The peritoneal cavity is the largest cavity in the body, the surface area of its lining membrane

(2 m2 in an adult) being nearly equal to that of the skin.

This membrane is conveniently divided into two parts – the visceral peritoneum surrounding
the viscera and the parietal peritoneum lining the other surfaces of the cavity. Beneath the
peritoneum, supported by a small amount of areolar tissue, lies a network of lymphatic vessels
and rich plexus of capillary blood vessels from which all absorption and exudation must occur.
In health, only a few millilitres of peritoneal 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.

Functions of the peritoneum

In health
●● Visceral lubrication
●● Fluid and particulate absorption
In disease
●● Pain perception (mainly parietal)
●● Inflammatory and immune responses
●● Fibrinolytic activity

The peritoneum has the capacity to absorb large volumes of fluid: this ability is used during
peritoneal dialysis in the treatment of renal failure. However, the peritoneum can also produce
large volumes of fluid (ascites) and an inflammatory exudate when injured (peritonitis).

The peritoneum, mesentery and omentum may be the site of a variety of

conditions that reflect their relationship to other anatomical structures or, in
some instances, their primary
functions.

Scope of disease
Intraperitoneal disease
●● Peritonitis
Primary
Secondary
●● Abscess
●● Ascites
Transudate
Exudate
●● Tumours
Primary
Secondary
●● Adhesions
Omental disease
●● Hernia
●● Adhesions
●● Torsion
●● Neoplasia
Mesenteric disease
●● Trauma
●● Ischaemia
●● Inflammation
●● Cysts
●● Neoplasia
Retroperitoneal disease
●● Chronic inflammation/fibrosis
●● Abscess
●● Tumours

Peritonitis is simply defined as inflammation of the peritoneum and may be localised or

generalised.

In this instance, free fluid spills into the peritoneal cavity and circulates, largely directed by the
normal peritoneal attachments and gravity. For example, spillage from a perforated
peptic ulcer may run down the right paracolic gutter, leading to presentation with pain in the
right iliac fossa (Valentino’s syndrome). Even in patients with non-bacterial peritonitis
(e.g. acute pancreatitis, intraperitoneal rupture of the bladder or haemoperitoneum), the
peritoneum often becomes infected by transmural spread of organisms from the bowel. Such
translocation is a feature of the systemic inflammatory response on the bowel and it is not long
(often a matter of hours) before a bacterial peritonitis develops. Most duodenal and gastric
perforations are initially sterile for up to several hours before becoming secondarily infected

Causes of peritoneal inflammation

●● 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

Although acute bacterial peritonitis most commonly arises from a perforation of a viscus of the
alimentary tract, other routes of infection can include the female genital tract and exogenous
contamination. There are also less common forms in which the aetiology is a primary
‘spontaneous’ peritonitis, in which a pure infection with streptococcal, pneumococcal or
haemophilus bacteria occurs.

Paths to peritoneal infection

●● 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 inflammatory disease
●● Haematogenous spread (rare), e.g. septicaemia

Bacteria from the gastrointestinal tract

The number of bacteria within the lumen of the gastrointestinal tract is normally low until the
distal small bowel is reached. However, disease leading to stasis and overgrowth (e.g.
obstruction, and chronic and acute motility disturbances)may increase proximal colonisation.

Peritoneal infection is usually caused by two or more bacterial strains. Gram-

negative bacteria contain endotoxins (lipopolysaccharides) in their cell walls
that have multiple toxic effects on the host, primarily by causing the release
of tumour necrosis factor (TNF) from host leukocytes. Systemic absorption of
endotoxin may produce endotoxic shock, with hypotension and impaired
tissue perfusion.

Other bacteria such as Clostridium perfringens produce harmful exotoxins.

Bacteroides spp. are commonly found in peritonitis. These gram-negative,
non-sporing organisms, although predominant in the lower intestine, often
escape detection because they are strictly anaerobic and slow to grow on
culture media unless there is an adequate carbon dioxide tension in the
anaerobic apparatus.

Non-gastrointestinal causes of peritonitis

Pelvic infection via the fallopian tubes is responsible for a high proportion of
‘non-gastrointestinal’ infections. The most common offending organisms are
Chlamydia spp. and gonococci. These organisms lead to a thinning of
cervical mucus and allow bacteria from the vagina into the uterus and
oviducts, causing infection and inflammation.

