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
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
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).