The peritoneum - PowerPoint Presentation

Slide1

The peritoneum

The

peritoneal cavity is the largest cavity in the body

,

the

surface area

of its lining membrane

being nearly equal

to that of the skin

.

The

peritoneal membrane is

composed of 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 plexuses of capillary blood vessels from

which all absorption

and exudation must

occur.

In

health, only a

few millilitres

of peritoneal fluid is 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

.

Slide2

The parietal portion is richly supplied with nerves and, when irritated, causes severe pain that is accurately localised to the affected area.

The visceral peritoneum, in contrast, is poorly supplied with nerves and its irritation causes pain that is usually poorly localised to the midline

.

The

peritoneum can also produce large volumes of fluid (ascites) and an inflammatory exudate when injured (peritonitis).

The circulation of peritoneal fluids may be responsible for the occurrence of abscesses distant from primary disease

Slide3

The peritoneum has the capacity to absorb large volumes of fluid: this ability is used during

peritoneal

dialysis in the treatment of renal failure.

.

When parietal peritoneal defects are created, healing occurs not from the edges but by the development of new mesothelial cells throughout the surface of the defect. In this way, large defects heal as rapidly as small defects.

Functions of the peritoneum

In health

Visceral lubrication

Fluid and particles absorption

In disease

Pain perception (mainly parietal)

Inflammatory and immune responses

Fibrinolytic activity

Slide4

PERITONITIS

Peritonitis

is

inflammation of the peritoneum

Localized

Generalised.

Most of cases are

caused by an invasion of the peritoneal cavity by

bacteria, free

fluid spills into the peritoneal cavity and circulates

largely directed

by the normal peritoneal attachments and

gravity.

S

pillage

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

.

Slide5

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

Slide6

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.

Slide7

Paths to peritoneal infection

Gastrointestinal perforation, e.g. perforated ulcer, appendix, diverticulum

Transmural translocation (no perforation), e.g. pancreatitis, ischaemic bowel

Exogenous contamination, e.g. drains, open surgery,

trauma

Female genital tract infection, e.g. pelvic inflammatory disease

Haematogenous spread (rare), e.g. septicaemia

Slide8

Microbiology

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.

Disease leading to stasis and overgrowth (e.g. obstruction, chronic and acute motility disturbances) may increase proximal colonisation.

The biliary and pancreatic tracts are also normally free from bacteria, although they may be infected in disease, e.g. gallstones.

Slide9

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.

Clostridium welchii

produce harmful exotoxins

.

Slide10

Bacteroides

are commonly found in peritonitis. These anaerobic Gramnegative, non-sporing organisms, although predominant in the lower intestine. These organisms are resistant to penicillin and streptomycin but sensitive to metronidazole, clindamycin, lincomycin and cephalosporin compounds. Since the widespread use of metronidazole (Flagyl), Bacteroides infections have greatly diminished

.

Slide11

Non-gastrointestinal causes of peritonitis

Pelvic infection via the Fallopian. The most common organisms are chlamydia and gonococcus.

These organisms lead to a thinning of cervical mucus and allow bacteria from the vagina into the uterus and oviducts.

Perihepatitis which can cause scar tissue to form on Glisson’s capsule, a thin layer of connective tissue surrounding the liver.

Tuberculosis and other mycobacterial strains and those causing primary peritonitis (pneumococcus, staphylococcus and streptococcus spp).

Fungal peritonitis is uncommon but may complicate severely ill patients.

Slide12

Localised peritonitis

Anatomical and pathological factors may favour the localisation of peritonitis.

Anatomical

The greater sac of the peritoneum is divided into

The subphrenic spaces

The pelvic space

The peritoneal cavity proper, divided into a ;

Supracolic compartment

Infracolic compartment

Slide13

Pathological

Inflamed

peritoneum

loses its glistening appearance and becomes reddened and velvety.

Flakes of fibrin appear and cause loops of intestine to become adherent to one another.

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

Slide14

Diffuse (generalised) peritonitis

A number of factors may favour the development of diffuse peritonitis:

Speed of peritoneal contamination is a prime factor. If an inflamed appendix or other hollow viscus perforates before localisation has taken place, there will be an efflux of contents into the peritoneal cavity, which may spread over a large area.

Perforation proximal to an obstruction or from sudden anastomotic separation is associated with severe generalised peritonitis and a high mortality rate.

Slide15

Stimulation of peristalsis by the ingestion of food or water.