Microorganisms in peritonitis
Gastrointestinal source
●● Escherichia coli
●● Streptococci
●● Enterococci
●● Bacteroides spp.
●● Clostridium spp.
●● Klebsiella pneumoniae
Other sources
●● Chlamydia trachomatis
●● Neisseria gonorrhoeae
●● Haemolytic streptococci
●● Staphylococci
●● Streptococcus pneumoniae
●● Mycobacterium tuberculosis and other species
●● Fungal infections

Localised peritonitis
The greater sac of the peritoneum is divided into:

1) the subphrenic spaces,

2) the pelvis
3) the peritoneal cavity proper,

The last is divided into a supracolic and an infracolic compartment by the transverse colon
and transverse mesocolon, which deters the spread of infection from one to the other

There is an outpouring of serous inflammatory exudate rich in leukocytes and plasma proteins
that soon becomes turbid; if localisation occurs, the turbid fluid becomes frank pus. Peristalsis
is retarded in affected bowel and this helps to prevent distribution of the infection. The greater
omentum, by enveloping and becoming adherent to inflamed structures, often forms a
substantial barrier to the spread of infection

Diffuse (generalised) peritonitis, factors:

●●Speed of peritoneal contamination

●●Stimulation of peristalsis by the ingestion of food or even water hinders localisation
●●The virulence of the infecting organism may be so great as to render the localisation of
infection difficult or impossible.
●● Young children have a small omentum, which is less effective
in localising infection.
●● Disruption of localised collections may occur with injudicious handling, e.g. appendix mass
or pericolic abscess.
●● Deficient natural resistance (‘immune deficiency’) may result from use of drugs (e.g.
steroids), disease [e.g. acquired immune deficiency syndrome (AIDS)] or old age.

With appropriate treatment, localised peritonitis usually resolves; in about 20% of cases, an
abscess follows. Infrequently, localised peritonitis becomes diffuse. Conversely, in favourable
circumstances, diffuse peritonitis can become localised, most frequently in the pelvis or at
multiple sites within the abdominal cavity.

Localised peritonitis
The initial symptoms and signs of localised peritonitis are those of the
underlying condition – usually visceral inflammation (hence abdominal pain,
specific GI symptoms + malaise,
anorexia and nausea). When the peritoneum becomes inflamed, abdominal
pain will worsen and in general temperature and pulse rate will rise. The
pathognomonic signs are localised guarding (involuntary abdominal wall
contraction to protect the viscus from the examining hand), a positive
‘release’ sign (rebound tenderness) and sometimes rigidity (involuntary
constant contraction of the abdominal wall over the inflamed parietes). If
inflammation arises under the diaphragm, shoulder-tip (‘phrenic’) pain may
be felt. In cases of pelvic peritonitis arising from an inflamed appendix in the
pelvic position or from salpingitis, the abdominal signs are often slight; there
may be deep tenderness of one or both lower quadrants alone, but a rectal
or vaginal examination reveals marked tenderness of the pelvic peritoneum.

Diffuse (generalised) peritonitis symptoms:

EARLY
Abdominal pain is severe and made worse by moving or breathing. It is first experienced at the
site of the original lesion and spreads outwards from this point. The patient usually lies still.
Tenderness and generalised guarding are found on palpation, when the peritonitis affects the
anterior abdominal wall. Infrequent bowel sounds may still be heard for a few hours but they
cease with the onset of paralytic ileus. Pulse and temperature rise in accord with degree of
inflammation and infection.

LATE
If resolution or localisation of generalised peritonitis does not occur, the abdomen will become
rigid (generalised rigidity). Distension is common and bowel sounds are absent. Circulatory
failure ensues, with cold, clammy extremities, sunken eyes, dry tongue, thready (irregular)
pulse, and drawn and anxious face (hippocratic face)

Clinical features of peritonitis

●● Abdominal pain, worse on movement, coughing and deep respiration
●● Constitutional upset: anorexia, malaise, fever, lassitude
●● GI 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 inflammatory response syndrome [SIRS] and multi-organ
dysfunction syndrome [MODS]) in later stages
Diagnostic aids
Investigations may elucidate a doubtful diagnosis, but the importance of a
careful history and repeated examination must not be forgotten.

Bedside
●● Urine dipstix for urinary tract infection.
●● ECG if diagnostic doubt (as to cause of abdominal pain)
or cardiac history.

Bloods
●● Baseline urea and electrolytes (U&Es) for treatment.
●● Full blood count for white cell count (WCC).
●● Serum amylase estimation may establish the diagnosis of acute pancreatitis provided that it
is remembered that moderately raised values are frequently found following other abdominal
catastrophes and operations, e.g. perforated duodenal ulcer.
●● Group and save may be taken as an adjunct to impending
surgery.

