56.peritoneum,omentum,mesentry and retro peritoneal space

8/3/2019 56.Peritoneum,Omentum,Mesentry and Retro Peritoneal Space

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56 The peritoneum, omentum, mesentery andretroperitoneal space

JEREMY THOMPSON

The peritoneumThe peritoneal membrane is conveniently divided into two parts — thevisceralsurrounding the viscera and the parietal lining the other surfaces of the cavity.The peritoneum has a number of functions (Table 56.1).The parietal portion is richlysupplied with nerves and, when irritated, causes severe pain accurately localised to theaffected area. The visceral peritoneum, in contrast, is poorly supplied with nerves, and

its irritation causes vague pain which is usually located to the midline.The peritoneal cavity is the largest cavity in the body, the surface area of its liningmembrane (2 m2 in an adult) being nearly equal to that of the skin. The peritonealmembrane is composed of flattened polyhedral cells (mesothelium), one layer thick,resting upon a thin layer of flbroelastic tissue. Beneath the peritoneum, supported by asmall amount of areolar tissue, lies a network of lymphatic vessels and rich plexusesof capillary blood vessels from which all absorption and exudation must occur. Inhealth, only a few millilitres of peritoneal fluid is found in the peritoneal cavity Thefluid is pale yellow, somewhat viscid and contains lymphocytes and other leucocytes;it lubricates the viscera allowing easy movement and peristalsis.In the peritoneal space mobile gas-filled structures float upwards under the influence

of posture, as does free air (‘gas’). In the erect position, when free fluid is present inthe peritoneal cavity, pressure is reduced in the upper abdomen compared with thelower abdomen. When air is introduced it rises, allowing all of the abdominal contentsto sink.During expiration intra-abdominal pressure is reduced and peritoneal fluid, aided bycapillary attraction, travels in an upward direction towards the diaphragm.Experimental evidence shows that particulate matter and bacteria are absorbed withina few minutes into the lymphatic network through a number of ‘pores’ within thediaphragmatic peritoneum. This upward movement of peritoneal fluids is responsiblefor the occurrence of many subphrenic abscesses.The peritoneum has the capacity to absorb large volumes of fluid: this ability is usedduring peritoneal dialysis in the treatment of renal failure. But the peritoneum can also

produce an inflammatory exudate when injured (Table 56.2). When a visceral perforation occurs the free fluid which spills into the peritoneal cavity runsdownwards, largely directed by the normal peritoneal attachments. For example,spillage from a perforated duodenal ulcer may run down the right paracolic gutter.When parietal peritoneal defects arecreated healing occurs, not from the edges, hutbythe development of new mesothelial cells throughout the surface of the defect. Inthisway large defects heal as rapidly as small defects.Acute peritonitisMost cases of peritonitis are due to an invasion of the peritoneal cavity by bacteria, sothat when the term ‘peritonitis’ is used without qualification, bacterial peritonitis isimplied. Bacterial peritonitis is usually polymicrobial, both aerobic and anaerobicorganisms being present. The exception is primary peritonitis (‘spontaneous’



peritonitis) in which a pure infection with streptococcal, pneumococcal or haemophilus bacteria occurs.BacteriologyBacteria 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, while

high concentrations are found in the colon. However, disease (e.g. obstruction,achlorhydria, diverticula) may increase proximal colonisation. The biliary and

pancreatic tracts are normally free from bacteria, although they may be infected indisease, e.g. gallstones. Peritoneal infection is usually caused by two or more bacterialstrains. The commonest are Escherichia coli, aerobic and anaerobic streptococci, andthe bacteroides. Less frequently Clostridium welchii is found; still less frequentlystaphylococci or Klebsiella pneumonlae (Friedländer’s bacillus). Gram-negative

bacteria contain endotoxins (lipopolysaccharides) in their cell walls which havemultiple toxic effects on the host, primarily by causing the release of tumour necrosisfactor (TNF) from host leucocytes. Systemic absorption of endotoxin may produceendotoxic shock with hypotension and impaired tissue perfusion. Other bacteria suchas C. welchii produce harmful exotoxins.Bacteroidesare commonly found in peritonitis. These Gram-negative, nonsporingorganisms, although predominant in the lower intestine, often escape detection

because they are strictly anaerobic, and slow to grow on culture media unless there isan adequate carbon dioxide tension in the anaerobic apparatus (Gillespie). In manylaboratories, the culture is discarded if there is no growth in 48 hours. Theseorganisms 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 diminished greatly.

Nongastrointestinal causes of peritonitis Nongastrointestinal causes of peritonitis include chlamydia, gonococcus, beta-haemolytic streptococcus, pneumococcus and Mycobacterium tuberculosis. Since theadvent of antibiotics haemolytic streptococcal peritonitis has lost many of its dreadedlethal properties. In young girls and women, pelvic infection via the Fallopian tubes isresponsible for a high proportion of ‘nongastrointestinal’ infections but bacteroides isalso found in the female genital tract.Immunodeficient patients, for example those withhuman immunodeficiency virus(HIV) infection (the acquired immunodeficiency syndrome — AIDS) or onimmunosuppressivetreatment, may present with opportunistic peritoneal infection,e.g. mycobacterium avis intracellulare(MAI).Route of infection

Infecting organisms may reach the peritoneal cavity via a number of routes (Table56.3).Even in patients with nonbacterial peritonitis (e.g. acute pancreatitis, intraperitonealrupture of the bladder or haemoperitoneum) the peritoneum often becomes infected

by transmural spread of organisms from the bowel, and itis not long (often a matter of hours) before a bacterial peritonitis develops. Most duodenal perforations are initiallysterile for up to several hours, and many gastric perforations are also sterile at first;intestinal perforations are usually infected from the beginning. The proportion of anaerobic to aerobic organisms increases with the passage of time. Mortality reflects:•the degree and duration of peritoneal contamination;•the age of the patient;

•the general health of the patient;•the nature of the underlying cause.



Localised peritonitisAnatomical, pathological and surgical factors may favour the localisation of

peritonitis.AnatomicalThe greater sac of the peritoneum is divided into (a) the subphrenic spaces, (b) the

pelvis, and (c) the peritoneal cavity proper. The latter is redivided into a supracolicand an infracolic compartment by the transverse colon and transverse mesocolon,which deter the spread of infection from one to the other. When the supracoliccompartment overflows, as is often the case when a peptic ulcer perforates, itdoes soover the colon into the infracolic compartment, or by way of the right paracolic gutter to the right iliac fossa, and thence to the pelvis. Posture can assist in directingcollections into the pelvis, as in the ‘Sherren’ regime for perforated appendicitis.PathologicalThe clinical course is determined in part by the manner in which adhesions formaround the affected organ. Inflamedperitoneum loses its glistening appearance and

becomes reddened and velvety. Flakes of fibrin appear and cause loops of intestine to become adherent to one another and to the parieties. There is an outpouring of serousinflammatory exudate rich in leucocytes and plasma proteins that soon becomesturbid; if localisation occurs, the turbid fluid becomes frank pus. Peristalsis is retardedin affected bowel, and this helps in preventing distribution of the infection. Thegreater omen-turn, by enveloping and becoming adherent to inflamed structures, oftenforms a substantial barrier to the spread of infection.SurgicalDrains are frequently placed during operation to assist localisation (and exit) of intra-abdominal collections: their value is disputed. They may act as conduits for exogenous infection. Collections detected postoperatively on ultrasound or computerised tomography (CT) scanning may be drained percutaneously.Diffuse peritonitisA number of factors may favour the development of diffuse peritonitis.Speed of peritoneal contamination is a prime factor in the spread of peritonitis. If aninflamed appendix (Fig. 56.1) or other hollow viscus perforates before localisationhas taken place, there is a gush of contents into the peritoneal cavity which mayspread over a large area almost instantaneously. Perforation proximal to anobstruction, or from sudden anastomotic separation, is associated with severegeneralised peritonitis and a high mortality.Stimulation of peristalsis by the ingestion of food, or even water, hinders localisation.Violent peristalsis occasioned by the administration of a purgative or an enema may

cause the widespread distribution of an infection that would otherwise have remainedlocalised.The virulence of the infecting organism may be so great as to render the localisationof infection difficult or impossible.Young children have a small omentum.Disruption of localised collections may occur with injudicious and rough handling,e.g. appendix mass or pericolic abscess.Deficient natural resistance (‘immune deficiency’) mayresult from drugs (e.g. steroids), disease (e.g. AIDS) or old age.Clinical featuresLocalised peritonitis

