Acute peritonitis

Most cases of peritonitis are due to an invasion of the peritoneal cavity by bacteria, so that when the term ‘peritonitis’ is used without qualification, bacterial peritonitis is implied. Bacterial peritonitis is usually polymicrobial, both aerobic and anaerobic organisms being present. The excep­tion is primary peritonitis (‘spontaneous’ peritonitis) in which a pure infection with streptococcal, pneumococcal or haemophilus bacteria occurs.

Bacteriology

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, 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 in disease, e.g. gallstones. Peritoneal infection is usually caused by two or more bacterial strains. The commonest are Escherichia coli, aerobic and anaerobic streptococci, and the bacteroides. Less frequently Clostridium welchii is found; still less frequently staphylococci or Klebsiella pneumonlae (Friedländer’s bacillus). Gram-negative bacteria contain endotoxins (lipopolysaccharides) in their cell walls which have multiple toxic effects on the host, primarily by causing the release of tumour necrosis factor (TNF) from host leucocytes. Systemic absorption of endotoxin may produce endotoxic shock with hypotension and impaired tissue perfusion. Other bacteria such as C. welchii produce harmful exotoxins.

Bacteroides are commonly found in peritonitis. These Gram-negative, nonsporing organisms, although predominant in the lower intestine, often escape detection because they are strictly anaerobic, and slow to grow on culture media unless there is an adequate carbon dioxide tension in the anaerobic apparatus (Gillespie). In many laboratories, the culture is discarded if there is no growth in 48 hours. 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 diminished greatly.

Nongastrointestinal causes of peritonitis

Nongastrointestinal causes of peritonitis include chlamydia, gonococcus, beta-haemolytic streptococcus, pneumococcus and Mycobacterium tuberculosis. Since the advent of antibiotics haemolytic streptococcal peritonitis has lost many of its dreaded lethal properties. In young girls and women, pelvic infection via the Fallopian tubes is responsible for a high proportion of ‘nongastrointestinal’ infections but bacteroides is also found in the female genital tract.

Immunodeficient patients, for example those with human immunodeficiency virus (HIV) infection (the acquired immunodeficiency syndrome AIDS) or on immunosuppressive treatment, 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 (Table 56.3).

Even in patients with nonbacterial 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, and it is not long (often a matter of hours) before a bacterial peritonitis develops. Most duodenal perforations are initially sterile 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 peritonitis

Anatomical, pathological and surgical factors may favour the localisation of peritonitis.

Anatomical

The 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 supracolic and an infracolic compartment by the transverse colon and transverse mesocolon, which deter the spread of infection from one to the other. When the supracolic compartment overflows, as is often the case when a peptic ulcer perforates, it does so over 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 directing collections into the pelvis, as in the ‘Sherren’ regime for perforated appendicitis.

Pathological

The clinical course is determined in part by the manner in which adhesions form around the affected organ. 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 and to the parieties. There is an outpouring of serous inflammatory exudate rich in leucocytes 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 in preventing distribution of the infection. The greater omen-turn, by enveloping and becoming adherent to inflamed structures, often forms a substantial barrier to the spread of infection.

Surgical

Drains 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 peritonitis

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

Speed of peritoneal contamination is a prime factor in the spread of peritonitis. If an inflamed appendix (Fig. 56.1) or other hollow viscus perforates before localisation has taken place, there is a gush of contents into the peritoneal cavity which may spread over a large area almost instantaneously. Perforation proximal to an obstruction, or from sudden anastomotic separation, is associated with severe generalised 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 remained localised.

The virulence of the infecting organism may be so great as to render the localisation of infection difficult or impossible.

Young children have a small omentum.

Disruption of localised collections may occur with injudicious and rough handling, e.g. appendix mass or pericolic abscess.

Deficient natural resistance (‘immune deficiency’) may

result from drugs (e.g. steroids), disease (e.g. AIDS) or old age.

Clinical features

Localised peritonitis

Localised peritonitis is bound up intimately with the causative condition and the initial symptoms and signs are those of that condition. When the peritoneum becomes inflamed the temperature, and especially the pulse rate, rise. Abdominal pain increases and usually there is associated vomiting. The most important sign is guarding and rigidity of the abdominal wall over the area of the abdomen which is involved, with a positive ‘release’ sign (rebound tenderness), if inflammation arises under the diaphragm shoulder tip (‘phrenic’) pain may be felt. In cases of pelvic peritonitis arising from an inflamed appendix in the pelvic position or from salpingitis the abdominal signs are often slight, deep tenderness of one or both lower quadrants alone being present, but a rectal or vaginal examination reveals marked tenderness of the pelvic peritoneum. With appropriate treatment localised peritonitis usually resolves. 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 sites within the abdominal cavity. A large collection of bile localised to the subhepatic space can remain dangerously ‘silent’ until a late stage.

Diffuse (generalised) peritonitis

Diffuse (generalised) peritonitis may present in differing ways dependent on the duration of infection.

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. 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 is unaffected, 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 but they 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 temperature changes are variable and can be subnormal.

