syndrome : named after the two physicians, Thomas Fitz-Hugh, Jr USA, and Arthur Hale Curtis 1881–1955, gynecologist, Chicago, IL, USA, who first reported this condition in 1934 and 1930, respectively . cocci. These organisms lead to a thinning of  cervical mucus and allow bacteria from the vagina to pass into the uterus and oviducts, causing infection and inflammation. A variant of  transperitoneal spread of  such org anisms is perihepatitis, which can cause scar tissue to form on Glisson’s capsule, a thin layer of  connective tissue surrounding the liver (Fitz - Hugh–Curtis syndrome). Fungal peritonitis is rare but may complicate severely ill patients.

PERITONEAL (MESOTHELIAL) SAC AND HERNIA FORMATION
PERITONEAL (MESOTHELIAL) SAC AND HERNIA FORMATION
The processus vaginalis refers to a peritoneal tube that advances into the inguinal ligament in tandem with migra tion of  the testes. The lumen of  the processus vaginalis is in continuity with the peritoneal cavity . Given this, it provides a conduit for herniation of  abdominal contents. Even a residual indentation at the ostium of  the processus v aginalis represents a mechanical defect at which repeated episodes of raised intraperitoneal pressure can lead to gradual extension of the parietal peritoneum into the inguinal canal. The mesothelial sac is a near constant feature of  incisional and parastomal hernias. In these instances, the peritoneum gradually advances over subcutaneous fat, or the serosal sur face of  the intestine, bringing that region of  anatom y directly in continuity with the peritoneal cavity . Not surprisingly , inci sional or parastomal hernias gradually increase in size with time. In addition, they are frequently complicated by para stomal her niation of  intestinal contents and intestinal com promise.

PERITONEAL INCLUSION CYSTS Introduction
PERITONEAL INCLUSION CYSTS Introduction
These are benign cysts lined by peritoneal mesothelium. They can arise at any location of  the peritoneum, in continuity with the surface of  either parietal or visceral peritoneum. They can gradually expand and rarely rupture. Most are asymptomatic and are identified incidentally on cross-sectional imaging for other indications. There is a loose association with ovarian malignancy and thus MRI evaluation of  the ovaries is advisable in the premenopausal context. If  symptomatic an inclusion cyst may be drained under imaging control, deroofed or excised. Recurrent rates are high.

PERITONITIS
PERITONITIS
Peritonitis is inflammation of  the peritoneum and can be cate gorised as localised or di ff use, acute or chronic or according to the primary underlying pathology . In the clinical setting, the most useful categorisation of  peritonitis is based on whether it is localised or di ff use. Summary box 65.2 Causes of peritoneal inflammation /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF /uni25CF - Summary box 65.3 Paths to peritoneal infection /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF
Ascending
Right
colon
mesocolon
Fascia in
retroperitoneal
space
Divided
re
/f_l
ection
(d)
Mesoileum
Fascia in
retroperitoneal
space
Peritoneal
re
/f_l
ection
Mesenteric principles of gastrointestinal surgery: basic and applied
Bacterial, gastrointestinal and non-gastrointestinal
Chemical, e.g. bile, barium
Allergic, e.g. starch peritonitis
Traumatic, e.g. operative handling
Ischaemia, e.g. strangulated bowel, vascular occlusion
Miscellaneous, e.g. familial Mediterranean fever
Gastrointestinal perforation, e.g. perforated ulcer, appendix,
diverticulum
Transmural translocation (no perforation), e.g. pancreatitis,
ischaemic bowel, primary bacterial peritonitis
Exogenous contamination, e.g. drains, open surgery, trauma,
peritoneal dialysis
Female genital tract infection, e.g. pelvic in
/f_l
ammatory disease
Haematogenous spread (rare), e.g. septicaemia
This is where a localised area of  the peritoneum has become inflamed. If  the parietal peritoneum is involved, the patient complains of  pain (somatic pain) in the area a ff ected. Vital signs may be normal, but tachycardia and pyrexia are common. The characteristic signs are involuntary guarding (reflex abdominal wall contraction to reduce further peritoneal irritation) and rebound tenderness (worsening of  pain on lifting the examin ing hand o ff the abdominal wall). Collectively these signs and symptoms are termed peritonism and the patient is described as peritonitic (see Chapter 63 ). If  inflammation arises under the diaphragm, shoulder tip (‘phrenic’) pain may be felt. This is referred pain to the C5 dermatome. In cases of  pelvic peritonitis, e.g. from an inflamed appendix or salpingitis, abdominal signs may be limited; dee seated tenderness may be detected by digital rectal or vagi nal examination. Signs may be limited in obese patients or in patients on immunosuppressive medications. The aim is to diagnose the underlying cause and guide treatment. Diagnosis of  the underlying condition is made through a combination of  history and physical examina supplemented by laboratory and radiological investigations Laboratory biomarkers will support a diagnosis of  acute inflammation, but are rarely diagnostically specific. The inves tigation of  choice is computed tomography (CT) scanning. Modalities such as ultrasound can be used but lack specificity except in the case of  tubo-ovarian pathology (see Chapter 87 Laparoscopy may be required if  the above investigations are inconclusive. The aims of  treatment are to remove the underlying cause and to lavage or dilute residual contamination. At surgery the inflamed peritoneum appears reddened, thickened and has a velvety texture. Plaques of  yellow/white fibrin may be appar ent, causing loops of intestine (and mesentery) to adhere to themselves and to the parietes. There is a reactionary , serous exudate (rich in leukocytes and plasma proteins) that gradually becomes turbid in appearance. The fluid may transfor frank pus if  not evacuated.