Localised peritonitis is bound up intimately with the causative condition and theinitial symptoms and signs are those of that condition. When the peritoneum becomes



inflamed the temperature, and especially the pulse rate, rise. Abdominal painincreases and usually there is associated vomiting. The most important sign isguarding and rigidity of the abdominal wall over the area of the abdomen which isinvolved, with a positive ‘release’ sign (rebound tenderness), if inflammation arisesunder 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 salpingitisthe abdominal signs are often slight, deep tenderness of one or both lower quadrantsalone being present, but a rectal or vaginal examination reveals marked tenderness of the pelvic peritoneum. With appropriate treatment localised peritonitis usuallyresolves. In 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 siteswithin the abdominal cavity. A large collection of bile localised to the subhepaticspace can remain dangerously ‘silent’ until a late stage.Diffuse (generalised) peritonitisDiffuse (generalised) peritonitis may present in differing ways dependent on theduration of infection.Early. Abdominal pain is severe and made worse by moving or breathing. It is firstexperienced at the site of the original lesion, and spreads outwards from this point.Vomiting may occur. The patient usually lies still. Tenderness and rigidity on

palpation are typically found when the peritonitis affects the anterior abdominal wall.Abdominal tenderness and rigidity are diminished or absent if the anterior wall isunaffected, as in pelvic peritonitis or, rarely, peritonitis in the lesser sac. Patients with

pelvic peritonitis may complain of urinary symptoms; they are tender on rectal or vaginal examination. Infrequent bowel sounds may still be heard for a few hours butthey cease with the onset of paralytic ileus. The pulse rises progressively, but if the

peritoneum is deluged with irritant fluid, there is a sudden rise. The temperaturechanges are variable and can be subnormal.Late. If resolution or localisation of generalised peritonitis does not occur, theabdomen remains silent and increasingly distends. Circulatory failure ensues, withcold, clammy extremities, sunken eyes, dry tongue, thready (irregular) pulse, anddrawn and anxious face (Hippocratic facies, Fig.56.2). The patient finally lapses intounconsciousness. With early diagnosis and adequate treatment, this condition is rarelyseen in modern surgical practice.Diagnostic aidsA number of investigations may elucidate a doubtful diagnosis, but the importance of a careful history and repeated examination must not be forgotten

A leucocytosis is usually seen in peritonitis but is often delayed for many hours.Peritoneal diagnostic aspiration may be helpful but is usually unnecessary. After infiltrating the skin of the abdomen with local anaesthetic, the peritoneum is enteredin one or more quadrants with a sterile needle an or intravenous cannula attached to asyringe into which is sucked any free fluid. Bile-stained fluid indicates perforated

peptic ulcer or gall bladder, the presence of pus indicates bacterial peritonitis; blood isaspirated in a high proportion of patients with intraperitoneal bleeding. Whenaspiration fails, the introduction of a small quantity of sterile physiological saline,followed after a few minutes by peritoneal aspiration may produce fluid of diagnosticvalue. Microscopy of the fluid may show neutrophils (indicative of acuteinflammation) and bacteria (confirming infection).

An X-ray film of the abdomen may confirm the presence of dilated gas-filled loops of bowel (consistent with a paralytic ileus) or show free gas, although the latter is best



shown on an erect chest X-ray (Fig. 56.3). If the patient is too ill for an ‘erect’ film todemonstrate free air collecting under the diaphragm, a lateral decubitus film is just asuseful showing gas beneath the abdominal wall. Serum amylase estimation mayuphold the diagnosis of acute pancreatitis provided itis remembered that moderatelyraised values are frequently found following other abdominal catastrophes and

operations, e.g. perforated duodenal ulcer.Ultrasound and CT scanning, when available, may also he helpful in some patients byidentifying a cause of peritonitis e.g. perforated appendicitis, acute pancreatitis (Fig.56.4). Such knowledge may influence operative approach or contraindicate operation.TreatmentIt cannot be stressed too strongly that in any case of doubt, early surgical interventionis to be preferred to a ‘wait and see’ policy; for greaten numbers of patients die fromdelay than from an ‘unnecessary’ laparotomy. This rule is particularly true for

postoperative peritonitis.Treatment consists of:•general care of the patient;

• specific treatment for the cause;• peritoneal lavage when appropriate.

General care of the patientCorrection of circulating volume and electrolyte imbalance. Patients are frequentlyhypovolaemic with electrolyte disturbances. The plasma volume must be restored andthe plasma electrolyte concentrations corrected. Central venous catheterisation and

pressure monitoring may be helpful in correcting fluid and electrolyte balance particularly in patients with concurrent disease. Plasma protein depletion may alsoneed correction as the inflamed peritoneum leaks large amounts of protein. If the

patient’s recovery is delayed for more than 7—10 days, intravenous feeding (‘hyper-alimentation’ or ‘total parenteral nutrition’) is required.Gastrointestinal decompression. A nasogastnic tube is passed into the stomach andaspirated. Intermittent aspiration is maintained until the paralytic ileus resulting from

peritonitis has recovered. Measured volumes of water are allowed by mouth whenonly small amounts are being aspirated. If the abdomen is soft and not tender, and

bowel sounds return, oral feeding may be progressively introduced. It is important notto prolong the ileus by missing this stage.Antibiotic therapy. Administration of antibiotics prevents the multiplication of

bacteria and the release of endotoxins. As the infection is usually a mixed one,initially parenteral broad-spectrum antibiotics active against aerobic and anaerobic

bacteria should be given.

A fluid balance chart must be started so that daily output by gastric aspiration andurine is known. Additional losses from the lungs, skin, and in faeces are estimated, sothat the intake requirements can be calculated and seen to have been administered.Throughout recovery, the haematocrit and serum electrolytes and urea must bechecked regularly.Analgesia. The patient should be nursed in the sitting-up position and must berelieved of pain before and after operation. Once the diagnosis has been mademorphine may be given, and continued as necessary. If appropriate expertise isavailable epidural infusion may provide excellent analgesia. Freedom from painallows early mobilisation and adequate physiotherapy in the postoperative periodwhich help to prevent basal pulmonary collapse, deep-vein thrombosis and pulmonary

embolism.



Vital system support. Especially if septic shock is present, special measures may beneeded for cardiac, pulmonary and renal support. Administration of oxygen

postoperatively canhelp to prevent and mitigate the effects of septic shock, especiallyadult respiratory distress syndrome (ARDS) which may require a period of mechanical ventilation. If oligunia persists despite adequate fluid replacement, both

diuretics and inotropic agents such as dopamine may be needed.Specific treatment of the causeIf the cause of peritonitis is amenable to surgery, such as in perforated appendicitis,diverticulitis, peptic ulcer, gangrenous cholecystitis or in rare cases of perforation of the small bowel, operation must be carried out as soon as the patient is fit for anaesthesia. This is usually within a few hours. In peritonitis due to pancreatitis or salpingitis, or in cases of primary peritonitis of streptococcal or pneumococcal origin,nonoperative treatment is preferred (if the diagnosis can be made with certainty).Peritoneal lavageIn operations for general peritonitis itis essential that after the cause has been dealtwith the whole penitoneal cavity should be explored with the sucker and mopped dry,if necessary until all seropurulent exudate is removed. The use of a large volume of saline (1—2 litres) containing dissolved antibiotic (e.g. tetracycline) has been shownto be very effective (Matheson).PrognosisWith modern treatment diffuse peritonitis carries a mortality of about 10 per cent. Thesystemic complications and lethal factors are listed in Table 56.4.Complications of peritonitisAll of the complications of a severe bacterial infection are possible, but the specificabdominal complications of peritonitis are listed in Table 56.5.Acute intestinal obstruction due to peritoneal adhesionsThis usually gives central colicky abdominal pain with evidence of small bowel gasand fluid levels sometimes confined to the proximal intestine on X-ray. Bowel soundsare increased. It is more common with localised peritonitis. It is essential todistinguish this from paralytic ileus.Paralytic ileusThere is usually little pain and gas-filled loops with fluid levels are seen distributedthroughout the small and large intestines on abdominal X-ray. In paralytic ileus,

bowel sounds are reduced or absent.AbscessesAbscess formation following local or diffuse peritonitis usually occupies one of thesituations shown in Fig. 56.5. The symptoms and signs of a purulent collection may

be very vague and consist of nothing more than lassitude, anorexia and failure tothrive; pyrexia (often low-grade), tachycardia, leucocytosis and localised tendernessare also common. Later on a palpable mass may develop. When palpable anintraperitoneal abscess should be monitored by marking out its limitations on theabdominal wall, and meticulous daily examination. More commonly its course ismonitored by repeat ultrasound or CT scanning. In the majority of cases with the aidof antibiotic treatment, the abscess or mass becomes smaller and smaller, and finallyis undetectable. In others, the abscess fails to resolve, or becomes larger, in whichevent it must be drained. In many situations, by waiting for a few days the abscess

becomes adherent to the abdominal wall, so that it can be drained without opening thegeneral peritoneal cavity; If facilities are available ultrasound or CT-guided drainage

may avoid further operation. Open drainage of an intraperitoneal collection should be



carried out by cautious blunt finger exploration to minimise the risk of an intestinalfistula.Pelvic abscessThe pelvis is the commonest site of an intraperitoneal abscess because the vermiformappendix is often pelvic in position and also the Fallopian tubes are frequent sites of