Late. If resolution or localisation of generalised peritonitis does not occur, the abdomen remains silent and increasingly distends. Circulatory failure ensues, with cold, clammy extremities, sunken eyes, dry tongue, thready (irregular) pulse, and drawn and anxious face (Hippocratic facies, Fig.56.2). The patient finally lapses into unconsciousness. With early diagnosis and adequate treatment, this condition is rarely seen in modern surgical practice.

Diagnostic aids

A 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 entered in one or more quadrants with a sterile needle an or intravenous cannula attached to a syringe 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 is aspirated in a high proportion of patients with intraperitoneal bleeding. When aspiration fails, the introduction of a small quantity of sterile physiological saline, followed after a few minutes by peritoneal aspiration may produce fluid of diagnostic value. Microscopy of the fluid may show neutrophils (indicative of acute inflammation) 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 to demonstrate free air collecting under the diaphragm, a lateral decubitus film is just as useful showing gas beneath the abdominal wall. Serum amylase estimation may uphold the diagnosis of acute pancreatitis provided it is remembered that moderately raised 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 by identifying a cause of peritonitis e.g. perforated appendicitis, acute pancreatitis (Fig. 56.4). Such knowledge may influence operative approach or contraindicate operation.

Treatment

It cannot be stressed too strongly that in any case of doubt, early surgical intervention is to be preferred to a ‘wait and see’ policy; for greaten numbers of patients die from delay 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 patient

Correction of circulating volume and electrolyte imbalance. Patients are frequently hypovolaemic with electrolyte disturbances. The plasma volume must be restored and the 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 also need 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 (‘hyper­alimentation’ or ‘total parenteral nutrition’) is required.

Gastrointestinal decompression. A nasogastnic tube is passed into the stomach and aspirated. Intermittent aspiration is maintained until the paralytic ileus resulting from peritonitis has recovered. Measured volumes of water are allowed by mouth when only 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 not to 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 and urine is known. Additional losses from the lungs, skin, and in faeces are estimated, so that the intake requirements can be calculated and seen to have been administered. Throughout recovery, the haematocrit and serum electrolytes and urea must be checked regularly.

Analgesia. The patient should be nursed in the sitting-up position and must be relieved of pain before and after operation. Once the diagnosis has been made morphine may be given, and continued as necessary. 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 help to prevent basal pulmonary collapse, deep-vein thrombosis and pulmonary embolism.

Vital system support. Especially if septic shock is present, special measures may be needed for cardiac, pulmonary and renal support. Administration of oxygen postoperatively can help to prevent and mitigate the effects of septic shock, especially adult 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 cause

If 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 lavage

In operations for general peritonitis it is essential that after the cause has been dealt with 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 shown to be very effective (Matheson).

Prognosis

With modern treatment diffuse peritonitis carries a mortality of about 10 per cent. The systemic complications and lethal factors are listed in Table 56.4.

Complications of peritonitis

All of the complications of a severe bacterial infection are possible, but the specific abdominal complications of peritonitis are listed in Table 56.5.

Acute intestinal obstruction due to peritoneal adhesions

This usually gives central colicky abdominal pain with evidence of small bowel gas and fluid levels sometimes confined to the proximal intestine on X-ray. Bowel sounds are increased. It is more common with localised peritonitis. It is essential to distinguish this from paralytic ileus.

Paralytic ileus

There is usually little pain and gas-filled loops with fluid levels are seen distributed throughout the small and large intestines on abdominal X-ray. In paralytic ileus, bowel sounds are reduced or absent.

Abscesses

Abscess formation following local or diffuse peritonitis usually occupies one of the situations 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 to thrive; pyrexia (often low-grade), tachycardia, leucocytosis and localised tenderness are also common. Later on a palpable mass may develop. When palpable an intraperitoneal abscess should be monitored by marking out its limitations on the abdominal wall, and meticulous daily examination. More commonly its course is monitored by repeat ultrasound or CT scanning. In the majority of cases with the aid of antibiotic treatment, the abscess or mass becomes smaller and smaller, and finally is undetectable. In others, the abscess fails to resolve, or becomes larger, in which event 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 the general 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 intestinal fistula.

Pelvic abscess

The pelvis is the commonest site of an intraperitoneal abscess because the vermiform appendix 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 peritonitis and is a common sequel of anastomotic leakage following large bowel and rectal surgery. Pus can accumulate in this area without serious constitutional disturbance and unless the patient is examined carefully from day to day, such abscesses may attain considerable proportions before being recognised. The most characteristic symptoms of a pelvic abscess are diarrhoea and the passage of mucus in the stools. It is 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 pelvic abscess. Rectal examination reveals a bulging of the anterior rectal wall which, when the abscess is ripe, becomes softly cystic. Left to nature, a proportion of these abscesses bursts into the rectum, after which the patient nearly always recovers rapidly. If this possible happy termination does not readily occur the abscess should be drained deliberately. In women vaginal drainage through the posterior fornex is often 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 pus can be confirmed by ultrasound or CT scanning or by an aspirating needle introduced through 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 can also be inserted percutaneously or via the vagina or rectum under radiological (ultrasonic or CT) guidance (Fig. 56.7).