RETROPERITONEAL SPACE COLLECTIONS
RETROPERITONEAL SPACE COLLECTIONS
These are fluid collections in the retroperitoneal space and these di ff er from intraperitoneal collections because of  their location ( Figure 65.21 ). They are a common finding in moder ate to severe acute pancreatitis. Fluid accumulates as a result of  pancreatic inflammation, dissecting the left mesocolon o ff the underlying fascia and posterior abdominal wall. With continued expansion retroperitoneal space collections track subperitoneally ar ound the flanks. A rapidly expanding retro peritoneal collection, such as occurs with a ruptured aortic aneurysm, may rupture intraperitoneally .
Mesorectum
Fascia
(b)
Intraoperative appearance
Mesenteric principles of gastro
(b)

ROTATIONAL DISORDERS Malrotation
ROTATIONAL DISORDERS Malrotation
Malrotation refers to a failure of  formation of  the mid-region switch (described in Development of the mesentery and peritoneum ) ( Figure 65.13 ) and is the most common abdom inal surgical emergency in the neonatal period. Early during development, the right and left side of  the mid-region fold of the mesentery are aligned from the central to peripheral zones. Later, the sides switch position at the periphery but not at the central zone. Adjoining intestine similar ly changes position to take up the normal conformation. In malrotation, the switch does not occur, and the sides of  the mid-region fold remain aligned. This explains why the duodenum, jejunum and ileum William Edwards Ladd , 1880–1967, Surgeon in Chief, Boston Children’s Hospital, Boston, MA, USA. are aligned in the right flank of the abdomen. Malrotation in itself  is not pathogenic. However, the small intestine and adjoining mesentery are abnormally mobile and can undergo torsion around the superior mesentery artery , which can be life-threatening. History The neonate with a volvulus due to malrotation is patently distressed, vomiting and has a distended abdomen. Investigation Urgent CT is mandated and clarifies the position of  the duode - nojejunal junction. Normally the duodenojejunal flexure is positioned at or to the left of  the midline. In volvulus due to malrotation, the duodenojejunal junction is on the right of  the midline (i.e. the mid-region switch has not occurred). Treatment The mainstay of  treatment is Ladd’s procedure, in which the volvulus is first reversed and then the intestine is secured to the posterior abdominal wall. Although this does not correct the underlying mesenteric abnormality , it does reduce the mobility of  the intestine and mesentery and reduces the likelihood of further volvulus. It is possible however to address the under - lying mesenteric abnormality by recapitulating the mid-region switch. This returns the intestine and mesentery to a normal conformation. They can then be fixed to the posterior abdom - inal wall. -
Mesenteric
transition zone
Fat wrapping
Creeping fat
Normal
mesentery
(b)
The mesenteric transition zone and
Mesenteric principles of gastrointestinal surgery: basic and

Retroperitoneal lipoma
Retroperitoneal lipoma
The patient may seek advice on account of  a swelling or because of  indefinite abdominal pain. The swelling sometimes reaches an immense size. Diagnosis is usually by CT scan. A retroperitoneal lipoma sometimes undergoes myxomatous degeneration, a complication that does not occur in a lipoma rance.
Figure 65.22
Representative sagittal computed tomography recon
struction of a right-sided psoas abscess (arrow) (courtesy of Dr K
Patel, Homerton University Foundation Trust, London, UK).
size is often malignant (liposarcoma).

Retroperitoneal sarcoma
Retroperitoneal sarcoma
Retroperitoneal sarcomas are rare tumours accounting for only 1–2% of  all solid malignancies (10–20% of  all sarcomas are retroperitoneal). The peak incidence is in the fifth decade of  life, although they can occur at almost any age. The most frequently encountered cell types are: /uni25CF liposarcoma; /uni25CF leiomyosarcoma; /uni25CF malignant fibrous histiocytoma. History and examination Patients with sarcomas present late because these tumours arise in the large potential spaces of  the retroperitoneum and can grow to a considerable size without producing symptoms. Moreover, when symptoms do occur, they are non-specific, such as abdominal pain and fullness, and are easily dismissed as being caused by other less serious processes. Retroperitoneal sarcomas are therefore often very large at the time of presentation. Investigation Detailed multiplanar imaging (CT and MRI) with reconstruc tions is required not only for tumour detection, staging and surgical planning but also for guiding percutaneous or surgical biopsy of  these tumours. Treatment The definitive treatment of  primary retroperitoneal sarcomas is surgical resection. Chemotherapy and radiotherapy without surgical debulking have rarely been beneficial, when used alone or in combination. A multidisciplinary treatment approach with imaging review will be required when assessing operabil ity (based on adjacency or involvement of vital structures) and approach. Up to 75% of  retroperitoneal sarcoma resections visceral organ (commonly large or small bowel or kidney). The most common types of  v ascular involvement precluding resection are involvement of the proximal superior mesenteric vessels or involvement of  bilateral renal vessels. Prognosis Survival rates are in general poor, even after complete resec - tion, being of  the order of  35–50% (excluding low-grade liposarcomas, which may frequently be cured by resection).