infection. A pelvic abscess can also occur as a sequel to any case of diffuse peritonitisand is a common sequel of anastomotic leakage following large bowel and rectalsurgery. Pus can accumulate in this area without serious constitutional disturbanceand unless the patient is examined carefully from day to day, such abscesses mayattain considerable proportions before being recognised. The most characteristicsymptoms of a pelvic abscess are diarrhoea and the passage of mucus in the stools. Itis no exaggeration to say that the passage of mucus, occurring for the first time in a

patient who has, or is recovering from, peritonitis, is pathognomonic of pelvicabscess. Rectal examination reveals a bulging of the anterior rectal wall which, whenthe abscess is ripe, becomes softly cystic. Left to nature, a proportion of theseabscesses bursts into the rectum, after which the patient nearly always recoversrapidly. If this possible happy termination does not readily occur the abscess should

be drained deliberately. In women vaginal drainage through the posterior fornex isoften chosen. In other cases, where the abscess is definitely pointing into the rectum,rectal drainage (Fig. 56.6) is employed. If any uncertainty exists, the presence of puscan be confirmed by ultrasound or CT scanning or by an aspirating needle introducedthrough the rectum or abdominal wall into the swelling. Laparotomy is almost never necessary. Rectal drainage of a pelvic abscess is far preferable to suprapuhic drainage,which risks exposing the general peritoneal cavity to infection. Drainage tubes canalso be inserted percutaneously or via the vagina or rectum under radiological(ultrasonic or CT) guidance (Fig. 56.7).

Subphrenic abscessAnatomyThe complicated arrangement of the peritoneum results in the formation of four

peritoneal and three extraperitoneal spaces in which pus may collect. Three of thesespaces are on either side of the body, and one is approximately in the midline (Figs56.8 and 56.9).Left superior (anterior) intraperitoneal (‘left subphrenic’) is hounded above by thediaphragm, and behind by the left triangular ligament and the left lobe of the liver, thegastrohepatic omentum and 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.Leftinferior (posterior) intraperitoneal (‘left subhepatic’) is another name for the‘lesser’ sac. The commonest 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 superior (anterior) intraperitoneal (‘right subphrenic’) lies between the rightlobe 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 falciformligament. Common causes here are perforating cholecystitis, a perforated duodenal

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



Right inferior (posterior) intraperitoneal (‘right subhepatic’) lies transversely beneaththe right lobe of the liver in Rutherford Morison’s pouch. It is bounded on the right bythe 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, the upper part of the right kidney and diaphragm. The space is bounded

above by the liver, and below by the transverse colon and hepatic flexure. It is thedeepest space of the four and the commonest site of a subphrenic abscess whichusually arises from appendicitis, cholecystitis, a perforated duodenal ulcer or following upper abdominal surgery.Extraperitoneal. There are three of these:•right and left extra peritoneal which are terms given to perinephric abscesses(Chapter 64);•midline extraperitoneal which is another name for the ‘bare’ area of the liver whichmay develop an abscess in amoebic hepatitis (the commonest cause) or a pyogenicliver abscess (Chapter 52).Clinical featuresThe symptoms and signs of subphrenic infection are frequently nonspecific, and it iswell to remember the aphorism, ‘pus somewhere, pus nowhere else, pus under diaphragm’.SymptomsA common history is that when some infective focus in the abdominal cavity has beendealt with, the condition of the patient improves temporarily, but after an interval of afew days or weeks, symptoms of toxaemia reappear. The condition of the patientsteadily, and often rapidly, deteriorates. Sweating, wasting and anorexia are present.There is sometimes epigastric fullness and pain, or pain in the shoulder on theaffected side, owing to irritation of sensory fibres in the phrenic nerve, referred alongthe descending branches of the cervical plexus. Persistent hiccup may be a presentingsymptom.SignsA swinging pyrexia is usually present, unless antibiotics or drugs (steroids) haveinterfered. If the abscess is anterior, abdominal examination will reveal sometenderness, rigidity or even a palpable swelling. Sometimes the liver is displaceddownwards, but more often itis fixed by adhesions. Examination of the chest isimportant, and in the majority of cases collapse of the lung or evidence of basaleffusion or empyema is to be found.InvestigationsAnumber of these may be helpful as follows. Blood count usually shows a

leucocytosis.A plain radiograph sometimes demonstrates the presence of gas or a pleural effusion.On screening, the diaphragm is often seen to be elevated (so-called ‘tented’diaphragm) and its movements impaired.Ultrasound or CT scanning is the investigation of choice and permits early detectionof subphrenic collections (Fig. 56.10).Radiolabelled white cell scanning may occasionally prove helpful when other imagingtechniques have failed.Differential diagnosis. Pyelonephritis, amoebic abscess, pulmonary collapse and

pleural empyema give rise to most of the diagnostic difficulties.Treatment

The clinical course of suspected cases is watched, and blood and imaginginvestigations are made at suitable intervals. If suppuration seems probable,



intervention is indicated. If skilled help is available it is possible to insert a percutaneous drainage tube under ultrasound or CT control. The same tube can beused to instil antibiotic solutions or irrigate the abscess cavity. To pass an aspiratingneedle at the bedside through the pleura and diaphragm invites potentiallycatastrophic spread of the infection into the pleural cavity.

If an operative approach is necessary and a swelling can be detected in the subcostalregion or in the loin, an incision is made over the site of maximum tenderness, or over any area where oedema or redness is discovered. The parietes usually form part of theabscess wall so that contamination of the general penitoneal cavity is unlikely.If no swelling is apparent, the subphrenic spaces should be explored either by ananterior subcostal approach or from behind after removal of the outer part of the 12thrib according to the position of abscess on imaging. With the posterior approach the

pleura must not be opened and after the fibres of the diaphragm have been separated afinger is inserted beneath the diaphragm so as to explore the adjacent area. The aimwith all techniques of drainageis to avoid dissemination of pus into the penitoneal or

pleural cavities.When the cavity is reached, all of the fibrinous loculi must be broken down with thefinger and one or two drains or drainage tubes must be fully inserted. These drains arewithdrawn gradually during the next 10 days and the closure of the cavity is checked

by sinograms or scanning. The appropriate antibiotics are also given.

Special forms of peritonitisPostoperativeThe patient is ill, with raised pulse and peripheral circulatory failure. Following ananastomotic dehiscence the general condition of a patient is usually more serious thanif the patient had suffered leakage from a perforated peptic ulcer with no precedingoperation. Local symptoms and signs are less definite. Abdominal pain may not be

prominent and is often difficult to assess because of normal wound pain and postoperative analgesia. The patient’s deterioration may be wrongly attributed tocardiopulmonary collapse which is usually concomitant.Peritonitis follows abdominal operations more frequently than is realised. The

principles of treatment do not differ from those of peritonitis of other origin.Antibiotic therapy alone is inadequate; no antibiotic can stay the onslaught of

bacterial peritonitis due to leakage from a suture line, which must be dealt with byoperation.In patients under treatment with steroids

Pain is frequently slight or absent. Physical signs are similarly vague and misleading.In childrenThe diagnosis is in some ways more difficult, in other ways easier, than in adults. If ahistory can be taken itis plain and unembroidered. Any physical signs elicited by agentle, patient and sympathetic examiner are meaningful.In senile patientsThese can be as fractious as children and unable to give a reliable history. Abdominaltenderness is usually well localised, but guarding and rigidity are less marked becausethe abdominal muscles are thin and weak.

Bile peritonitis

Unless there is reason to suspect that a bile duct was damaged at an operation, it isimprobable that bile as a cause of peritonitis will be thought of until the abdomen has



been opened and bile is seen therein. The common causes of bile peritonitis are shownin Table 56.6. Unless the bile has extravasated slowly and the collection becomes shutoff from the general peritoneal cavity there are signs of diffuse peritonitis. After a fewhours a tinge of jaundice is not unusual. Laparotomy (or laparoscopy) should beundertaken with evacuation of the bile and penitoneal lavage. The source of bile

leakage should be identified. A leaking gall bladder is excised or a cystic duct ligated.An injury to the bile duct may simply be drained or alternatively intubated; later reconstructive operation is often required. Infected bile is more lethal than sterile bile.A ‘blown’ duodenal stump must be drained as it is too oedematous to repair, butsometimes itcan be covered by a jejunal patch. The patient is often jaundiced fromabsorption of peritoneal bile, but the surgeon must ensure that the abdomen is notclosed until any obstruction to a major bile duct has been either excluded or relieved.Post cholecystectomy bile leaks may be dealt with by percutaneous (ultrasoundguides) drainage and endoscopic biliary stenting to reduce bile duct pressure. Thedrain is reduced when dry and the stent at 4—6 weeks.Meconium peritonitisMeconium is a sterile mixture of epithelial cells, mucin, salts, fats and bile and isformed when the foetus commences to swallow amniotic fluid. By the third month of intrauterine life the upper third of the small intestine has become filled withmeconium; by the fourth month the accumulation has reached the ileocaecal valve;during the remainder of intrauterine life the colon becomes increasingly filled.Meconium peritonitis is an aseptic peritonitis which develops late in intrauterine lifeor during, or just after, delivery. Meconium enters the peritoneal cavity through anintestinal perforation and in over 50 percent of cases the perforationis the resultof some form of neonatal intestinal obstruction; in the remainder no cause for the