Imaging
●● Erect chest radiograph to demonstrate free sub diaphragmatic gas
●● A supine radiograph of the abdomen may confirm the presence of dilated gas-filled loops of
bowel (consistent with a paralytic ileus), and occasionally show other gas filled structures that
may aid diagnosis, e.g. biliary tree; the faecal pattern may act as a guide to colonic disease
(absent in sites of significant inflammation, e.g. diverticulitis). In the patient who is too ill for an
‘erect’ film, a lateral decubitus film can show gas beneath the abdominal wall ( if CT
unavailable).
●● Multiplanar computed tomography (CT) is increasingly used to identify the cause of
peritonitis and may also influence management decisions, e.g. surgical strategy.
●● Ultrasonography has undoubted value in certain situations such as pelvic peritonitis in
women and localized right upper quadrant peritonism.

Invasive
●● In the era of access to high-quality CT scanning, peritoneal diagnostic aspiration has little
residual value.

Management of peritonitis
General care of patient
●● Correction of fluid 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
●● Remove or divert cause
●● Peritoneal lavage ± drainage

Systemic complications of peritonitis

●● Septic shock
●● Systemic inflammatory response syndrome
●● Multi-organ dysfunction syndrome
●● Death
Abdominal complications of peritonitis
●● Paralytic ileus
●● Residual or recurrent abscess/inflammatory mass
●● Portal pyaemia/liver abscess
●● Adhesional small bowel obstruction

SPECIAL FORMS OF PERITONITIS

1. Bile peritonitis
Unless there is reason to suspect that the biliary tract was damaged during
surgery or the patient has proven acute cholecystitis, it is improbable that
bile will be thought of as a
cause of peritonitis until the abdomen has been opened. Unless the bile has
extravasated slowly and the collection becomes shut off from the general
peritoneal cavity, there are
symptoms (often severe pain) and signs of diffuse peritonitis. After a few
hours a tinge of jaundice is not unusual. Laparotomy (or laparoscopy) should
be undertaken with evacuation
of the bile and peritoneal lavage. The source of bile leakage should be
identified and treated accordingly. Infected bile is more lethal than sterile
bile.

Causes of bile peritonitis

●● Perforated gall bladder secondary to inflammation or obstruction (especially empyema)
●● Post-cholecystectomy:
Cystic duct stump leakage
Leakage from an accessory duct in the gall-bladder bed
Bile duct injury
T-tube drain dislodgement (or tract rupture on removal)
●● Following other operations/procedures:
Duodenal injury
Leaking duodenal stump post gastrectomy
Leaking biliary–enteric anastomosis
Leakage around percutaneously placed biliary drains
●● Blunt or penetrating hepatobiliary or duodenal trauma

2. Spontaneous bacterial peritonitis

Spontaneous bacterial peritonitis (SBP; sometimes called primary bacterial peritonitis) is an
acute bacterial infection of ascitic fluid. It can occur in children and adults and can in theory
occur as a complication of any disease state that produces the clinical syndrome of ascites.
Clinical features usually include local symptoms and/or signs of peritonitis, GI
upset (secondary to ileus, e.g. nausea and vomiting), signs of systemic
inflammation (hyper- or
hypothermia, chills, tachycardia and tachypnoea ± signs of septic shock),
worsening liver and renal function, hepatic encephalopathy and GI bleeding.
It should, however, be noted that evolving infection may be asymptomatic,
especially in outpatients.

3. Tuberculous peritonitis
Intra-abdominal tuberculosis (TB) is very common in resource-poor countries where all general
surgeons are familiar with its presentation and management. The incidence is, however, also
rising in resource-rich countries as a consequence of migration and immunosuppression where
Mycobacterium avium - intracellulare is becoming increasingly prevalent with the widespread
increase in human immunodeficiency virus (HIV) co-infection. The abdomen is involved in 11%
of patients with extrapulmonary TB and includes intraperitoneal, GI tract and solid organ
disease forms, with TB peritonitis being a common site-specific variant (ileocaecal is the most
common site of involvement). Although still uncommon, TB peritonitis requires some specific
mention because it is often diagnosed late in the course of the disease, resulting in undue
patient morbidity and mortality.
In the most common form of the disease, ascites may be localised or generalised throughout
the peritoneal cavity. Multiple tubercle deposits appear on both layers of the peritoneum.
Diagnosis is via abdominal ultrasonography or CT to detect ascites and lymphadenopathy ±
diffuse thickening of the peritoneum, mesentery and/or omentum.
TB management is principally supportive (nutrition and hydration) and medical (systemic
antituberculous therapy, noting that multiple-drug resistance may be higher for abdominal than
for pulmonary TB), although surgery may be required for specific complications such as
intestinal obstruction.
Tuberculous peritonitis
●● 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-tuberculous
treatment without surgery