Violent peristalsis occasioned by the administration of a purgative or an enema may cause

the widespread

distribution of an infection.

The virulence of the infecting organism may be so great.

Slide16

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.

Slide17

With

appropriate treatment, localised peritonitis usually resolves

;

I

n

about 20 per cent 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

.

Slide18

Clinical features

Localised peritonitis

The initial symptoms and signs are ( 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).

Slide19

If

inflammation arises under the diaphragm, shoulder tip (‘phrenic’) pain may be felt as the pain is referred to the C5 dermatome.

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.

Slide20

Diffuse (generalised) peritonitis

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.

Tenderness and generalised guarding are found on palpation.

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.

Slide21

Late

The

abdomen will become rigid (generalised rigidity).

Distension

is common and bowel sounds are absent.

Circulatory

failure, with cold, clammy extremities, sunken eyes, dry tongue, thready (irregular) pulse and drawn and anxious face (Hippocratic facies).

The

patient finally lapses into unconsciousness.

With

early diagnosis and adequate treatment, this condition is rarely seen in modern surgical practice

Slide22

The Hippocratic facies in terminal diffuse peritonitis.

Slide23

Diagnostic aids

Bedside

G

eneral

u

rine examination for urinary tract infection

ECG if diagnostic doubt (as to cause of abdominal pain) or cardiac history.

Bloods

Full blood count for white cell count (WCC)

Serum amylase estimation may establish the diagnosis of acute pancreatitis.

Group and save serum may be taken as an adjunct to impending surgery.

Slide24

Imaging

Erect chest radiograph to demonstrate free subdiaphramatic gas.

A supine radiograph of the abdomen may confirm the presence of dilated gas-filled loops of bowel (consistent with a paralytic ileus). 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.

Ultrasound scanning has undoubted value in certain situations such as pelvic peritonitis in females and localised right upper quadrant peritonism.

Slide25

Management

General care of the patient

Correction of fluid loss and circulating volume

Patients are frequently hypovolaemic with electrolyte disturbances.

The plasma volume must be restored and electrolyte concentrations corrected.

Special measures may be needed for cardiac, pulmonary and renal support, especially if septic shock is present, including central venous pressure monitoring in patients with concurrent disease.

Slide26

Urinary

catheterisation ± gastrointestinal decompression

A urinary catheter will give a guide to central perfusion and will be required if abdominal surgery is to proceed

.

A nasogastric tube is commonly passed to allow drainage ± aspiration

until paralytic

ileus has resolved.

Antibiotic therapy

Administration of parenteral broad-spectrum (aerobic and anaerobic) antibiotics prevents the multiplication of bacteria and the release of endotoxins.

Slide27

Analgesia

The patient should be nursed in the sitting-up position and must be relieved of pain before and after operation.

If appropriate expertise is available, epidural infusion may provide excellent analgesia.

Freedom from pain allows early mobilisation and adequate physiotherapy in the postoperative period, which helps to prevent basal pulmonary collapse, deep-vein thrombosis and pulmonary embolism.

Slide28

Specific treatment of the cause

In patients where specific treatment has not been guided by CT scanning, early surgical intervention is to be preferred to a ‘wait and see’ policy assuming that the patient is fit for anaesthesia and that resuscitation has resulted in a satisfactory restitution of normal body physiology.

More caution is, of course, required in patients at high operative risk because of

comorbidity or

advanced age.

Slide29

In those patients with a preoperative diagnosis, if the cause of

peritonitis

is amenable to surgery, operation must be carried out

as soon

as the patient is fit.

This is usually within a few hours.

In peritonitis caused by pancreatitis or salpingitis, or in cases of primary peritonitis of streptococcal or pneumococcal origin, non-operative treatment is preferred provided the diagnosis can be made with confidence

Slide30

In general, surgery is directed to removing (or diverting) the cause and subsequent adequate peritoneal lavage ± drainage.

In operations for generalised peritonitis it is essential that, after the cause has been dealt with, the whole peritoneal cavity is explored with the sucker and, if necessary, mopped dry until all seropurulent exudate is removed.

The use of a large volume of saline (typically 3 litres) containing dissolved antiseptic or antibiotic has been shown to be effective.

Slide31

Prognosis

D

iffuse peritonitis carries a mortality rate of about 10 per cent reflecting;

The degree and duration of peritoneal contamination

.

Age

of the

patient.

F

itness of the patient.

T

he nature of the underlying cause.