Retroperitoneal fibrosis
Retroperitoneal fibrosis
This is a relatively rare diagnosis characterised by development of  a flat grey/white plaque of  tissue that usually develops in the low lumbar region and later spreads laterally and upwards to encase the common iliac vessels, ureters and aorta. Histo logical appearances vary from active inflammation with a high cellular content interspersed with bundles of  collagen through to one of  relative acellularity and mature fibrosis/calcification. Its aetiology is obscure in most cases (idiopathic; synonym Or mond’s disease), being allied to other fibromatoses (others being Dupuytren’s contracture and Peyronie’s disease). Summary box 65.11 Causes of retroperitoneal fibrosis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF John Kelso Ormond , 1886–1978, urologist, Ann Arbor, MI, USA. Baron Guillaume Dupuytren , 1777–1835, Surgeon in Chief, Hôtel Dieu, Paris, France. François Gig ot de la Peyronie , 1678–1747, surgeon to King Louis XIV of  F Percival Pott , 1714–1788, surgeon, St Bartholomew’s Hospital, London, UK. The psoas abscess is an abscess of  the retroperitoneum ( Figure 6.22 ). At the start of  the twentieth century , psoas abscess was mainly caused by TB of the spine (Pott’s disease). With the decline of M. tuberculosis as a major pathogen in resource-rich countries, a psoas abscess was mostly found secondary to direct spread of  infection from the inflamed digestive or urinary tract with or without perforation. In more recent years it is most commonly seen in advanced Crohn’s disease. Rarely , it arises due to haematogenous spread from an occult source in immunocompromised patients and in association with intra - venous drug misuse. History Clinical presentation is with back pain, lassitude and fever. A swelling may point to the groin as it tracks distally along the iliopsoas muscle, under the inguinal ligament. Pain may be elicited by passive extension of  the hip or a fixed flexion of  the hip evident on inspection. Investigation and treatment Radiological investigation is by CT scanning and treatment is usually by percutaneous CT-guided drainage and appropriate antibiotic therapy . Surgical intervention is required if  these are unsuccessful. -
Figure 65.21
Computed tomography scan demonstrating retroperi
toneal space collection in acute pancreatitis. The collection (arrows)
has dissected the right mesocolon (asterisk) and duodenum, off the
underlying retroperitoneum. Fluid is apparent in the retroperitoneal
space.
Benign
Idiopathic (Ormond’s disease)
Chronic in
/f_l
ammation
Extravasation of urine
Retroperitoneal irritation by leakage of blood or intestinal
content
Aortic aneurysm (in
/f_l
ammatory type)
Trauma
Drugs (chemotherapeutic agents and previously methysergide)
Malignant
Lymphoma
Carcinoid tumours
Secondary deposits (especially from carcinoma of stomach,
colon, breast and prostate)

Secondary peritoneal malignancy
Secondary peritoneal malignancy
Peritoneal carcinomatosis Peritoneal carcinomatosis is common and refers to malignant nodules on the surface of the peritoneum. It normally arises in conjunction with ovarian malignancy or malignancy in an organ of  the mesenteric domain. It can be localised or di ff use. Any peritoneal surface can be involved. Sometimes the omen Paul H Sugerbaker , b. 1941, Director of  Surgical Oncology , Washington Cancer Institute, Washington, DC, USA. tum is di ff usely involved, forming a mass termed an omental cake. The symptoms and signs are mainly related to the primary pathology . If  the tumour burden is considerable, a mass may be palpable and the accompanying ascites substantial. Radio - logical cross-sectional imaging with CT or magnetic resonance imaging (MRI) is usually diagnostic; however, histological or cytological confirmation is essential to distinguish it from peri - toneal TB. The visceral origin of peritoneal carcinomatosis is important as this can guide chemotherapy and cytoreductive or extirpative surgery . The visceral origin of peritoneal car cinomatosis is import - ant because if curative resection of the primary tumour is deemed feasible and the peritoneal disease considered resect - able, resection with peritonectomy and HIPEC should be con - sidered. HIPEC is a highly concentrated, hea ted (41–42°C) chemotherapy delivered directly into the abdomen for 90 min - utes after cytoreductive surgery . HIPEC is particularly valu - able in trea tment of  pseudomyxoma peritonei and has become the standard of  care in carefully selected patients assessed in specialist centres (Sugerbaker) (see Chapter 76 ). -
Figure 65.8
(a)
Plain chest radiograph from a 55-year-old man
showing miliary tuberculosis (TB);
(b, c)
representative computed
tomography images from the same patient showing gross ascites,
nodular stranding in the omentum and mesentery, as well as nodular
enhancement of the peritoneum – TB peritonitis (courtesy of Dr S
Burke, Homerton University Foundation Trust, London, UK).
treatment is palliative. Subacute intestinal obstruction may require intestinal bypass or a defunctioning stoma (see Chapter 78 ). Malignant ascites may be drained externally or via a peritoneovenous shunt (LeV een).

Special considerations  Abscess formation followin
Special considerations: Abscess formation following intestinal surgery and anastomosis
The development of  an abscess following intestinal resection and anastomosis signifies infection of  a haematoma or an anas - tomotic leak. Locules of  gas or free contrast (Gastrografin) on CT support anastomotic leak. Pelvic abscess formation is not uncommon following excision of  the rectum and formation of - a pelvic anastomosis.