perforation is discernible. When meconium, which is sterile, enters the peritonealcavity an exudate is secreted that organises rapidly; matting of intestinal loopsoccurs,and in many cases in a matter of weeks the extruded meconium becomescalcified.Meconium remains sterile until about 3 hours after birth; thereafter, unless the

perforation has become sealed, sterile meconium peritonitis gives place to acute bacterial peritonitis which, unless treated promptly, is rapidly fatal.Clinical features. Meconiumperitonitis should always he considered when a baby is

born with a tense abdomen. There is vomiting and failure to discharge meconium. Thedifferential diagnosis between neonatal intestinal obstruction and peritonitis is, inmany cases, virtually impossible; indeed in half the cases both are present. Free fluidin theperitoneal cavity is often sufficient to give a fluid thrill. Meconium ileus occurs

in 5—10 per cent of newborn babies with cystic fibrosis (mucoviscidosis) who havean inherited autosomal recessive abnormality of mucus secretion. This leads tosecondary damage to the pancreas, lungs, liver and small bowel. Bronchialobstruction by mucus plugs can cause fatal pneumonia.Radiography (Fig. 56.11). Free air in the peritoneal cavity, an abundant quantity of abdominal fluid, fluid levels, calcification (often most distinct on the surface of theliver or the spleen and most readily seen in a lateral view) are characteristic findings,all of which are unlikely to be present in every case. Meconium peritonitis has beendiagnosed by radiography of the foetus in utero 2 days before birth.Treatment.The prognosis is bad, but recovery may follow prompt operation. Thegreatest chance of survival is in those patients who have an intestinal perforation but

no intestinal obstruction, in which case closure of the perforation and drainage of the peritoneal cavity are performed expeditiously. Intestinal lavage can prevent



reformation of meconium bolos obstruction and supplements of pancreatic exocrineenzymes are often necessary throughout life. If there is an associated pulmonary

problem, the condition requires special treatment (e.g. oxygen, bronchial lavage,nebulisers and long-term use of antibiotics).Pneumococcal peritonitis

There are two forms of this disease: (1) primary, and (2) secondary to pneumonia.Primary pneumococcal peritonitis is much more common. The patient is often anundernourished girl between 3 and 6 years of age, and itisprobable that the infectionsometimes occurs via the vagina and Fallopian tubes, for pneumococci have beencultured from patients’ vaginas. At other times, and always in males, the infection is

blood-borne from the upper respiratory tract or the middle ear. After the age of10years pneumococcal peritonitis is most unusual. Children with nephritis are moreliable to this condition than others. During the past 30 years the instance of

pneumococcal peritonitis has declined greatly and the condition is now rare.Clinical features. The onset is sudden and the earliest symptom is pain localised to thelower half of the abdomen. The temperature is raised to 39.80Cor more and there isusually frequent vomiting. After 24—48 hours profuse diarrhoea, occasionally blood-stained, is characteristic.There is usually increased frequency of micturition. The lasttwo symptomsare due to severe pelvic peritonitis. Herpes on the lip or nostril is often

present. In acute forms of the disease, even in cases where there is no involvement of a lung, there is a tinge of cyanosis of the lips and cheeks and movement of the alaenasi is often discernible. On examination rigidity is usually bilateral but is less than inmost cases of acute appendicitis with peritonitis.Differential diagnosis. A leucocytosis of 30000/mm3 (30 x 109/litre) or more withapproximately 90 per cent polymorphs suggests pneumococcal peritonitis rather thanappendicitis. Even so, itis often impossible, especially in males to exclude perforatedappendicitis. The other condition which is extremely difficult to differentiate from

primary peritonitis in its early stage is pneumonia. An unduly high respiratory rateand the absence of abdominal rigidity are the most important signs supporting thediagnosis of pneumonia, which is usually clarified by a chest X-ray.Treatment. Early operation is always required. After starting antibiotic therapy andcorrecting dehydration and electrolyte imbalance, a short midline incision is made.The peritoneum is incised. Should the exudate be odourless and sticky, the diagnosisof pneumococcal peritonitis is practically certain, hut itis essential to perform aroutine laparotomy to exclude other lesions. Assuming that no other cause for the

peritonitis is discovered some of the excudate is removed with a syringe and senttothe laboratoryfor culture and sensitivity tests. Thorough peritoneal lavage is carried

out and the incision closed. The patient is returned to bed, and antibiotic and fluidreplacement therapy continued. Nasogastric suction drainage is essential. Recovery isusual.Primary streptococcal peritonitis of infants and childrenPrimary streptococcal peritonitis of infants and children is rather more frequent than

pneumococcal peritonitis but still uncommon. When a streptococcus is the infectingorganism the peritoneal exudate is thin and slightly clouded and contains flecks of fibrin. The clinical presentation and treatment of streptococcal peritonitis in infantsand children are similar to those of pneumococcal peritonitis (see above), hut the mor-tality is higher. An intravaginal foreign body should always be looked for in female

patients.

Idiopathic streptococcal and staphylococcal peritonitis in adults



Idiopathic streptococcal and staphylococcal peritonitis in adults is fortunately rare, for prior to the antibiotic era it was nearly always fatal and the mortality is still very high.Rightly, in early cases the abdomen is opened, usually on a diagnosis of acuteappendicitis. In streptococcal peritonitis the peritoneal exudate is odourless, thin,contains some flecks of fibrin and may he blood stained. In these circumstances pus is

removed by suction, the abdomen closed with drainage and nonoperative treatment of peritonitis performed. Recently the use of intravaginal tampons has led to anincreased incidence of Staphylococcus aureus infections: these can be associated withtoxic shock syndrome’ and disseminated intravascular coagulopathy.Peritonitis following abortion/patturitionThe abortionist has usually pushed an instrument through the uterine vault andstreptococcal peritonitis follows. Peritonitis following puerperal infection is morecommon after first deliveries. Rigidity is seldom much in evidence; this, at any rate in

part, is due to the stretched condition of the abdominal musculature. The lochia mayhe offensive but not necessarily so. Diarrhoea is common.Treatment. Provided the infection is limited strictly to the pelvis, the correct treatmentis to rest the gastrointestinal tract and provide intravenous fluids, the requiredantibiotics and attention to electrolyte balance. Posterior colpotomy may be necessaryif a pelvic abscess forms. If the peritonitis is generalised, the patient is usuallyextremely ill and drainage is advisable. This may be carried out by making a smallsuprapubic incision under local anaesthesia and inserting a drain, which can be donewith the patient in bed, if necessary.In the pre antibiotic era the mortality of general peritonitis following parturitionorabortion was at least 50 per cent; with antibiotic therapy and timely operation, themortality has fallen to less than 10 per cent (Brews).Familial Mediterranean fever (periodic peritonitis)Familial Mediterranean fever (periodic peritonitis) is characterised by abdominal painand tenderness, mild pyrexia, polymorphonuclear leucocytosis and occasionally painin 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, islimited principally to Arabs, Armenians and Jews; other races are occasionallyaffected. The aetiology is unknown. Usually children are affected hut it is not rare for the disease to make its first appearance in early adult life when females outnumber males by two toone. Exceptionally the disease becomes manifest in patients over 40years of age. At laparotomy, which may be necessary to exclude other causes, the

peritoneum —particularly in the vicinity of the spleen and the gall bladder — is

inflamed. There is no evidence that the interior of these organs is abnormal.Colchicine may prevent recurrent attacks.Differential diagnosis. Patients with abdominal epilepsy do not have positive physicalsigns of pyrexia and their attacks are usually controlled by anticonvulsive medication. Tuberculous peritonitisAcute tuberculous peritonitisTuberculous peritonitis sometimes has an onset that resembles so closely acute

peritonitis that the abdomen is opened. Straw-coloured fluid escapes and tuberculesare seen scattered over the peritoneum and greater omentum. Early tubercles aregreyish and translucent. They soon undergo caseation, and appear white or yellow and

are then less difficult to distinguish from carcinoma. Occasionally they appear like patchy fat necrosis. On opening the abdomen and finding tuberculous peritonitis the



fluid is evacuated, some being retained for bacteriological studies. A portion of thediseased omentum is removed for histological confirmation of the diagnosis and thewound closed without drainage.Atother times, although acute abdominal symptoms arise, the presence of ascitesmakes diagnosis of acute tuberculous peritonitis reasonably evident.