Slide32

Complications of peritonitis

Abdominal complications

Paralytic ileus

Residual or recurrent abscess/inflammatory mass

Portal pyaemia/liver abscess

Adhesional small bowel obstruction

Systemic

complications

Bacteraemic/endotoxic shock

Systemic inflammatory response syndrome

Multiorgan dysfunction syndrome

Death

Slide33

SPECIAL FORMS OF PERITONITIS

Bile peritonitis

Causes of bile peritonitis

Perforated cholecystitis

Postcholecystectomy due to;

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

Leaking duodenal stump postgastrectomy

Leaking biliary–enteric anastomosis

Leakage around percutaneous placed biliary drains

Following liver trauma

Slide34

Clinical features and treatment

S

evere abdominal 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.

Slide35

A

‘blown’ duodenal stump should be drained as it is too oedematous to repair, but sometimes it can be covered by a jejunal patch.

The patient is often jaundiced from absorption of peritoneal bile, but the surgeon must ensure that the abdomen is not closed until any obstruction to a major bile duct has been either excluded or relieved.

Bile leaks after cholecystectomy or liver trauma may be dealt with by percutaneous (ultrasoundguided) drainage and endoscopic biliary stenting to reduce bile duct pressure.

The drain is removed when dry and the stent at 4–6 weeks.

Slide36

Primary peritonitis

Primary pneumococcal peritonitis may complicate nephrotic syndrome or cirrhosis in children.

Healthy children, particularly girls between three and nine years of age, may also be affected, and it is likely that the route of infection is sometimes via the vagina and Fallopian tubes.

Always in males, the infection is blood-borne and secondary to respiratory tract or middle ear disease.

The prevalence of pneumococcal peritonitis has declined greatly and the condition is now rare.

Slide37

Clinical features

Sudden pain localised to the lower half of the abdomen.

Fever with vomiting.

After 24–48 hours, profuse diarrhoea is characteristic.

There is usually increased frequency of micturition.

The last two symptoms are caused by severe pelvic peritonitis

On examination, peritonism is usually diffuse

Slide38

Investigation and treatment

A leukocytosis 30 000 μL with approximately 90 per cent polymorphs suggests pneumococcal peritonitis rather than another cause, e.g. appendicitis.

Antibiotic therapy, correcting dehydration and electrolyte imbalance.

Early surgery is required (Laparotomy or laparoscopy).

In pneumococcal peritonitis the exudate is odourless and sticky, but it is essential to perform a careful exploration to exclude other pathology, some of the exudate is aspirated and sent to the laboratory for microscopy, culture and sensitivity tests

.

Slide39

Peritoneal

lavage is carried out and the incision closed.

Antibiotic and fluid replacement therapy.

Other organisms are now known to cause some cases of primary peritonitis in children, including

Haemophilus, other streptococci

and a few Gram-negative bacteria.

Underlying pathology (including an intravaginal foreign body in girls) must always be excluded before primary peritonitis can be diagnosed with certainty.

Idiopathic streptococcal and staphylococcal peritonitis can also occur in adults.

Slide40

Slide41

Tuberculous peritonitis

Intra-abdominal tuberculosis is very common in the developing world.

The incidence is however also rising in areas of the developed world as a consequence of migration and immunosuppression where

Mycobacterium avium-intracellulare

is becoming increasingly prevalent with the widespread increase in human immunodeficiency virus (HIV) coinfection.

Abdominal tuberculosis (TB) includes intraperitoneal, GI tract and solid organ disease forms with TB peritonitis being a common site-specific variant.

TB peritonitis is resulting in morbidity and mortality.

Slide42

Tuberculosis can spread to the peritoneum through the GI tract (typically ileocaecal region) via mesenteric lymph nodes or directly from the blood, usually from the ‘miliary’ but occasionally the ‘cavitating’ form of pulmonary TB, lymph and the Fallopian tubes.

50–83 per cent of patients with abdominal TB can be expected to have peritoneal involvement.

Clinical or subclinical ascites is reported in all patients with TB peritonitis and is frequently a presenting feature.

In the most common form of the disease, wet-type peritonitis, ascites may be localised or generalised throughout the peritoneal cavity.

Multiple tubercle deposits appear on both layers of the peritoneum.

Slide43

Diagnosis is via abdominal ultrasound or CT to detect ascites and lymphadenopathy ± diffuse thickening of the peritoneum, mesentery and/or omentum.

Ascitic fluid is typically a straw-coloured exudate (protein >25–30 g/L) with white cells >500 mm3 and lymphocytes >40 per cent.