Special considerations  Prevention of abscess form
Special considerations: Prevention of abscess formation after appendicitis
During appendectomy , it is important to aspirate the pelvic, paracolic and subhepatic spaces prior to closure of  the abdom - - inal wall. This simple measure can reduce the incidence of postoperative abscess, which is common after appendectomy , occurring in up to 30% of  patients following appendectomy for a perforated appendix. It can lead to frustration f or patients if not forewarned of  the possibility .

Special considerations  Subphrenic abscess
Special considerations: Subphrenic abscess
This refers to the presence of  pus immediately beneath the diaphragm. Patients may complain of  shoulder tip pain. The diaphragm also develops at the same level as the C5 dermatome. If  the parietal peritoneum under the diaphragm is irritated, - pain is referred to the shoulder tip. This also explains why patients frequently complain of  shoulder tip pain following laparoscopic or robotic surgery . In the era preceding that of cross-sectional imaging via CT , the adage ‘pus somewhere, pus nowhere, pus under the diaphragm’ was useful. The pelvis is the most common site of abscess formation because the vermiform appendix is often pelvic in position and the Fallopian tubes are also frequent sites of  infection. A pelvic abscess can also occur as a sequel to di ff use peritonitis and is common after anastomotic leakage following colorectal surgery . Clinical features The most characteristic symptoms are pelvic pain, diarrhoea and passage of  mucus in the stools. The patient may complain of  lower back pain or a pressure sensation in the pelvis. This symptom can be quite severe in intensity . The abscess may discharge into the anal canal as the pelvic collection points through an anastomotic leak (the point of least resistance). Rectal or vaginal examination can be extremely uncomfortable for the patient. Investigation and management If  any uncertainty exists, the presence of  pus should be confirmed by ultrasonography or CT scanning. Pelvic abscesses can be drained transanally or transgluteally . The past vogue for transintestinal drainage is no longer practised because of  the high incidence of  complications such as fistulae. Laparotomy may sometimes be indicated.

Spontaneous bacterial peritonitis
Spontaneous bacterial peritonitis
Spontaneous bacterial peritonitis (SBP; sometimes called primary bacterial peritonitis) is an acute bacterial infection of ascitic fluid. There is often a history of  cirrhosis and ascites. The clinical picture is highly variable as the patient may be asymptomatic. The course can be prolonged. The diagnosis is made by paracentesis and should be con - sidered in cirrhotic patients and those with ascites even when there is a low index of  suspicion. The diagnosis is confirmed by 3 finding an increased neutrophil count of  250/mm in aspirated ascitic fluid. Culture of  ascites is negative in as many as 60% of  patients with clinical manifestations of  SBP . When culture - is positive the most common pathogens include Gram-negative bacteria, usually Escherichia coli, and Gram-positive cocci (mainly streptococci and enterococci). Empirical treatment of  SBP must be initiated immedi - ately after diagnosis and before the results of culture have been received. Although the choice of  antibiotic may vary , a third-generation cephalosporin, e.g. cefotaxime, is a reason - ab le first-line treatment that avoids the renal toxicity of  amino - glycosides. Alternatives are amoxicillin/clavulanic acid and quinolones such as ciprofloxacin. 1894–1963, physician, University of  Pennsylvania, Philadelphia, PA,
(b)
Axial
The incidence of  pneumococcal peritonitis has declined greatly and the condition is now rare. It may complicate nephrotic syndrome or cirrhosis in children; however, otherwise healthy children may also be a ff ected. In girls, the route of  infection may be via the vagina and Fallopian tubes, while a blood-borne route secondary to respiratory tract or middle-ear disease is also possible. The clinical onset is usually sudden, with pain usually local ised to the lower half  of  the abdomen. The temperature is raised to 39°C or more and there is usually frequent vomiting. After 24–48 hours, profuse diarrhoea is characteristic. There is usually increased frequency of  micturition. The last two symp toms are caused by severe pelvic peritonitis. On examination, peritonism is usually di ff use but less prominent than in cases of a perforated viscus, leading to peritonitis. An underlying pathology must always be excluded before primary peritonitis can be diagnosed with certainty . Causative organisms include Haemophilus spp., group A streptococci and a few Gram-negative bacteria. Idiopathic streptococcal and staphylococcal peritonitis can also occur in adults. After starting antibiotic therapy and correcting dehydra tion and electrolyte imbalance, early surgery is required unless spontaneous infection of pre-existing ascites is strongly suspected, in which case a diagnostic peritoneal tap is useful. Laparotomy or laparoscopy ma y be used. Assuming that no other cause for the peritonitis is discovered, some of the exudate is aspirated and sent to the laboratory for microscopy , culture and sensitivity tests. Thorough peritoneal lavage is carried out and the incision closed. Antibiotics and fluid replacement therapy are continued and recovery is usual.