Chronic tuberculous peritonitisAlthough the incidence of tuberculous peritonitis has declined in Britain, in many

parts of the world where measures for eradicating tuberculosis (especially the diseasein cows) are enforced less strictly, the condition still occurs. The condition presentswith abdominal pain (90 per cent of cases), fever (60 per cent), loss of weight (60 per cent), ascites (60 per cent), night sweats (37 per cent) and abdominal mass (26 per cent).Origin of the infectionInfection originates from:• tuberculous mesenteric lymph nodes;• tuberculosis of the ileocaecal region;• a tuberculous pyo salpinx;• blood-borne infection from pulmonary tuberculosis, usually the ‘miliary’ butoccasionally the ‘cavitating’ form.Varieties of tuberculous peritonitisThere are four varieties of tuberculous peritonitis: ascitic, encysted, fibrous and

purulent.Ascitic formThe peritoneum is studded with tubercules and the peritoneal cavity becomes filledwith pale, straw-coloured fluid. The onset is insidious. There is loss of energy, facial

pallor and some loss of weight. The patient is usually brought for advice because of enlargement of the abdomen. Pain is often completely absent; in other cases there isconsiderable abdominal discomfort which may be associated with constipation or diarrhoea. On inspection, dilated veins can be seen coursing beneath the skin of theabdominal wall. Shifting dullness can be elicited readily. In the male child congenitalhydroceles sometimes appear, due to the patent procesus vaginales becoming filledwith ascitic fluid from the peritoneal cavity. Because of the increased intra-abdominal

pressure an umbilical hernia commonly occurs. On abdominal palpation a transversesolid mass can often be detected. This is rolled-up greater omentum infiltrated withtubercules.Diagnosis is seldom difficult except when itoccurs in an acute form or when it firstappears in an adult, in which case it has to be differentiated from other forms of

ascites, especially from malignant secondary deposits. A positive Mantoux test in achild with ascites strongly suggests, and a negative test is good evidence against,tuberculosis. In adults this test is of negligible value. Laparoscopy is useful byallowing inspection of the peritoneal cavity, where the appearance is often diagnostic.Areas of caseation can be biopsied for histology and microbiological studies. The‘open’ (Hassan) technique of trocar insertion should be used because of the risk of adhesions to the abdominal wall. The diagnosis of tuberculous peritonitis having beenmade, it is always important to look for tuberculous disease elsewhere. The possibilityof tuberculous salpingitis in females should be remembered. A chest X-ray shouldalways be taken before laparoscopy or laparotomy is performed.The ascitic fluid is pale yellow, usually clear and rich in lymphocytes. The specific

gravity is comparatively high, often 1.020 or over. Even after centrifugation, rarely



can M.tuberculosis be found, but its presence can be demonstrated by culture or byguinea-pig inoculation.Treatment. See guidelines, Chapter 8. If the general condition is good, the patient canreturn home and, if an adult, to light work, before the course of chemotherapy has

been completed.

Encysted formEncysted (syn. loculated) form is similar to the above, but one part of the abdominalcavity alone is involved. Thus, a localised intra-abdominal swelling is producedwhich gives rise to difficulty in diagnosis. In a female above the age of puberty whenthe swelling is in the pelvis, an ovarian cyst will probably be diagnosed. In the case of a child it is sometimes difficult to distinguish the swelling from a mesenteric cyst. For these reasons laparotomy is often performed, and if an encapsulated collection of fluidis found, it is evacuated and the abdomen is closed. The general treatment alreadydetailed is required, but the response to this treatment is more rapid. Late intestinalobstruction is a possible complication.Fibrous formFibrous (syn. plastic) form is characterised by the production of widespreadadhesions, which cause coils of intestine, especially the ileum, to become mattedtogether and distended. These distended coils act as a ‘blind loop’ and give rise tosteatorrhoea, wasting and attacks of abdominal pain. On examination, the adherentintestine with omentum attached, together with the thickened mesentery, may giverise to a palpable swelling or swellings. The first intimation of the disease may besubacute or acute intestinal obstruction. Sometimes the cause of the obstruction can

be remedied easily by the division of bands. Lateral anastomosis between anobviously dilated loop and a collapsed loop of small intestine should not be done, asthe ‘blind loop’ syndrome is a certain outcome. If the adhesions are accompanied byfibrous strictures of the ileum as well it is best to excise the affected bowel, providednot too much of the small intestine needs to be sacrificed. If adhesions only are

present a plication may be performed (see Chapter 58). Chemotherapy after adequatesurgery will rapidly cure the condition.Purulent formThe purulent form is rare. When it occurs, usually it is secondary to tuberculoussalpingitis. Amidst a mass of adherent intestine and omentum, tuberculous pus is

present. Sizeable cold abscesses often form, and point on the surface, commonly near the umbilicus, or burst into the bowel. In addition to prolonged general treatment,operative treatment may be necessary for the evacuation of cold abscesses and

possibly for intestinal obstruction. If a faecal fistula forms it usually persists because

of distal intestinal obstruction. Closure of the fistula must therefore be combined withsome form of anastomosis between the segment of intestine above the fistula and anunobstructed area below. The prognosis of this variety of tuberculous peritonitis isrelatively poor.Peritoneal bands and adhesionsCongenital bands and membranes. Congenital bands and membranes occur in the

peritoneum at various sites as described in textbooks of anatomy. Intestinalobstruction is rarely seen except by an obliterated vitellointestinal duct.Peritoneal adhesions. Peritoneal adhesions are abnormal deposits of fibrous tissue thatform after peritoneal injury. They follow operation or peritonitis and are thecommonest cause of small bowel obstruction and secondary female infertility in

developed countries. They are discussed in detail in Chapter 58.



Talc granuloma. Talc (silicate of magnesium) should never be used as a lubricant for rubber gloves for itis a cause of peritoneal adhesions and granulomas in the Fallopiantubes. Potassium bitartrate which is completely soluble is free from these seriouscomplications.Starch peritonitis. Like talc, starch powder has found disfavour as a surgical glove

lubricant. In a few starch-sensitive patients it causes a painful ascites, fortunately of limited duration. Should laparotomy be performed any small granulomas in, say, theomentum will be found to contain birefringent starch particles. Starch-free surgicalgloves are now widely available AscitesAscites, an excess of serous fluid within the penitoneal cavity, can be recognisedclinically only when the amount of fluid present exceeds 1500 ml; in the obese agreater quantity than this is necessary before there is clear evidence of the presence of intrapenitoneal fluid. Ultrasound and CT scanning can detect much smaller volumesof ascitic fluid.Mechanism of ascitesThe balanced effects ofplasma and peritoneal colloid osmotic and hydrostatic

pressures determine the exchange offluid between the capillaries and the peritonealfluid. Normal intrapenitoneal pressure and normal peritoneal fluid colloid osmotic

pressure cannot be measured. Protein rich fluidenters theperitoneal cavitywhencapillary permeability to protein 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. Capillary pressure israised selectively in the portal venous system in the Budd—Chiari syndrome,cirrhosis of the liver or extra-hepatic portal venous obstruction (see Chapter 52).Plasma colloid osmotic pressure may be lowered in patients with reduced nutritionalintake, diminished intestinal absorption, abnormal protein losses, or defective proteinsynthesis as occurs in cirrhosis. Peritoneal lymphatic drainage may be impairedresulting in the accumulation of protein-rich fluid.Clinical featuresThe 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 largeaccumulation of fluid this sign is absent. In such cases, on flicking the abdominalwall, a characteristic fluid thrill is transmitted from one side to the other. In women,ascites must be differentiated from an enormous ovarian cyst. The causes of ascitesare listed in Table 56.7.

Congestive heart failure, the commonest cause of ascites, causes increased venous pressure in the vena cava and consequent obstruction to the venous outflow from theliver. This increased pressure can be seen as engorgement of the veins of the neck — a striking sign in this condition. The ascitic fluid is light yellow and of low specificgravity, about 1.010, with a low protein concentration (<25 g/litre). Patients withconstrictive pericarditis (syn. Pick’s disease) have both penitoneal and pleuraleffusions due to engorgement of the venae cavae consequent upon the diminishedcapacity of the right side of the heart.In cirrhosis there is obstruction to the portal venous system which is caused byobliterative fibrosis of the intrahepatic venous bed. Lymph flow may be increased. Inthe Budd—Chiari syndrome (Chapter 52), 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 due to excessive exudationof fluid and lymphatic blockage. The fluid is dark yellow and frequently bloodstained. The specific gravity, 1.020 or over, and the protein content (>25g/litre) arehigh. Microscopical examination often reveals cancer cells especially if largequantities of fluid are ‘spun-down’ to produce a concentrated deposit for sampling.