4. Familial Mediterranean fever

Familial Mediterranean fever (periodic peritonitis) is characterised by

abdominal pain and tenderness, mild pyrexia, polymorphonuclear
leukocytosis and, occasionally, pain in
the thorax and joints. The duration of an attack is 24–72 hours, when it is
followed by complete remission, but exacerbations recur at regular intervals.
Most of the patients have
undergone appendicectomy in childhood. This disease, often familial, is
limited principally to Arab, Armenian and Jewish populations; other races are
occasionally affected. Mutations
in the MEFV (Mediterranean fever) gene appear to cause the disease. This
gene produces a protein called pyrin, which is expressed mostly in
neutrophils; however, the exact function
of pyrin is not known.

Clinical features of an abdominal/pelvic abscess

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
exam)

Anatomy
The complicated arrangement of the peritoneum results in the formation of
four intraperitoneal spaces in which pus may commonly collect.

LEFT SUBPHRENIC SPACE

This is bounded above by the diaphragm and behind by the left triangular
ligament and the left lobe of the liver, the gastrohepatic omentum and the
anterior surface of the stomach To the right is the falciform ligament and to
the left the spleen, gastrosplenic omentum and diaphragm. The common
cause of an abscess here is an operation on the stomach, the tail of the
pancreas, the spleen or the splenic flexure of the colon.

LEFT SUBHEPATIC SPACE/LESSER SAC

The most common cause of infection here is complicated acute pancreatitis.
In practice, a perforated gastric ulcer rarely causes a collection here because
the potential space is obliterated by adhesions.

RIGHT SUBPHRENIC SPACE

This space lies between the right lobe of the liver and the diaphragm. It is
limited posteriorly by the anterior layer of the coronary and the right
triangular ligaments, and to the left by the falciform ligament. Common
causes of abscess here are perforating cholecystitis, a perforated duodenal
ulcer and a duodenal cap ‘blow-out’ following gastrectomy and appendicitis.

RIGHT SUBHEPATIC SPACE

This lies transversely beneath the right lobe of the liver in Rutherford
Morison’s pouch. It is bounded on the right by the right lobe of the liver and
the diaphragm. To the left is situated the foramen of Winslow and below this
lies the duodenum. In front are the liver and the gall bladder, and behind are
the upper part of the right kidney and the diaphragm. The space is bounded
above by the liver and below by the transverse colon and hepatic flexure. It
is the deepest space of the four and the most common site of a subphrenic
abscess, which usually arises from appendicitis, cholecystitis, a perforated
duodenal ulcer or following upper abdominal surgery.

Ascitis

Causes of ascites
Transudates (protein <25 g/L)
●● Low plasma protein concentrations:
Malnutrition
Nephrotic syndrome
Protein-losing enteropathy

●● High central venous pressure:

Congestive cardiac failure

●● Portal hypertension
Portal vein thrombosis
Cirrhosis
Exudates (protein >25 g/L)
●● Peritoneal malignancy
●● Tuberculous peritonitis
●● Budd–Chiari syndrome ( an uncommon disorder characterized by
obstruction of hepatic venous outflow. The obstruction may be thrombotic or
non-thrombotic anywhere along the venous course from the hepatic venules
to junction of the inferior vena cava (IVC) to the right atrium.)
●● Pancreatic ascites
●● Chylous ascites
●● Meigs’ syndrome (an uncommon presentation, where a benign ovarian
tumor presents along with ascites and pleural effusion. About 1% of ovarian
tumors can present as Meigs syndrome. A similar presentation can be seen
in many metastatic malignancies.)

Clinical features
Ascites can usually be recognised clinically only when the amount of fluid
present exceeds 1.5 L depending on body habitus: in obese individuals a
greater quantity than this is necessary before there is clear evidence. 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, on flicking the
abdominal wall, a characteristic fluid thrill is transmitted from one side to the
other. In women, ascites must be differentiated from an enormous ovarian
cyst. Congestive heart failure results in increased venous pressure in the
vena cava and consequent obstruction to the venous outflow from the liver.
The ascitic fluid is light yellow and of low specific gravity, about 1.010, with a
low protein concentration (<25 g/L). Ascites occurs with low plasma albumin
concentrations, e.g. in patients with albuminuria or starvation.
In cirrhosis, now the most common cause of ascites internationally, there is
obstruction to the portal venous system, which is caused by obliterative
fibrosis of the intrahepatic venous bed. In the Budd–Chiari syndrome,
thrombosis or obstruction of the hepatic veins is responsible for obstruction
to venous outflow from the liver. The ascites seen in patients with peritoneal
metastases is caused by excessive exudation of fluid and lymphatic
blockage.