THE GREATER OMENTUM
THE GREATER OMENTUM
The greater omentum corresponds to the anterior wall of the upper region of  the mesentery . Rutherford Morison called the greater omentum ‘the abdominal policeman’. The greater omentum attempts, often successfully , to limit intraperitoneal infective and other noxious processes. For instance, an acutely inflamed appendix is often found wrapped in omentum, and this saves many patients from developing di ff use peritonitis. The omentum often plugs the neck of  a hernial sac and prevents a coil of  intestine from entering and becoming strangulated. The omentum can also be a cause of  obstruction (acting as a large adhesion). The omentum is usually involved in tuberculous peritonitis and carcinomatosis of  the peritoneum. The mesoappendix arises from the posterior aspect of the ileocaecal region of  the mesentery ( Figure 65.18 a result, it often occupies a retrocaecal position, as does the adjoining appendix. The position of  the mesoappendix is thus a determinant of  the symptoms and signs associated with acute appendicitis (see Chapter 76 ). A Meckel’s diverticulum (see Chapter 74 ) resembles the appendix in that it comprises an intestinal diverticulum at the periphery of  a flange of  mesentery . The latter arises from a nearby small intestinal region of  mesentery . The bloodless fold of  Treves, a flange of  mesentery at the antimesenteric side of  the ileum just proximal to the ileocaecal valve, is a mesenteric remnant that arises after di ff erentiation of  the intestine at that level. James Rutherford Morison , 1853–1939, Professor of  Surgery , University of  Durham, Durham, UK. Sir Fredrick Treves , 1853–1923, surgeon, the London Hospital, London, UK, renowned for operating on King Edward VII for appendicitis, resulting in the postponement of  the coronation and his care for Joseph Merrick, the ‘elephant man’. Carl T oldt , 1840–1920, Professor of  Anatomy in Prague, the former Czechoslovakia, and later Vienna, Austria. Wilhelm von Waldeyer-Hartz , 1836–1921, Professor of  Anatomy , Berlin, Germany . Charles-Pierre Denonvilliers , 1808–1872, Professor of  Surgery and Anatomy , Paris, France. Dimitrie Gerota , 1867–1939, Professor of  Surgical Anatomy , Bucharest, Romania. Pierre Fredet , 1870–1946, surgeon, Paris, France.
Mesoappendix
Ileocaecal
Mesoappendix
mesentery
Mesenteric principles of gastrointestinal

THE MESENTERY GENERAL CONSIDERATIONS
THE MESENTERY GENERAL CONSIDERATIONS
The arterial supply and venous and lymphatic drainage of  each digestive organ are located in the mesentery . Thus diseases of individual organs can have significant e ff ects on the adjoining mesentery and its components. The pancreas and the e ff ects of  pancreatitis are a good example. The pancreas is positioned on the mesentery ( 65.5 ). It arches are intramesenteric). The neck of  the pancreas is anterior to the region of  the mesentery that contains the portal vein. The body and tail of the pancreas are in the dorsal mesogastrium (i.e. the posterior wall of  the upper region sack) and the tip of the tail of  the pancreas is located at the hilum of  the spleen (see Development of the mesentery and peritoneum ). Given these anatomical relations, acute inflammation of  the pancreas can a ff ect any of  these structures . Complications of acute pancreatitis thus include thrombosis in the portal and splenic vein, gastric outlet obstruction and arterial haemor - rhage (see Chapter 72 ). The mesentery is remarkably well preserved in most diseases. Although rarely encountered in clinical practice, mesenteric necrosis is mostly seen in advanced necrotising pancreatitis. Primary defects (i.e. non-sur gical causes) of  the mesentery are rare. These are always accompanied by failure of  normal development of  the adjoining organ. For example, intestinal atresia arises when a section of  the adjoining mes - entery fails to develop. The mesentery comprises adipose, connective tissue, neurological, lymphatic and vascular components. Abnormalities can arise in any of  these and lead to either solid (tumour deposits, lymphatic metastases) or cystic lesions. The supportive capacity of  the mesentery is reflected in the finding of  splen unculi, heterotopic pancreas, ossification, teratomas and even ectopic pregnancies in di ff erent regions of  the mesentery .

THE PERITONEUM
THE PERITONEUM
The peritoneal cavity is the largest cavity in the body , the 2 surface area of  its lining membrane (2 /uni00A0 m in an adult) being nearly equal to that of  the skin ( 65.3 ). The peritoneal membrane is composed of  flattened polyhedral cells (meso thelium), one layer thick, resting on a thin layer of  fibroelastic tissue. Beneath the peritoneum, supported by a small amount of  areolar tissue, lies a network of  lymphatic vessels and a rich plexus of  capillary blood vessels from w hich all absorption and exudation must occur. In health, only a few millilitres of  peri - toneal fluid are found in the peritoneal cavity . The fluid is pale yellow , somewhat viscid and contains lymphocytes and other leukocytes; it lubricates the viscera, allowing easy movement and peristalsis. The parietal portion is richly innervated and, when irritated, causes sev ere pain that is accurately localised to the a ff ected area. The visceral peritoneum, in contrast, is poorly innervated and irritation causes pain that is usually poorly localised to the midline. - Summary box 65.1 Functions of the peritoneum /uni25CF /uni25CF - /uni25CF /uni25CF /uni25CF
Non-mesenteric
domain
In health
Visceral lubrication
Fluid and particulate absorption
In disease
Pain perception (mainly parietal)
In
/f_l
ammatory and immune responses
Fibrinolytic activity
The peritoneum has the capacity to absorb large volumes of fluid; however, the peritoneum can also produce large volumes of  fluid (ascites) and an inflammatory exudate when injured (seen in peritonitis). During expiration, intra-abdominal pressure is reduced and peritoneal fluid, aided by capillary attraction, travels in an upward direction towards the dia phragm. Particulate matter and bacteria are absorbed within a few minutes into the lymphatic network through a number of ‘pores’ in the diaphragmatic peritoneum. The circulation of  peritoneal fluids may be responsible for the occurrence of abscesses anatomically remote from primary disease. The two sites most prone to collection are the pelvis and subdiaphrag matic areas, reflecting the e ff ects of  gravity while standing and lying, respectively .
Peritoneal
re
/f_l
ection
(c)
Descending
colon
Peritoneal
re
/f_l
ection
Figure 65.6
The re
/f_l
ection at the periphery of the mesenteric domain, i.e. the junction between the mesenteric and non-mesenteric domains.
(Reproduced with permission from Coffey JC, Lavery I, Sehgal R (eds).
principles.
Boca Raton: CRC Press, 2017.)