Ascites occurs with low plasma albumin concentrations; for example in patients withalbuminunia or starvation. The ascites in this instance is due to alterations in theosmotic pressure of the capillary blood, and has a low specific gravity.Rarely ascites and pleural effusion are associated with solid fibroma of the ovary(Meigs’ syndrome). The effusions disappear when the tumour is excised.TreatmentAscites may be tapped (paracentesis abdominis) but unless other measures are taken,the fluid soon reaccumulates and repeated tappings remove valuable protein.Treatment of the specific cause is undertaken whenever possible, for example if portalvenous pressure is raised, it may be possible to lower it by treatment of the primarycondition (Chapter 52). Dietary sodium restriction to 200 mg per day may be helpful

but diuretics are usually required.Paracentesis abdominisThe bladder having been emptied by a catheter, under local anaesthesia puncture of the peritoneum is carried out with a moderate sized trocar and cannula at one ofthe

pointsshown in Fig. 56.12. Alternatively a peritoneal drain may be inserted under ultrasound guidance to minimise the risk of visceral injury. In cases where theeffusion is due to cardiac failure the fluid must be evacuated slowly. In other circumstances this precaution is unnecessary. If the cannula becomes blocked withfibrin it is cleared with a stylet or the drain is flushed. After the fluid has beenevacuated the puncture is sealed and a tight hinder is applied to the abdomen. Somesurgeons prefer to perform the ‘tap’ over the liver beneath the costal margin or in themidline beneath the xiphisternum.Permanent drainage of ascitic fluidIn rare cases where ascites accumulates rapidly after paracentesis and the patient isotherwise fit, permanent drainage of the ascitic fluid via a peritoneovenous shunt (e.g.LeVeen) may render the patient more comfortable. Similar in concept to shunts for hydrocephalus (Chapter 35), a catheter (e.g. of silicone) is constructed with a valve soas 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 manualcompression. Insertion is relatively simple. The complications include overloading thevenous system, cardiac failure and disseminated intravascular coagulopathy. The

frequency of these complications may he reduced by evacuating ascitic fluid and partially replacing itwith normal saline at the time of shunt insertion. The proceduremay also be used forpatients with terminal malignant ascites giving improved qualityof life, despite the risk of further dissemination of malignant cells.Chylous ascitesIn some patients the ascitic fluid appears milky due to an excess of chylomicrons(triglycerides). Most cases are associated with malignancy, usually lymphomas; other causes are cirrhosis, tuberculosis, filariasis, nephrotic syndrome, abdominal trauma(including surgery), constrictive pericarditis, sarcoidosis and congenital lymphaticabnormality. The condition is rare. The prognosis is poor unless the underlyingcondition can be cured. In additionto other measures used to treat ascites, patients

should be placedon a fat-free diet with medium-chain triglyceride supplements.Peritoneal loose bodies (peritoneal mice)



Peritoneal loose bodies almost never cause symptoms. One or more may be found in ahernial sac or in the pouch of Douglas. Theloose body may come from an appendixepiploica that has undergone axial rotation followed by necrosis of its pedicle anddetachment, 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.

Neoplasms of the peritoneumCarcinoma peritonei is a common terminal event in many cases of carcinoma of thestomach, colon, ovary or other abdominal organs and also of the breast and bronchus.The peritoneum, both parietal and visceral, is studded with secondary growths, andthe penitoneal cavity becomes filled with clear, straw-coloured or blood-stainedascitic fluid.The main forms of penitoneal 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,sometimes, to a ‘frozen pelvisGravity probably determines the distribution of free malignant cells within the

penitoneal cavity. Cells not caught in penitoneal folds along the attachments of mesenteries gravitate into the pelvic pouches or into a hernial sac, enlargement of which is occasionally the first indication of the condition. Implantation occurs also onthe greater omentum, the appendices epiploicae and the inferior surface of thediaphragm. It is remarkable how often patients riddled with intraperitoneal carcinoma

preserve their nutrition and look and feel comparatively well until the terminal stage.Differential diagnosisEarly discrete tubercles common in tuberculous peritonitis are greyish and translucentand closely resemble the discrete nodules of penitoneal carcinomatosis, but the latter feel hard when rolled between the finger and thumb, making the differential diagnosistolerably simple. Fat necrosis usually can be distinguished from a carcinomatousnodule by its opacity. Penitoneal hydatids can also simulate malignant disease after rupture of a hydatid cyst, with seeding of daughter cysts.TreatmentAscites due to carcinomatosis of the peritoneum may respond to systemicchemotherapy. In other cases intrapenitoneal chemotherapy with cisplatin, mitomycinC or methotrexate after drainage ofascites may be effective.

Tamoxifen (an oestrogen receptor site competitor) can dramatically reduce ascites dueto breast cancers which are oestrogen dependent.Pseudomyxoma peritoneiThis rare condition occurs more frequently in females. The abdomen is filled with ayellow jelly, large quantities of which are oftenmore or less encysted. The condition isassociated with bothmucinous cystic tumours of the ovary andappendix. Recentstudies suggest that most cases arise from a primary appendiceal tumour withsecondary implantation on to one or both ovaries. It is often painless and there isfrequently no impairment of general health for a long time. Although an abdomendistended with what seems to be fluid that cannot be made to shift should raise the

possibility, 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. Unfortunately



recurrence is usual. Pseudomyxoma peritonei is locally malignant but does not giverise to extraperitoneal metastases. Occasionally the condition responds to radioactiveisotopes or intraperitoneal chemotherapy which may be used in recurrent cases.MesotheliomaAs in the pleural cavity, this is a highly malignant tumour. Asbestos is a recognised

cause. It has a predilection for the pelvic peritoneum,but it is not radiosensitive.Alkylatingagents have given remissions. Benign forms arereported. Recentregimensof multiple chemocytotoxic agents have been reported as curative for early formsof malignant mesothelioma.DesmoidThis is considered under familial adenomatous polyposis (Chapter 57).

Laparoscopy (peritoneoscopy)Laparoscopic surgery has developed rapidly over recent years (Chapter 70).Previously used largely as a diagnostic procedure, laparoscopy with the aid of modernvideo technology is now used to perform many ‘minimally invasive operations (Table56.8).The primary trocar for laparoscopy is inserted using either the ‘open’ or ‘closed’technique. In the latter method a‘pneumopenitoneum’ is created by the insertion of aspecial needle (e.g. Verres’) through which carbon dioxide is delivered. Once the

penitoneal cavity is adequately distended a sharp-ended trocar is inserted ‘blindly’and the laparoscope then introduced. In the ‘open’ method, which is to be preferred, asmall incision (usually subumbilical) is made through the abdominal wall down to the

penitoneum which is opened under direct vision. This reduces the risk of visceralinjury and eliminates the rare major vascular injuries (iliac, vena caval and aortic) thatoccur with the ‘closed’ method.The greater omentumRutherford Morison called the greater omentum ‘the abdominal policeman’ [but it hasnot any feet, i.e. itdoes not move across the abdomen of its own volition, but passivelydue to peristalsis, and itmay bepushed by the movements of the abdominal wall intoan area of immobility (rigidity) where there is local peritoneal irritation]. Relativelylarger and structurally more substantial in the adult than in the child, the discharge of its life-saving constabulary duties becomesmore effective after puberty, and remainsunabated throughout life. The greater omentum attempts, often successfully, to limitintraperitoneal infective and other noxious processes (Fig. 56.13). For instance, an

acutely inflamed appendix is often found wrapped in omentum and this saves many patients from developing diffuse peritonitis. Some sufferers of herniae are also greatlyindebted to this structure, for itoften plugs the neck of a hernial sac and prevents a coilof intestine from entering and becoming strangulated.Apart from a small portion of it becoming gangrenous while performing the last-mentioned duty (strangulated omentocele) this Good Samatitan1 of the peritonealcavity seldom itself becomes diseased; when it does become overwhelmed, as intuberculous peritonitis and carcinomatosis peritonei, it becomes rolled like a scroll.Torsion of the omentum. Torsion of the omentum is a rare emergency andconsequently is seldom diagnosed correctly. It is usually mistaken for appendicitiswith somewhat abnormal signs. It may be primary or secondary to an adhesion ofthe

omentum, to an old focus of infection, or to a hernia. Successive herniations of a



portion of the omentum into a hernial sac of irregular bore are credited with giving thenecessary stimulus to omental torsion.The patient is most frequently a middle-aged, obese male. A tender lump may be

present in the abdomen. The blood supply having been jeopardised, the twisted masssometimes becomes gangrenous, in which case bacterial peritonitis soon follows.

Treatment. The abdomen having been opened, the pedicle above the twist is ligatedsecurely and the mass removed.Omental cyst (see below).