Diagnostic smears for acid-fast bacilli are diagnostic in <3 per cent of patients and culture may take up to 4–8 weeks with no guarantee of a positive result.

Laparoscopy and peritoneal biopsy may thus be helpful to couple typical appearances with histology.

Slide44

Tuberculous peritonitis

Acute (may be clinically indistinguishable from acute bacterial peritonitis)

C

hronic

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 antituberculous treatment without surgery

Slide45

Management is principally;

Supportive (nutrition and hydration)

Medical (systemic antituberculous therapy)

Surgery may be required for specific complications such as intestinal obstruction.

Slide46

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.

Slide47

Mutations in the

MEFV

(Mediterranean fever) gene. This gene produces a protein called pyrin.

Usually, children are affected.

Exceptionally, the disease becomes manifest in patients over 40 years of age.

At operation, which may be necessary to exclude other causes, the peritoneum is inflamed, particularly in the vicinity of the spleen and the gall bladder.

Colchicine therapy is used during attacks and to prevent recurrent attacks

.

Slide48

INTRAPERITONEAL ABSCESS

Following intraperitoneal sepsis, abscess development usually occupies one of a number of specific abdominal or pelvic sites.

Larger abscesses will give rise to the picture of swinging pyrexia, pulse and a palpable mass.

Blood tests will reveal elevated inflammatory markers.

Slide49

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)

Slide50

Pelvic abscess

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 any case of diffuse peritonitis and is common after anastomotic leakage following colorectal surgery.

Clinical features

The most characteristic symptoms are of pelvic pain, diarrhoea and the passage of mucus in the stools.

Rectal examination reveals a bulging of the anterior rectal wall, which, when the abscess is ripe, becomes softly cystic.

Slide51

Investigation and management

The presence of pus should be confirmed by ultrasound or CT scanning

Left to nature, a proportion of these abscesses burst into the rectum.

In women, vaginal drainage through the posterior fornix is often chosen.

When the abscess is definitely pointing into the rectum, rectal drainage is employed.

Laparotomy is almost never necessary and rectal drainage of a pelvic abscess is far preferable to suprapubic drainage, which risks exposing the general peritoneal cavity to infection.

Drainage tubes can also be inserted percutaneously or via the vagina or rectum under ultrasound or CT guidance.

Slide52

Intraperitoneal abscess

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.

Slide53

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, a duodenal cap ‘blow-out’ following gastrectomy and appendicitis.

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.

Slide54

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.

Slide55

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.

Slide56

Clinical features

Sweating and anorexia are present.

There is sometimes epigastric fullness and pain, or pain in the shoulder on the affected side due to irritation of sensory fibres in the phrenic nerve, this being referred along the descending branches of the cervical plexus.

Persistent hiccoughs may be a presenting symptom.

A swinging pyrexia is usually present.

If the abscess is anterior, abdominal examination will reveal some tenderness, rigidity or even a palpable swelling.

Sometimes the liver is displaced downwards but more often it is fixed by adhesions.

Slide57

Investigation and management

CXR , as in the majority of cases, collapse of the lung or evidence of basal effusion or even an empyema are evident.

Ultrasound or CT guidance followed by drainage. The same tube can be used to instill antibiotic solutions or irrigate the abscess cavity if necessary.

Radiolabelled white cell scanning may occasionally prove helpful when other imaging techniques have failed.

In most cases, with the aid of percutaneous drainage and antibiotic treatment, the abscess or mass gradually reduces in size until, finally, it is undetectable.

Open drainage of an intraperitoneal collection is thus now uncommon but may be necessary.

Slide58

If a swelling can be detected in the subcostal region or in the loin, an incision is made over the site of maximum tenderness or over any area where oedema or redness is discovered.

Cautious blunt finger exploration can then be used to avoid dissemination of pus into the peritoneal or pleural cavities and minimise the risk of an intestinal fistula.

When the cavity is reached, all of the fibrinous loculi must be broken down with the finger and one or two drainage tubes fully inserted.

These drains are withdrawn gradually during the next 10 days and the closure of the cavity can be checked by sinograms or scanning.

Appropriate antibiotics are also given.

Slide59

ASCITES

Ascites is defined as an accumulation of excess serous fluid within the peritoneal cavity.

Pathophysiology

The balanced effects of plasma and peritoneal colloid osmotic and hydrostatic pressures determine the exchange of fluid between the capillaries and the peritoneal fluid.