Chylous ascites
In some patients the ascitic fluid appears milky because of an excess of
chylomicrons (triglycerides). Most cases are associated with malignancy,
usually lymphomas; other causes
are 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.

THE RETROPERITONEAL SPACE

Retroperitoneal fibrosis
This is a relatively rare diagnosis characterised by the development of a flat grey/white plaque
of tissue, which is found first in the low lumbar region but then spreads laterally and upwards
to encase the common iliac vessels, ureters and aorta. Its aetiology is obscure in most cases
(idiopathic) being allied to other fibromatoses (others being Dupuytren’s contracture and
Peyronie’s disease). In other patients the cause is known.
The clinical presentation may be one of ill-defined chronic backache or occur as a result of
compromise to involved structures, e.g. lower limb or scrotal oedema secondary to venous
occlusion, or chronic renal failure secondary to ureteric obstruction. Treatment will be directed
to the cause, the modification of disease activity when appropriate, e.g. immunomodulation
with steroids, tamoxifen and restoration of flow in affected structures, e.g. ureteric stenting

Causes of retroperitoneal fibrosis

Benign
●● Idiopathic (Ormond’s disease)
●● Chronic inflammation
●● Extravasation of urine
●● Retroperitoneal irritation by leakage of blood or intestinal content
●● Aortic aneurysm (inflammatory type)
●● Trauma
●● Drugs (chemotherapeutic agents and previously methysergide)
Malignant
●● Lymphoma
●● Carcinoid tumours
●● Secondary deposits (especially from carcinoma of stomach, colon, breast and prostate)

Clinical features of an abdominal/pelvic abscess

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
exam)

Retroperitoneal (psoas) abscess

The retroperitoneal space can also be a site for abscess formation, which for practical purposes
is almost synonymous with psoas abscess. Psoas abscess is a relatively uncommon diagnosis,
the true incidence of which is not well described. 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 ± perforated digestive or urinary
tract. In recent years a primary psoas abscess due to haematogenous spread from an occult
source is more common, especially in immunocompromised and older patients, as well as in
association with intravenous drug misuse. Clinical presentation is with back pain, lassitude and
fever. A swelling may point to the groin as it tracks along iliopsoas. Pain may be elicited by
passive extension of the hip or a fixed flexion of the hip evident on inspection. Radiological
investigation is via CT scanning and treatment usually by percutaneous CT-guided drainage and
appropriate antibiotic therapy

Retroperitoneal tumours
Although swellings in the retroperitoneum may include abscess, haematoma,
cysts and spread of malignancy from retroperitoneal organs (kidney, ureter,
adrenal), the term retroperitoneal tumour is usually confined to primary
tumours arising in other tissues in this region e.g. muscles, fat, lymph nodes
and nerves. The management of such tumours is now frequently by referral
to a specialist centre and this should be done before biopsy which may
compromise subsequent surgical cure.

1) Retroperitoneal lipoma
The patient may seek advice on account of a swelling or because of indefinite abdominal pain.
Women are more often affected. These swellings sometimes reach an immense size. Diagnosis
is usually by ultrasonography and CT scanning. A retroperitoneal lipoma sometimes undergoes
myxomatous degeneration, a complication that does not occur in a lipoma in any other part of
the body. Moreover, a retroperitoneal lipoma is often malignant (liposarcoma) (see below) and
may increase rapidly in size.

2)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 common types of retroperitoneal soft-
tissue sarcomas in adults vary from study to study.

●● liposarcoma;
●● leiomyosarcoma;
●● malignant fibrous histiocytoma (MFH).

CLINICAL FEATURES
Patients with sarcomas present late, because these tumours arise in the
large potential spaces of the retroperitoneum and can grow very large
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, usually very large at the
time of presentation.

INVESTIGATION
Detailed multiplanar imaging (CT + MRI) with reconstructions is required not
only for tumour detection, staging and surgical planning, but also for guiding
percutaneous or surgical
biopsy of these tumours. Such biopsies have a greater role than for other
sarcomas.

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
operability (based on adjacency or involvement of vital structures) and
approach. Up to 75% of retroperitoneal sarcoma resections involve resection
of at least one adjoining intraabdominal visceral organ (commonly large or
small bowel or kidney). The most common types of vascular involvement
precluding resection are involvement of the proximal superior mesenteric
vessels or involvement of bilateral renal vessels.