THE RETROPERITONEAL SPACE AND RETROPERITONEUM
THE RETROPERITONEAL SPACE AND RETROPERITONEUM
The non-mesenteric domain is posterior to the mesenteric domain. The space between both is termed the retroperitoneal space ( Figure 65.19 ) ( 65.4 ). It is a conceptual space as it contains areolar connective tissue. Regions of  the connective tissue were separately named Toldt’s, Waldeyer’s, Denonvil - liers’, Gerota’s and Fredet’s fascia, as if  they are separate enti - ties. These are merely di ff erent zones of  the same connective tissue layer that is interposed between the mesenteric domain in front and the non-mesenteric domain behind. The space continues into the thorax and thereafter into the neck. This explains why , on occasion, a patient with an intestinal perforation during colonoscopy de velops surgical ). As emph ysema and crepitus at the neck level. In these cases, per - foration occurs into the retroperitoneal space ( Figure 65.20 ). Gas tracks along the space into the thorax and thereafter into the neck, where it accesses subcutaneous tissue to generate sur - gical emphysema and crepitus. The volume of  gas insu ffl ated can be considerable given that the peritoneal cavity will not ha ve been entered and the endoscopist may not recognise the perforation. The space may be obliterated following radia tion treatment, in Crohn’s disease or in longstanding diverticular inflammation. This presents considerable challenges for the surgeon who needs access to the plane whenever conducting visceral surgery .
Left mesocolon
Fascia
Peritoneal
re
/f_l
ection
Figure 65.19
The retroperitoneal space.
(a)
Digital image of the fascia (green) located in the retroperitoneal space.
of fascia in the retroperitoneal space. (Reproduced with permission from Coffey JC, Lavery I, Sehgal R (eds).
intestinal surgery: basic and applied principles
. Boca Raton: CRC Press, 2017: 11–40 and 57–68.)
(a)
Figure 65.20
Perforation into the retroperitoneal space. Axial computed tomography section of the abdomen demonstrating gas (arrows) in the
retroperitoneal space
(a)
and mediastinum
(b)
.

THE RETROPERITONEUM
THE RETROPERITONEUM
The retroperitoneum is the region of  the non-mesenteric domain deep to the retroperitoneal space. It contains the kidneys, adrenal glands, major vessels, ureters and gonadal vessels and is surrounded by adipose tissue. - Swellings in the retroperitoneum include abscess, haema - toma, cysts and malignancy from retroperitoneal organs (kid - ney , ureter, adrenal). The term retroperitoneal tumour refers to primary tumours arising in connective tissues in this region. -

TUBERCULOSIS OF THE MESENTERIC L YMPH NODES
TUBERCULOSIS OF THE MESENTERIC L YMPH NODES
Tuberculous mesenteric lymphadenitis is considerably less common than acute non-specific lymphadenitis. Tubercle bacilli, usually , but not necessarily , bovine, are ingested and enter the mesenteric lymph nodes by way of  Peyer’s patches. Sometimes only one lymph node is infected; usually there are several, and occasionally massive involvement occurs. The presentation may be with abdominal pain (a rare di ff erential for appendicitis) or with general constitutional symptoms (pyrexia, weight loss, etc.). Calcified lymph nodes may be demonstrated on a plain radiograph of  the abdomen, where they must be distinguished from other calcified lesions, e.g. renal or ureteric stones. Johann Conrad Peyer , 1653–1712, Professor of  Logic, Rhetoric and Medicine, Scha ff hausen, Switzerland, described the lymph follicles in the intestine in 1677. Sir David Drummond , 1852–1932, born Dublin, Ireland, pathologist and physician at the Royal Victoria Infirmary , Newcastle (1878–1920), President of the British Medical Association (1921–1922) and vice chancellor of  the University of  Durham (1920–1922). - - -
mesocolon
adenitis
Mesoileum
Figure 65.11
Mesenteric adenitis. (Reproduced with permission from
Coffey JC, Lavery I, Sehgal R (eds).
Mesenteric principles of gastro
intestinal surgery: basic and applied principles
. Boca Raton: CRC
Press, 2017: 69–84.)

TUMOURS OF THE PERITONEUM Primary peritoneal malig
TUMOURS OF THE PERITONEUM Primary peritoneal malignancy
Primary tumours of  the peritoneum are rare. They arise in the mesothelium of  the peritoneum. Mesothelioma of the peritoneum is less frequent than in the pleural cavity but is equally lethal. Asbestos is a recognised cause. It has a predilection for the pelvic peritoneum. Cytoreductive surgery with heated intraperitoneal chemotherapy (HIPEC) or systemic cisplatin-based chemotherapy are the mainstays of  treatment.

