Acute Peritonitis pdf - د. باسم

Baghdad College of Medicine / 4

grade

Student’s Name :

Dr. Basim Rassam
Lec. 3

Acute Peritonitis & intra
abdominal abscesses

Thurs. 19 / 11 / 2015

DONE BY : Ali Kareem

مكتب اشور لالستنساخ

2015 – 2016

Acute Peritonitis Dr. Basim Rassam

19-11-2015

©Ali Kareem 2015-2016

Acute Peritonitis

ACUTE PERITONITIS AND INTRA-ABDOMINAL AND PELVIC
ABSCESSES

INTRA-ABDOMINAL infections result in two major manifestations..

1-early or diffuse infection result in localized or generalized peritonitis.

2-late and localized infection produces.. intra-abdominal and pelvic abscesses.

Learning Objectives

To recognize and understand:

* The clinical features of localized and generalized peritonitis.

* The common causes and complications of peritonitis.

* The principles of surgical management in patients with peritonitis.

* The clinical presentations and treatment of abdominal/pelvic abscesses.

* The clinical presentations of tuberculosis peritonitis.

The Peritoneum:

The peritoneal membrane is conveniently divided into two parts – the visceral
peritoneum surrounding the viscera and the parietal peritoneum lining the other
surfaces of the cavity. The peritoneum had a number of functions.

Summary box .

Functions of the peritoneum

o Pain perception (parietal peritoneum).

Acute Peritonitis Dr. Basim Rassam

19-11-2015

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o  Visceral lubrication.
o  Fluid and particulate absorption.
o  Inflammatory and immune responses.
o  Fibrinolytic activity.

 The parietal portion is richly supplied with nerves and, when irritated,

causes severe pain accurately localized to the affected area. The visceral
peritoneum, in contrast, is poorly supplied with nerves and its irritation
causes vague pain that is usually located to the midline.

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

lining membrane (2m2 in an adult) being nearly equal to that of the skin.
The peritoneal membrane is composed of flattened polyhedral cells
(mesothelium), one layer thick, resting upon a thin layer of fibroblastic
tissue. Beneath the peritoneum, supported by a small amount of areola
tissue, lies a network of lymphatic vessels and rich plexuses of capillary
blood vessels from which all absorption and exudation must occur. In
health, only a few milliliters of peritoneal fluid is found in the peritoneal
cavity. The fluid is pale yellow, somewhat viscid and contains lymphocytes
and other leucocytes; it lubricates the viscera, allowing easy movement and
peristalsis.

 In the peritonea space, mobile gas-filled structures float upwards, as does

free air(„gas‟). In the erect position, when free fluid is present in the
peritoneal cavity, pressure is reduced in the upper abdomen compared with
the lower abdomen. When air is introduced, it rises, allowing all of the
abdominal contents to sink.

 During expiration, intra-abdominal pressure is reduced and peritoneal fluid,

aided by capillary attraction, travels in an upward direction towards the
diaphragm. Experimental evidence shows that particulate matter and
bacteria are absorbed within a few minutes into the lymphatic network
through a number of „pores‟ within the diaphragmatic peritoneum. This
upward movement of peritoneal fluids is responsible for the occurrence of
many subphrenic abscesses.

Acute Peritonitis Dr. Basim Rassam

19-11-2015

©Ali Kareem 2015-2016

 The peritoneum has the capacity to absorb large volumes of fluid: this

ability is used during peritoneal dialysis in the treatment of renal failure.
But the peritoneum can also produce an inflammatory exudates when
injured.

Summary box .

CAUSES OF PERITONIAL INFLAMMATORY EXUDATE..

o  Bacterial infection, e.g. appendicitis, tuberculosis.
o  Chemical injury, e.g. bile peritonitis.
o  Ischemic injury, e.g. strangulated bowel, vascular occlusion.
o  Direct trauma, e.g. operation.
o  Allergic reaction, e.g. starch peritonitis.

 When a visceral perforation occurs, the free fluid that spills into the

peritoneal cavity runs downwards, largely directed by the normal peritoneal
attachments. For example, spillage from a perforated duodenal ulcer may
run down the right parabolic gutter.

 When parietal peritoneal defects are created, healing occurs not from the

edges but by the development of new mesothelial cells throughout the
surface of the defect. In this way, large defects heal as rapidly as small
defects.

Acute Peritonitis

 Most cases of peritonitis are caused by 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.

Acute Peritonitis Dr. Basim Rassam

19-11-2015

©Ali Kareem 2015-2016

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, whereas high
concentrations are found in the colon. However, disease (e.g. obstruction,
achlorhydria, diverticulitis) may increase proximal colonization. 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. Gram-negative bacteria contain end toxins
(lip polysaccharides) in their cell walls that have multiple toxic effects on
the host, primarily by causing the release of tumor necrosis factor (TNF)
from host leucocytes. Systemic absorption of end toxin may produce end
toxic shock with hypotension and impaired tissue perfusion. Other bacteria
such as Clostridium wheelchair produce harmful serotoxins.

 Bactericides are commonly found in peritonitis. These Gram-negative, non-

sporing organisms, although predominant in the lower intestine, often
escape detection because they are strictly anaerobic and slow to growth 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 greatly diminished.

Non- gastrointestinal caused of peritonitis

o Pelvic infection via the fallopian tubes is responsible for a high proportion

of “non- gastrointestinal” infections.

o Immunodeficient patients, for example those with human immunodeficiency

virus (HIV) infection or those on immunosuppressive treatment, may present
with opportunistic peritoneal infection, e.g. Mycobacterium avium –
intracellulare (MAI).