Protein-rich fluid enters the peritoneal cavity when capillary permeability is increased, as in peritonitis and carcinomatosis peritonei.

Capillary pressure may be increased because of generalised water retention, cardiac failure, constrictive pericarditis or vena cava obstruction.

Slide60

Capillary pressure is raised selectively in the portal venous system in the Budd–Chiari syndrome, cirrhosis of the liver 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.

Slide61

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

Slide62

Exudates (protein >25 g/L)

Tuberculous peritonitis

Peritoneal malignancy

Budd–Chiari syndrome (hepatic vein occlusion or thrombosis)

Pancreatic ascites

Chylous ascites

Meigs’ syndrome

Slide63

Clinical features

Ascites can usually only be recognised clinically when the amount of fluid present exceeds 1.5 L depending on body habitus: in the obese a greater quantity than this is necessary before there is clear evidence.

The abdomen is distended 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.

Slide64

Congestive heart failure, the most common cause of ascites, 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).

Patients with constrictive pericarditis (Pick’s disease) have both peritoneal and pleural effusions because of engorgement of the venae cavae consequent upon the diminished capacity of the right side of the heart.

Ascites occurs with low plasma albumin concentrations, for example in patients with albuminuria or starvation.

The ascites in this instance is caused by alterations in the osmotic pressure of the capillary blood and has a low specific gravity

.

Slide65

In cirrhosis, 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. The fluid is dark yellow and frequently blood-stained. The specific gravity, 1.020 or over, and the protein content (>25 g/L) are high.

Slide66

Microscopic

examination often reveals cancer cells, especially if large quantities of fluid are ‘spun down’ to produce a concentrated deposit for sampling.

Rarely

, ascites and pleural effusion are associated with solid fibromas of the ovary (Meigs’ syndrome).

The

effusions disappear when the tumour is excised

Slide67

Investigation

Liver and cardiac function tests.

Ultrasound and/or CT imaging will ;

determine much smaller quantities of ascites.

diagnose aetiology, e.g. carcinomatosis, liver disease.

Ascitic aspiration or tap is now most commonly performed under imaging guidance to minimise the risk of visceral injury,

t

he bladder having been emptied, puncture of the peritoneum is carried out under local anaesthetic using a moderately sized trocar and cannula.

Slide68

Alternatively

, a peritoneal drain may be inserted.

In cases where the effusion is caused by cardiac failure, the fluid must be evacuated slowly.

Fluid

is sent for microscopy/cytology, culture, including mycobacteria, and analysis of protein content and amylase.

Unless

other measures are taken the fluid soon reaccumulates, and repeated tappings remove valuable protein.

Slide69

Treatment

Treatment of the specific cause;

If portal venous pressure is raised, it may be possible to lower it by treatment of the primary condition.

Dietary sodium restriction to 200 mg/day may be helpful.

Diuretics are usually required.

Slide70

In

rare cases in which ascites accumulates rapidly after paracentesis and the patient is otherwise fit, permanent drainage of the ascitic fluid via a peritoneovenous shunt (e.g. LeVeen, Denver) may render the patient more comfortable.

A

catheter (e.g. of silicone) is constructed with a valve so as to allow one-way flow from the peritoneum to a central vein (e.g. internal jugular).

A

chamber placed subcutaneously over the chest wall may be included for manual

compression.

Slide71

The complications include;

Overloading the venous system.

Cardiac failure

Disseminated intravascular coagulopathy.

Dissemination of malignant cells

The frequency of these complications may be reduced by evacuating ascitic fluid and partially replacing it with normal saline at the time of shunt insertion.

The procedure may also be used for patients with terminal malignant ascites, giving improved quality of life.

Slide72

Special cases

Chylous ascites

The ascitic fluid appears milky because of an excess of chylomicrons (triglycerides).

Most cases are associated with;

Malignancy, usually lymphomas;

Cirrhosis,

Tuberculosis,

Filariasis,

Nephrotic syndrome,

Abdominal trauma

(including surgery),

Constrictive pericarditis,

Sarcoidosis,

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 fatfree diet with medium-chain triglyceride supplements.

Slide73

TUMOURS OF THE PERITONEUM

Primary tumours

Are rare and in most cases take their origin not from the serous layer but from some adjacent structure, e.g

. lipoma

from appendices epiploicae

, fibroma

from connective tissue.