Treatment
Treatment
Abscesses less than 5 /uni00A0 cm in diameter normally resolve with intravenous antibiotic treatment. As antibiotics take e ff ect, the magnitude of  the swinging pyrexia can decrease with each successive spike in temperature. Serial monitoring of C-reactive protein levels is useful to non-invasively monitor response to treatment. Abscesses greater than 5 /uni00A0 cm require either percutaneous aspiration/drainage or surgical intervention. If percutaneous radiological approaches fail, then operative washout is indi cated. This can be conducted laparoscopically (laparoscopic vage) or via an open approach. The technical challenges la involved are such that this should only be undertaken by an wel may be matted and di ffi cult experienced surgeon. The bo to separate in order to access the abscess. All regions of  the peritoneal cavity should be accessed, with a view to drainage of any residual collections. The entirety of  the small intestine and adjoining mesentery should be exposed to ensure that there are no residual interloop abscesses. If  a phlegmon is appar ent, then only in the setting of  life-threatening circumstances should the components of  this be separated. Treatment
This is normally supportive. Viral mesenteric adenitis normally resolves spontaneously but can recur. The symp toms in bacterial mesenteric adenitis include cramping pain, vomiting and diarrhoea. They can be severe and require hospitalisation. Treatment
Sigmoid volvulus can be quickly reversed with endoscopic decompression, but recurrence is common. Most patients will ultimately require surgery to resect the intestine and adjoining mesentery . These patients often have multiple comorbidities and present challenging anaesthetic and ethical dilemmas (see Chapter 77 ).
Malrotation
Intestine aligned
Sehgal R (eds).
Mesenteric principles of gastrointestinal

Tuberculous peritonitis
Tuberculous peritonitis
Intra-abdominal tuberculosis (TB) is common in resource- poor countries; however, the incidence is rising in resource-rich countries as a consequence of  migration and immunosuppres sion. Mycobacterium avium intracellulare is becoming increasingly prevalent with the widespread increase in human immuno deficiency virus (HIV) co-infection. The abdomen is involved in approximately 11% of  patients with extrapulmonary TB and includes intraperitoneal, gastrointestinal tract and solid organ disease for ms. TB peritonitis requires specific mention because it is often diagnosed late, resulting in undue patient morbidity and mortality . TB can spread to the peritoneum through the gastrointesti nal tract (typically the ileocaecal region) via mesenteric lymph nodes or directly from the blood, usually from the ‘miliary’ ( Figure 65.8a ) but occasionally from the ‘cavitating’ form of pulmonary TB, lymph and the F allopian tubes; 50–80% of patients with abdominal TB can be expected to have perito neal involvement. The most common form of  TB peritonitis is the wet, ascitic type disease (90%), which is characterised by generalised or loculated ascites. Multiple tubercle deposits are present on both layers of the peritoneum. In the less common form fibrotic fixed loops of  bowel and omentum are matted together and may present with subacute intestinal obstruction. Ascites is not with abdominal pain, weight loss and abdominal distension. Distinction from di ff use peritoneal metastases is di ffi cult and may require biopsy . Diagnosis is via abdominal ultrasonography or CT to detect ascites and lymphadenopathy with/without di ff use thickening of the peritoneum, mesentery and/or omentum ( Figure 65.8b,c ). Ascitic fluid is typically a straw-coloured exudate (protein >25–30 /uni00A0 g/L) with white cells >500/mL - and lymphocytes >40%. Unfortunately , diagnostic smears for acid-fast bacilli are often not diagnostic and culture may take up to 4–8 weeks. Laparoscopy and peritoneal biopsy may thus be helpful to couple typical appearances with his - - tology . The value of  new laboratory investigations such as ® MTB/RIF assay and the interferon-gamma the Xpert release assay in diagnosing extrapulmonary TB remains to be determined; however, measurement of  adenosine deaminase activity in ascitic fluid has a high sensitivity and specificity in diagnosing peritoneal TB. TB management is principally supportive (nutrition and hydration) and medical (systemic anti-TB therapy , noting that multidrug resistance may be higher for abdominal than for - pulmonary TB), although surgery may be required f or specific complications such as intestinal obstruction. Summary box 65.6 Tuberculous peritonitis /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - -
Acute (may be clinically indistinguishable from acute bacterial
peritonitis) and chronic forms
Abdominal pain, sweats, malaise and weight loss are frequent
Ascites common, may be loculated
Caseating peritoneal nodules are common – distinguish from
metastatic carcinoma and fat necrosis of pancreatitis
Intestinal obstruction may respond to anti-TB treatment
without
/uni00A0
surgery