The mesenteryA wound of the mesentery can follow a severe abdominal contusion and is a cause of haemoperitoneum.Seat-belt syndromeIf a car accident occurs when a seat belt is worn, sudden deacceleration can result in atorn mesentery. This possibility should be borne in mind particularly as multipleinjuries may distract attention from this injury. If there is any bruising of theabdominal wall, or even marks of clothing impressed into the skin, laparotomy may

be indicated.Diagnostic peritoneal lavageDiagnostic peritoneal lavage may be helpful in this situation (Chapter 4). Under localanaesthetic a subumbilical incision is made down to the peritoneum in a similar wayto that used for ‘open’ laparoscopy (see above). A purse-string suture is placed in the

peritoneum which is then incised. Free fluid, e.g. blood or intestinal contents, may befound, but if not a peritoneal dialysis catheter is inserted and the purse-string suturetied. A litre of normal saline is run into the peritoneum and then drained off by

placing the bag and tubing below the patient’s abdomen. The presence of blood (>100000 red blood cells/mm3), bile or intestinal contents is an indication for laparotomy.In about 60 per cent of cases, the mesenteric laceration is associated with a rupture of the intestine. If the tear is a large one and especially if it is transverse (Fig.56.14a), the

blood supply to the neighbouring intestine is cut off and a limited resection of gut isimperative. Small wounds and wounds in the long axis (Fig. 56.14b) should besutured. If extensive damage to the mesenteric arcade of vessels is associated withdamage to contiguous intestine, exteriorisation of the damaged segment is preferableto excision and suture.Torsion of the mesenterySee volvulus neonatorum, and volvulus of the small intestine, Chapter 58.

Embolism and thrombosis of mesenteric vesselsSee Chapters 57 and 58. Acute nonspecific ileocaecal mesenteric adenitisAetiology

Nonspecific mesenteric adenitis was so named to distinguish it from specific(tuberculous) mesenteric adenitis. It is nowvery much more common than the tuberculous variety. Despite much investigation theaetiology often remains unknown although some cases are associated with Yersiniainfection of the ileum. In other cases an unidentified virus is blamed. In about 25 per cent of cases a respiratory infection precedes an attack of nonspecific mesenteric

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



There is a small increase in the amount of penitoneal fluid. The ileocaecal mesentericlymph nodes are enlarged and can be seen and felt between the leaves of themesentery. In very acute cases they are distinctly red and many of them are the size of a walnut. The nodes nearest the attachment of the mesentery are the largest. They arenot adherent to their peritoneal coats and if a small incision is made through the

overlying peritoneum, a node is extruded easily.Clinical featuresDuring childhood, acute nonspecific mesenteric adenitis is a common condition. It isunusual after puberty but is sometimes seen in teenage girls. The typical history is oneof short attacks of central abdominal pain lasting from 10 to 30 minutes, andassociated with circumoral pallor. They tend to come on when the patient is tired.Vomiting is common but there is no alteration of bowel habit. If vomiting is absent,itis more likely to be a case of mesenteric adenitis than appendicitis.On examinationThere are spasms of general abdominal colic, usually referred to the umbilicus, withintervals of complete freedom, which never appertains in obstructive appendicitis.The patient seldom looks ill. In more than half of the cases the temperature iselevated; in severe examples it exceeds 38.30C. Abdominal tenderness is greatestalong the line of the mesentery. When present, shifting tenderness is a valuable signfor differentiating the condition from appendicitis. After laying the patient on the leftside for a few minutes, the maximum tenderness moves to the left of the original site.The pelvic penitoneum is tender to rectal palpation in 30 per cent of cases. The neck,axillae and groins should be palpated for enlarged lymph nodes —if these nodes areenlarged, brucellosis should come to mind.Leucocyte countThere is often a leucocytosis of 10000—12000/mm3 (10—12 x 109/litre) or more onthe first day of the attack, but this falls on the second day.TreatmentWhen the diagnosis can be made with assurance, bed rest for a few days is the onlytreatment necessary. If at a second examination, an hour or two after confinement to

bed, acute appendicitis cannot be excluded, it is safer to perform either appendicectomy or diagnostic laparoscopy.Tuberculosis of the mesenteric lymph nodesTuberculous mesenteric lymphadenitis is considerably less common than acutenonspecific lymphadenitis. Tubercle bacilli, usually, but not necessarily, bovine, areingested and enter the mesenteric lymph nodes by way of Peyer’s patches. It is

possible for one draught of raw milk to start the infection; it is equally possible that a

toddler can become infected with human tubercle bacilli by placing one dust-coveredsmall object in its mouth. Sometimes only one lymph node is infected; usually thereare several; occasionally massive involvement occurs.Presentation.Demonstrated radiologically. The shadows cast by one or more calcifiedtuberculous lymph nodes are seen in a plain radiograph of the abdomen. They must bedistinguished from other calcified lesions, e.g. renal or ureteric stones. Their mobilityon repeated plain abdominal radiographs can clinch the diagnosis but orography can

be employed in doubtful cases. Oftenthe shadow cast by such a lymph node or nodesis situated in the ileocaecal region, but nearly as many are displayed along the line of attachment of the mesentery. Usually, the radiological characteristics areunmistakable. Each node is round or oval, not homogeneous, but mottled, and its

outline is not regular, hut bosselated like a blackberry. Calcification of these lymphnodes occurs at the earliest in 18 months. It is often assumed, wrongly, that because a



tuberculous lymph node is calcified, the infection is necessarily defunct. Especially inchildren, this assumption may not be valid.As a cause of general symptoms. The patient, usually a child under 10 years of age,loses appetite, looks pale and there is some loss of weight; sometimes evening pyrexiaoccurs. In children with these symptoms, especially those who live in the country, if

the Mantoux test is negative, brucellosis, the ‘disease of mistakes’ should be thoughtof and serological studies undertaken.As a cause of abdominal pain. Sometimes abdominal pain is the cause of the patient

being brought for advice; usually this pain is central, not severe but rather adiscomfort and is often constant. On examination the abdomen is somewhat

protuberant and there is tenderness on deep pressure to the right of the umbilicus. Inthese circumstances, the condition resembles acute nonspecific mesentericlymphadenitis. On deep palpation inflamed mesenteric lymph nodes are sometimes

palpable as firm, discrete, tender, bean-like objects most frequently to the right of andnear the umbilicus. A normal leucocyte count favours tuberculosis and, in a child, a

positive Mantoux test is confirmatory evidence of tuberculosis.Symptoms indistinguishable from those of appendicitis. On occasions the abdominal

pain is acute and may be accompanied by vomiting. This, combined with tendernessand some rigidity in the right iliac fossa, makes the diagnosis from appendicitisalmost impossible. When, as is sometimes the case, the tuberculous infection of themesenteric lymph nodes becomes reactivated in adolescent or adult life, the diagnosticdifficulties are even greater. A radiograph may show calcified lymph nodes, but assuch a condition can coexist with appendicitis, in some cases laparoscopy or laparotomy is necessary. If the mesentery is found to be in an inflamed state withcaseation of some of the lymph nodes, the diagnosis of active tuberculosis isconfirmed.As a cause of intestinal obstruction. Remote, rather than recent, tuberculousmesenteric adenitis can be the cause of intestinal obstruction. For instance, a coil of small intestine becomes adherent to a caseating node, and is thereby angulated, or afree coil may become imprisoned in the tunnel beneath the site of adherence and themesentery.As a cause of pseudomesentericcyst. When tuberculous mesenteric lymph nodes

break down, the tuberculous pus may remain confined between the leaves of themesentery, and a cystic swelling having the characteristics of a mesenteric cyst isfound. When such a condition is confirmed at operation, the tuberculous pus should

be aspirated without soiling the peritoneal cavity, the wound closed, the sensitivity of the organism should be sought and medical treatment continued until the infection has

been overcome.As ileocaecal lymph nodes.At laparotomy hard, enlarged lymph nodes may be foundlimited to the ileocaecal mesentery as a result of previous tuberculous infection. If thenodes have a yellow colour, they may well arise from a carcinoid tumour of theappendix or ileum (Chapter 57).Treatment. Therapy is similar to that of other tuberculous infections (Chapter 8). Mostcases subside but from time to time a local abscess forms, usually in the right iliacfossa when the tuberculous pus should be evacuated and the abdomen closed withoutdrainage.Mesenteric cystsMesenteric cysts are classified as:

•chylolymphatic;•enterogenous;



•urogenital remnant;•dermoid (teratomatous cyst).Chylolymphatic cyst, the commonest variety of mesenteric cyst, probably arises incongenitally misplaced lymphatic tissue that has no efferent communication with thelymphatic system; it arises most frequently in the mesentery of the ileum. The thin

wall of the cyst, which is composed of connective tissue lined by flat endothelium, isfilled with clear lymph or, less frequently, with chyle varying in consistency fromwatered milk to cream. Occasionally the cyst attains a great size. More oftenunilocular than multilocular, a chylolymphatic cyst is almost invariably solitary,although there is an extremely rare variety in which myriads of cysts are found in thevarious mesenteries of the abdomen. A chylolymphatic cyst has a blood supplyindependent of that of the adjacent intestine, thereby enucleation is possible withoutthe necessity of resection of gut.Enterogenous cyst is believed to be derived either from a diverticulum of themesenteric border of the intestine, which has become sequestrated from the intestinalcanal during embryonic life, or from a duplication of the intestine. An enterogenouscyst has a thicker wall than a chylolymphatic cyst, and itis lined by mucousmembrane, sometimes ciliated. The content is mucinous, and is either colourless or yellowish-brown from bygone haemorrhage into the cyst. As can be seen at operation,the muscle in the wall of an enterogenous cyst and the bowel with which it is incontact have a common blood supply; consequently removal of the cyst always entailsresection of the related portion of intestine.Clinical features of a mesenteric cyst. A mesenteric cyst is encountered mostfrequently in the second decade of life, less often between the ages of 1 and 10 yearsand, exceptionally, in infants under 1 year.The patient presents on account of:•a painless abdominal swelling. A cyst of the mesentery presentscharacteristic physical signs:

— there is a fluctuant swelling near the umbilicus (Fig. 56.15a), — the swelling moves freely in a plane at right angles to the attachment of themesentery (Fig. 56.15b),

— there is a zone of resonance around and, classically, a belt of resonance across thecyst;•recurrent attacks of abdominal pain withor without vomiting. Thepain results fromrecurring temporary impaction of a food bolos in a segment of bowel narrowed by thecyst, or possibly from torsion of the mesentery;•an acute abdominal catastrophe arises as a result of:

—torsion of that portion of the mesentery containing the cyst, — rupture of the cyst, often due to a comparatively trivial accident, — haemorrhage into the cyst, — infection.Radiography. In most instances, the patient should be submitted to a barium meal andfollow through. The hollow viscera will be found to be displaced around the cyst andnot infrequently some portion of the lumen of the small intestine will be narrowed. Inorder to exclude or confirm the diagnosis of a hydronephrosis, an ultrasoundexamination or a urogram should be performed. In cases of painless enlargement of the abdomen, an ultrasound scan should be undertaken first. Needle aspirationcombined with instillation of radio opaque water-soluble contrast media can transform

doubt into certainty.



Treatment. As has been indicated already, many chylolymphatic cysts can beenucleated in toto.When, after aspiration of about half the contents of the cyst, the major portion of thecyst has been dissected free, but one portion abutting on the intestine or a major bloodvessel seems too dangerous to remove, this portion can be left attached and its lining

destroyed by careful diathermy.In the case of an enterogenous cyst, enucleation must not be attempted. If acomparatively short segment of the intestine is involved,resection of the cyst with theadherent portion of the intestine, followed by intestinal anastomosis, is the correctcourse. Should a very large segment of small intestine be implicated, an anastomosisshould be made between the apex of the coil of small intestine and the cyst wallwhich, in this instance, holds sutures well.The older treatment of marsupialisation of a mesenteric cyst has little to recommendit;a fistula or recurrence results. Occasionally, however, on account of its simplicity it isadvisable in a poor-risk subject in whom surgery is necessary.Omental cystsOmental cysts occur nearly as frequently as mesenteric cysts. Preoperativedifferentiation is possible because a lateral radiograph, ultrasound orCT scan showsthe cyst in front of the intestines. Treatment is omentectomy.Cyst of the mesocolonCyst of the mesocolon is uncommon and itis differentiated from a mesenteric cystonly at operation. The treatment is similar.Cysts arising from a urogenital remnantCysts arising from a urogenital (Wolffian or MUllerian) remnant are essentiallyretroperitoneal, hut they are included in the classification because it is not impossiblefor such a cyst to project forward into the mesentery.The following, while not being mesenteric cysts in the true meaning of the term, giverise to the same physical signs and, in practice, they are mesenteric cysts:• serosanguineous cyst is probably traumatic in origin, hut a history of an accident isseldom obtained;•tuberculous abscess of the mesentery;•hydatid cyst of the mesentery.

Neoplasms of the mesenteryMesenteric tumours are classified as:•benign:

— lipoma,

— flbroma, — fibromyxoma;•malignant:

— lymphoma, — secondary carcinoma.Tumours situated in the mesentery give rise to physical signs similar to those of amesenteric cyst, the sole exception being that they sometimes feel solid.A benign tumour of the mesentery is excised in the same way as an enterogenousmesenteric cyst, i.e. with resection of the adjacent intestine. When possible, amalignant tumour of the mesentery is subjected to the same treatment. In inoperablecases, radiotherapy can be employed if the biopsy specimen reveals that the growth is

radiosensitive.The retroperitoneal space



Pus or blood in the retroperitoneal space tends to track to the corresponding iliacfossa. If a retroperitoneal abscess develops, it should be evacuated by the nearestroute through the abdominal wall, avoiding opening the peritoneum. Should theretroperitoneal collection be found at laparotomy, it must be drained by a counter-incision in the flank. Pus frequently develops from a renal or spinal source and is

sometimes tuberculous (‘cold abscess’): tracking can develop alongside the psoasmuscle and appear in the groin, where it must be distinguished from other swellings(e.g. hernia, Chapter 62). Retroperitoneal haematoma may be caused by fracturedspine, a leaking abdominal aneurysm, acute pancreatitis or a ruptured kidney.Retroperitoneal cystA cyst developing in the retroperitoneal space often attains very large dimensions, andhas at first to be distinguished from a hydronephrosis. Even after the latter conditionhas been eliminated by scanning or orography, a retroperitoneal cyst can seldom bediagnosed with certainty from a retroperitoneal tumour until displayed at operation.The cyst may be unilocular or multilocular. Many of these cysts are believed to bederived from a remnant of the Wolffian duct, in which case they are filled with clear fluid. Others are teratomatous and are filled with sebaceous material.Excision of these and other retroperitoneal swellings is best performed through atransperitoneal incision.Idiopathic retroperitoneal fibrosisThis is one of a group of fibromatoses (others being Dupuytren’s contracture andPeyronies disease). Most cases are idiopathic, hut many causes are known (Table56.9). Familial cases are known, involving mediastinal fibrosis, sclerosing cholangitis,Riedel’s thyroiditis and orbital pseudotumour. An autoimmune link has not beendemonstrated. Extensive collagen deposition surrounds the ureters, mostly at the levelof the pelvic brim or below. Most patients present with ureteric obstruction, oftenwith renal failure (Chapter 64): cases due to malignancy are treated appropriatelyaccording to the cause, but the prognosis is often poor.Primary retroperitoneal neoplasms arising from connective tissuesRetroperitoneal lipoma, in the first instance, is usually mistaken for a hydronephrosis,a diagnosis which is ruled out by ultrasonography, CT scan or orography. Women aremore often affected. These swellings sometimes reach an immense size. Aretroperitoneal lipoma sometimes undergoes myxomatous degeneration, acomplication which does not occur in a lipoma in any other part of the body.Moreover, a retroperitoneal lipoma is often malignant (liposarcoma) (Fig. 56.16) andmay increase rapidly in size.Retroperitoneal sarcoma presents signs similar to a retroperitoneal lipoma. The patient

may seek advice on account of a swelling or because of indefinite abdominal pain. Onother occasions the tumour, by pressure on the colon, causes symptoms of subacuteintestinal obstruction. On examination a smooth fixed mass, which is not tender, is

palpated. The most probable original diagnosis is that of a neoplasm of the kidney.This is ruled out by scanning or orography. The ureter, however, is liable to becomedisplaced by the tumour. Exploratory laparotomy should be performed and when

possible the tumour is removed. Often it is found widely disseminated in theretroperitoneal space, rendering complete removal impossible, in which case a portionis excised for microscopy. Even when excised at a comparatively early stage,recurrence always takes place, and these rumours must he looked upon as beingnecessarily fatal. Radiotherapy sometimes keeps recurrences in abeyance for a time.

Removal of a retroperitoneal cyst or neoplasm. After the anterior abdominal wall has been opened and the diagnosis of a retroperitoneal tumour has been confirmed, the



incision is extended as necessary. The small intestine is packed away in the upper abdomen or exteriorised and the caecum and the sigmoid colon are relegated to their respective fossae. The posterior peritoneum is then incised throughout its length over the area to be exposed, the incision being parallel to the left border of the aorta. The

peritoneum is dissected from the tumour which is removed as completely as possible.

Retroperitoneal tumours arising from specific organsThese may arise from:• lymph nodes (Chapter 17);•adrenal gland (Chapter 45);•kidney and ureter (Chapter 64);•nervous tissue (Chapter 34). Further reading

Jenkins, M.P, Alvaranga, J.C. and Thomas, J.M. (1996) The management of retroperitoneal soft tissue sarcomas.European Journal of Cances32A, 622—6.Krukowski, Z.H. and Matheson, N.A. (1983) The management of peritoneal and

parietal contamination in abdominal surgery. British Journal of Surgery, 10, 440.Paterson-Brown, S. (ed.) (1997) Emergency Surgery and Critical Care, WB.Saunders, London.Press, O.W, Press, N.O. and Kaufman, S.D. (1982) Evaluation and management of chylous ascites. Annals of Internal Medicine, 96, 358.Trentner, K.-H. and Schumpelick, V (eds) (1997) Peritoneal Adhesions,Springer,Berlin.

56.peritoneum,omentum,mesentry and retro peritoneal space

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