Mesothelioma

of the peritoneum is less frequent than in the pleural cavity but equally lethal. Asbestos is a recognised cause. It has a predilection for the pelvic peritoneum.

Chemocytotoxic agents are the mainstay of treatment.

Desmoid tumours

which have a relationship to the peritoneum are considered under familial adenomatous polyposis.

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Secondary tumours

Carcinomatosis peritonei

This is a common terminal event in many cases of carcinoma of the stomach, colon, ovary or other abdominal organs and also of the breast and bronchus.

The peritoneum, both parietal and visceral, is studded with secondary growths and the peritoneal cavity becomes filled with clear, straw-coloured or blood-stained ascitic fluid.

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The main forms of peritoneal metastases are:

discrete nodules – by far the most common variety;

plaques varying in size and colour;

diffuse adhesions – this form occurs at a late stage of the disease and gives rise, to a ‘frozen pelvis

’.

Gravity probably determines the distribution of free malignant cells within the peritoneal cavity.

The main differential diagnosis is from tuberculous peritonitis.

Treatment;

Are as for underlying malignancy.

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Pseudomyxoma peritonei

This rare condition occurs more frequently in women.

The abdomen is filled with a yellow jelly, large quantities of which are often encysted.

The condition is associated with mucinous cystic tumours of the ovary and appendix.

Recent studies suggest that most cases arise from a primary appendiceal tumour with secondary implantation on to one or both ovaries.

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It is often painless and there is frequently no impairment of general health.

Does not give rise to extraperitoneal metastases.

The diagnosis is more often suggested by ultrasound and CT scanning or made at operation.

At laparotomy, masses of jelly are scooped out.

The appendix, if present, should be excised together with any ovarian tumour.

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Unfortunately

, recurrence is inevitable, but patients may gain symptomatic benefit from repeated ‘debulking’ surgery.

Occasionally, the condition responds to radioactive isotopes or intraperitoneal chemotherapy.

The role of early radical peritoneal excision is uncertain.

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Peritoneal loose bodies (peritoneal mice

)

May be confused with a small tumour but almost never cause symptoms.

One or more may be found in a hernial sac or in the pouch of Douglas.

The loose body may come from an appendix epiploica that has undergone axial rotation followed by necrosis of its pedicle and detachment but they are also found in those who suffer from subacute attacks of pancreatitis.

These hyaline bodies attain the size of a pea or bean and contain saponified fat surrounded by fibrin

.

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ADHESIONS

Pathophysiology

Are strands of fibrous tissue that form, as a result of surgery, between surgically injured tissues.

After injury, there is bleeding and an increase in vascular permeability with extravasation of fibrinogen-rich fluid from the injured surfaces forming a temporary fibrin matrix.

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An

inflammatory response with cell migration, release of cytokines,

and

activation of

the coagulation cascade.

The

activation of the coagulation system results in thrombin formation, which is necessary for the conversion of fibrinogen to fibrin.

In the absence of fibrinolysis, adhesions will form within 5–7 days as the matrix gradually becomes more organised with collagen secretion by fibroblasts.

The ischaemic tissue loses its ability to break down fibrin and inhibits fibrinolysis in adjacent tissues.

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Complications

Small bowel obstruction (SBO). Adhesions are the most frequent cause of SBO in the developed world and are responsible for 60–70 per cent of SBO.

Major cause of secondary infertility.

Chronic abdominal and pelvic pain.

Unguided division of adhesions has not been shown to reduce chronic abdominal pain.

laparoscopy under local anaesthesia to direct lysis may improve success rates.

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Prevention

Minimising the production of ischaemic tissue by careful operative technique, including meticulous control of bleeding.

laparoscopic bowel surgery has been shown reduce adhesion.

The effect of a number of drugs including anti-inflammatory drugs like aspirin and steroids, some hormones, anticlotting agents, antibiotics, vitamin E and even methylene blue have been investigated in adhesion prevention but have not achieved widespread use either because of side effects or lack of consistent evidence of effectiveness.

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Interceed TC7® is a mesh-like product shown to significantly reduce the number of adhesions.

A

similar barriertype product (hyaluronic acid/carboxymethyl membrane), there was a significant reduction in the incidence,

extent and

severity of adhesions but no reduction in the incidence of intestinal obstruction or operative intervention.

Such barriers when placed around bowel anastomosis also led to a significant increase in the anastomotic leaks.

For

these reasons barrier approaches have not gained popularity.