Tumours of the mesentery
Tumours of the mesentery
Primary tumours of  the mesentery include carcinoid, lymphoma, sarcoma and desmoid tumours. The mesentery is a ff ected in local lymphatic spread of  carcinoma arising from abdominal viscera ( Figure 65.17 ). If  indicated, a benign tumour of  the mesentery may be excised with resection of the adjacent intestine. A malignant tumour of  the mesentery requires biopsy confirmation and specific, usually non-surgical, treatment, e.g. chemotherapy for lymphoma. Diffuse fibromatosis Fibromatosis is rare, characterised by an abnormal prolifer ation of  myofibroblasts. Although non-metastasising, and said to be benign, it can nevertheless prove widely invasive, Mesenteric cysts: clinical features /uni25CF /uni25CF /uni25CF /uni00A0 /uni25CF /uni25CF /uni25CF /uni25CF ). An /uni25CF /uni25CF /uni25CF /uni25CF compressing and infiltrating surrounding tissues such as the bowel and mesentery with complications thereof. There is an association with familial adenomatous polyposis (FAP). Summary box 65.10 Mesenteric tumours /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF - /uni25CF
(a)
Figure 65.17
Terminal ileal
carcinoid
(a)
and lymphatic
metastasis
(b)
. (Reproduced
with permission from Coffey
JC, Lavery I, Sehgal R (eds).
Mesenteric principles of
gastrointestinal surgery: basic
Carcinoid
and applied principles
. Boca
tumour
Raton: CRC Press, 2017:
85–108.)
Cysts occur most commonly in adults with a mean age of 45
years
Twice as common in women as in men
Rare: incidence around 1 per 140 000
Approximately a third of cases occur in children younger than
15 years
The mean age of children affected is 5 years
The most common presentation is of a painless
/f_l
uctuant
abdominal swelling near the umbilicus
Other presentations are with recurrent attacks of abdominal
pain with or without vomiting (pain resulting from recurring
temporary impaction of a food bolus in a segment of bowel
narrowed by the cyst or possibly from torsion of the mesentery)
and acute abdominal catastrophe due to:
torsion of that portion of the mesentery containing the cyst
rupture of the cyst, often as a result of a comparatively
trivial accident
haemorrhage into the cyst
infection
Benign
Malignant
Lipoma
Lymphoma
Fibroma
Secondary carcinoma
Fibromyxoma
Neuroendocrine tumours
Desmoid
Lymphatic metastases
Tumour deposits (lymphovascular
and perineural)
Peritoneal carcinomatosis
Mesoileum
(b)
Mesenteric
Terminal
lymphatic
ileum
metastasis
Ileocaecal
mesentery
Mesoappendix
Figure 65.18
The mesoappendix. (Reproduced with permission from Coffey JC, Lavery I, Sehgal R (eds).
surgery: basic and applied principles
. Boca Raton: CRC Press, 2017: 11–40.)

VASCULAR ABNORMALITIES OF THE MESENTERY Acute mese
VASCULAR ABNORMALITIES OF THE MESENTERY Acute mesenteric ischaemia
). The arterial inflow to the mesenteric domain is limited to three major vessels: the coeliac trunk and the superior and 65.5 ). Additional arterial inferior mesenteric arteries ( - inflow in the pelvis comes via the middle rectal arteries. The - limited number of  arterial inputs to the mesenteric domain mean that narrowing or occlusion at the origin of  any one vessel can have significant clinical e ff ects. Acute mesenteric ischaemia mostly follows embolisation to the origin of  either the coeliac or superior mesenteric arterial trunk. Unless quickly reversed, it can lead to ischaemia and necrosis of most of  the intestine. At first, the severity of  abdominal pain does not match clinical findings on examination. If ischaemia and necrosis occur, the patient develops peritonism as a result - of  irritation of  the parietal peritoneum by the necrotic intes tine. The inferior mesenteric artery (IMA) is usually divided at open repair of  an abdominal aortic aneurysm; however, anas - tomoses between peripheral branches of  the SMA and IMA, Drummond, usually pre - referred to as the marginal artery of vent critical ischaemia of  the sigmoid and descending colon. If ischaemia is limited to the mucosa, the patient may experience mally settles. cramping suprapubic pain and diarrhoea that nor If  ischaemia is transmural the colon may become necrotic and require resection.
Severe
mesenteric
Mild
Normal
disease
mesenteric
mesentery
disease
Fat
wrapping
Creeping
fat
Figure 65.12
The mesentery in Crohn’s disease.
(a)
Levels of mesenteric disease manifestations.
creeping fat. (Reproduced with permission from Coffey JC, Lavery I, Sehgal R (eds).
applied principles
. Boca Raton: CRC Press, 2017: 85–108.)

Volvulus of the intestine and adjoining mesentery
Volvulus of the intestine and adjoining mesentery
V olvulus can only be understood if  considered in mesenteric terms. Where a section of  intestine is curved, the adjoining mesentery is buckle-shaped or folded. If  the intestine progresses from a curve to a coil, the adjoining mesentery acquires a spiral shape. The resultant coil/spiral complex of the intestine and mesentery is termed a volvulus. Its formation is normally prevented by adhesion of  the mesentery to the posterior abdominal wall during development. Wherever mesenteric adhesion is inadequate, there is a risk of  volvulus formation. Sigmoid volvulus is the commonest type, followed by ileocaecal. However, the anatomy of the mesentery is such that volvulus can theoretically arise at any level from the oesophagogastric to anorectal junction.
Normal intestinal
conformation
Malrotation
Intestine aligned
Intestine non-aligned
Figure 65.13
Malrotation. (Reproduced with permission from Coffey JC, Lavery I,
surgery: basic and applied principles
. Boca Raton: CRC Press, 2017: 85–108.)