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Special forms of intraperitoneal fibrosis

Sclerosing encapsulating peritonitis

Is described in patients as a complication of long-term peritoneal dialysis or portovenous shunting.

The peritoneal cavity becomes obliterated as a result of gross subserosal thickening by fibrosis leading to bowel obstruction.

Surgery should be undertaken with trepidation and avoided if possible.

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Diffuse fibromatosis

A rare tumour characterised by an abnormal proliferation of myofibroblasts.

Although non-metastasising

,

benign, it can nevertheless prove widely invasive, compressing and infiltrating surrounding tissues such as the bowel and mesentery with complications thereof.

Intra-abdominal fibromatosis IAF is very rare within the general population but has a recognised association with familial adenomatous polyposis (FAP).

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THE OMENTUM

Rutherford Morison called the greater omentum ‘the abdominal policeman.

It limit intraperitoneal infective and other noxious processes.

An acutely inflamed appendix is often found wrapped in omentum, and this saves many patients from developing diffuse peritonitis.

It often plugs the neck of a hernial sac and prevents a coil of intestine from entering and becoming strangulated.

It can, of course, also be a cause of obstruction (acting as a large adhesion).

The omentum is usually involved in tuberculous peritonitis and carcinomatosis of the peritoneum.

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Torsion of the omentum

Torsion of the omentum is a rare emergency and consequently is seldom diagnosed correctly.

It is usually mistaken for appendicitis with somewhat abnormal signs.

It may be primary, or secondary to adhesion of the omentum to an old focus of infection or hernia.

The patient is most frequently a middle-aged, obese man. A tender lump may be present in the abdomen.

The blood supply having been jeopardised, the twisted mass sometimes becomes gangrenous, in which case bacterial peritonitis may follow.

Treatment is surgical; the pedicle above the twist is ligated securely and the mass removed.

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THE MESENTERY

Mesenteric injury

A wound of the mesentery can follow severe abdominal contusion and is a cause of haemoperitoneum.

More commonly, it is injured by a torsional force, so-called seatbelt syndrome.

Aside from control of any ongoing haemorrhage, associated ischaemic or ruptured gut will require resection.

Ischaemia

Torsion of the mesentery is lead to volvulus of the small intestine.

Embolism and thrombosis of mesenteric vessels leading to intestinal ischaemia

.

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Acute non-specific ileocaecal mesenteric adenitis

Non-specific mesenteric adenitis was so named to distinguish it from specific (tuberculous) mesenteric adenitis.

It is now much more common than the tuberculous variety.

The aetiology often remains unknown, although some cases are associated with

Yersinia infection of the ileum.

In about 25 per cent of cases, a respiratory infection precedes an attack of non-specific mesenteric adenitis.

This self-limiting disease is never fatal but may be recurrent.

Its significance thus mainly lies in its differential diagnosis with

appendicitis in children.

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Diagnosis

A common condition during childhood.

Central abdominal pain lasting from 10 to 30 minutes, commonly associated with vomiting.

More

than the half of the cases the temperature is elevated.

Abdominal tenderness is poorly localised.

The neck, axillae and groins should be palpated for enlarged lymph nodes.

Leukocytosis of 10 000–12 000 μL (10–12 × 109 L) or more on the first day of the attack, but this falls on the second day.

Treatment

Bed rest

Simple analgesia.

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Tuberculosis of the mesenteric lymph nodes

Tubercle bacilli, usually, but not necessarily, bovine, are ingested and enter the mesenteric lymph nodes by way of Peyer’s patches.

The presentation may be with abdominal pain or with general constitutional symptoms (pyrexia, weight loss, etc.).

Misty mesentery

The term ‘misty mesentery’ indicates a pathological increase in mesenteric fat attenuation at CT .

In patients suffering from acute abdominal disease, misty mesentery may be considered a feature of the underlying disease.

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Mesenteric cysts

Cysts may occur in the mesentery of either the small intestine(60 per cent) or the colon (40 per cent) and can be classified as:

• Chylolymphatic;

• Enterogenous;

• Urogenital remnant (actually retroperitoneal but project into peritoneum);

• Dermoid.

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Pathology

Chylolymphatic cyst

This

is the most common variety, probably arising in congenitally misplaced lymphatic tissue that has no efferent 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 lined by flat endothelium, is filled with clear lymph or, less frequently, with chyle varying in consistency from watered milk to cream.

Occasionally

, the cyst attains a great size. More often unilocular than multilocular, a chylolymphatic cyst is almost invariably solitary.

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 gut.

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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.

An enterogenous cyst has a thicker wall than a chylolymphatic cyst and it is lined by mucous membrane, sometimes ciliated.

The content is mucinous and is 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.

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Urogenital remnant

A cyst developing in the retroperitoneal space often attains very large dimensions and has first to be distinguished from a large hydronephrosis.

Even after the latter condition has been eliminated by scanning or urography, a retroperitoneal cyst can seldom be distinguished with certainty from a retroperitoneal tumour until displayed at operation.

The cyst may be unilocular or multilocular.

Many of these cysts are believed to be derived from a remnant of the Wolffian duct, in which case they are filled with clear fluid.

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Mesenteric cysts: clinical features

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 one-third of cases occur in children younger than 15 years

The mean age of children affected is 4-9 years

The most common presentation is of a painless abdominal swelling with characteristic physical signs there is a fluctuant swelling near the umbilicus the swelling moves freely in a plane at right angles to the attachment of the mesentery (Tillaux’s sign) there is a zone of resonance around the cyst

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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.

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Investigation and treatment

Ultrasound and CT scanning will demonstrate the lesion.

There are no suitable medical therapies.

The goal of surgical therapy is complete excision of the mass.

The

preferred treatment of mesenteric cysts is enucleation, although bowel resection is frequently required to ensure that the remaining bowel is viable.

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Differential diagnosis

S

erosanguinous

cyst

;

Tuberculous abscess of the mesentery;

Hydatid cyst of the mesentery.

Neoplasms of the mesentery

The mesentery is necessarily affected by local lymphatic spread of carcinoma arising from the peritoneal viscera.

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Other

benign and malignant tumours are less common

Tumours

situated in the mesentery give rise to physical signs that are similar to those of a mesenteric cyst, the sole exception being that they sometimes feel solid.

If

indicated, a benign tumour of the mesentery is excised in the same way as an enterogenous mesenteric cyst, i.e. 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.

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THE RETROPERITONEAL SPACE

Retroperitoneal chronic

inflammation/ 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.

Histological appearances vary from active inflammation with a high cellular content interspersed with bundles of collagen through to

one of

acellularity and mature fibrosis/calcification.

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Its aetiology is

idiopathic

.

In other patients the cause is known .

The

clinical presentation may be one of ill-defined chronic backache or may 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, to the modification of disease activity when appropriate, e.g. immune suppression with steroids and restoration of flow in affected structures,

e.g.

ureteric

stenting.

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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)

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Retroperitoneal (psoas) abscess

Psoas abscess is a relatively uncommon.

At the beginning of the twentieth century, psoas abscess was mainly caused by tuberculosis of the spine (Pott’s disease).

With the decline of

Mycobacterium tuberculosis as a major pathogen in developed

countries a psoas abscess was mostly found secondary to direct spread of infection from the inflamed ± perforated digestive or urinary tract.

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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 back pain, lassitude and fever.

A

swelling may point to the groin as it tracks along ileopsoas Pain may be elicited by passive extension of the hip or a fixed flexion of the hip evident on inspection.

Radiological investigation

CT

scanning.

Treatment

CT-guided drainage

Antibiotic therapy.

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Retroperitoneal tumours

Retroperitoneal tumour is usually confined to primary tumours arising in other tissues in this region, e.g. muscles, fat, lymph nodes and nerves.

Retroperitoneal lipoma

a swelling or abdominal pain.

Women are more often affected.

These swellings sometimes reach an large size.

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Diagnosis

Ultrasound and CT scanning.

A retroperitoneal lipoma is often malignant (liposarcoma) and may increase rapidly in size.

Retroperitoneal sarcoma

Retroperitoneal sarcomas are rare tumours accounting for only 1–2 per cent of all solid malignancies (10–20 per cent of all sarcomas are retroperitoneal).

The peak incidence is in the fifth decade of life, the most frequently encountered cell types are

:

liposarcoma;

leiomyosarcoma;

malignant fibrous histiocytoma (MFH).

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Clinical features

G

row very large without producing symptoms.

Abdominal pain and fullness.

Investigation

(CT + magentic resonance imaging)

Treatment

The definitive treatment of primary retroperitoneal sarcomas is surgical resection.

Chemotherapy and radiotherapy without surgical debulking have rarely been beneficial.

Prognosis

Survival rates are, in general, poor, even after complete resection, these being in the order of 35–50 per cent (excluding low grade liposarcomas, which may frequently be cured by resection).

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