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Summary box .

Bacteria in peritonitis

1- Gastrointestinal source

o  Escherichia coli
o  Streptococci (aerobic and anaerobic)
o  Bacteroides
o  Clostridium
o  Klebsiella pneumonia
o  Staphylococcus

2-  Other sources
3-  Chlamydia
4-  Gonococcus
5-  β-Haemolytic streptococci
6-  Pneumococcus
7-  Mycobacterium tuberculosis

Route of infection

o Infecting organisms may reach the peritoneal cavity via a number of

routes

Summary Box.

Paths to peritoneal infection

o  Gastrointestinal perforation, e.g. perforated ulcer, diverticular perforation.
o  Exogenous contamination, e.g. drains, open surgery, trauma.
o  Transmural bacterial translocation (no perforation), e.g. inflammatory

bowel disease, appendicitis, ischaemic bowel.

o Female genital tract infection, e.g. pelvic inflammatory disease.
o Haematogenous spread (rare), e.g. septicaemia.

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 Even in patients with non-bacterial peritonitis (e.g. acute pancreatitis,

intrapertioneal rupture of the bladder or haemoperitoneum), the peritoneum
ofter 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 and many gastric perforations are also sterile at first;
intestinal perforations are usually infected from the beginning. The
proportion of anaerobic to aerobic organisms increase with 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.

Localized peritonitis

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

Anatomical

 The greater sac of the peritoneum is divided into (1) the subphrenic, spaces

(2) the pelvis and (3) the peritoneal cavity proper. The last is divided into a
supracolic and an infrasonic compartment by the transverse colon and
transverse mescaline, which deters 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 infrasonic
compartment or by way of the right parabolic gutter to the right iliac fosse
and hence to the pelvis.

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

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cause loops of intestine to become adherent to one another and to the
parietals. There is an outpouring of serous inflammatory exudates rich in
leucocytes and plasma proteins that soon becomes turbid; if localization
occurs, the turbid fluid becomes frank pus. Peristalsis is retarded in affected
bowel and this helps to prevent distribution of the infection. The greater
momentum, 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 localization (and

exit) of intra-abdominal collections: their value is disputed. They may act as
conduits for exogenous infection.

Diffuse peritonitis

 A number of factors may favour the development of diffuce peritonitis:

 Speed of peritoneal contamination is a prime factor. If an inflamed

appendix . or other hollow viscus perforates before localization 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 rate.

 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, which is less effective in

localizing infection.

 Disruption of localised collections may occur with injudicious

handling, e.g. appendix mass or pericolic abscess.

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19-11-2015

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 Deficient natural resistance (“immune deficiency “) may result from

use of drugs (e.g. steroids), disease { e.g. acquired immune deficiency
syndrome(ADIS)} 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 increase and usually there is associated vomiting.
The most important sign is guarding and rigidity of the abdominal wall over
the area of the abdomen that is involved, with a positive ”release” sign
(rebound tenderness). If inflammation arises under the diaphragm, shoulder
tip (“phernic”) pain may be felt. In cases of pelvic peritonitis arising from
an inflamed appendix in the pelvic position or from salpingitis, the
abdominal signs are often slight; there may be deep tenderness of one or
both lower quadrants alone, but a rectal or vaginal examination reveals
marked tenderness of the pelvic peritoneum. With appropriate treatment,
localised peritonitis usually resolves; in about 20% of cases, an abscess
follows. Infrequently, localised peritonitis becomes diffuse. Conversely, in
favourable circumstances, diffuse peritonitis can become localised, most
frequently in the pelvis or at multiple sites within the abdominal cavity.

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 found typically when the peritonitis affects the

Acute Peritonitis Dr. Basim Rassam

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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 pluse 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, thread (irregular) pulse and drawn and anxious face (Hippocratic
fancies; The patient finally lapses into unconsciousness. With early
diagnosis and adequate treatment, this condition is rarely seen in modern
surgical practice.

Summary box .

Clinical features in peritonitis

o  Abdominal pain, worse on movement.
o  Guarding/rigidity of abdominal wall.
o  Pain/tenderness on rectal/ vaginal examination (pelvic peritonitis).
o  Pyrexia (may be absent).
o  Raised pulse rate.
o  Absent or reduced bowel sounds.
o

“Septic shock” {systemic inflammatory response syndrome (SIRS) in later
stages.

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Diagnostic aids

 Investigations may elucidate a doubtful

diagnosis, but the importance of a careful
history and repeated examination must
not be forgotten.

 A radiograph 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 radiograph .
If the patient is too ill for an “erect” film
to demonstrate free air under the diaphragm, a lateral decubitus film is just
as useful, showing gas beneath the abdominal wall.

 Serum amylase estimation may establish the diagnosis of acute pancreatitis

provided that it is remembered that moderately raised values are frequently
found following other abdominal catastrophes and operations, e.g.
perforated duodenal ulcer.

 Ultrasound and computerized tomography (CT) scanning are increasingly

used to identify the cause of peritonitis Such knowledge may influence
management decisions

 Peritoneal diagnostic aspiration may be helpful but is usually unnecessary.

Bile-stained fluid indicates a 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.

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©Ali Kareem 2015-2016

Summary box.

Investigations in peritonitis

o  Raised white cell count and C-reactive protein are usual.
o  Serum amylase >4x normal indicates acute pancreatitis.
o  Abdominal radiographs are occasionally helpful.
o   Erect chest radiographs may show free peritoneal gas (perforated viscus).
o   Ultrasound/CT scanning often diagnostic.
o  Peritoneal fluid aspiration (with or without ultrasound guidance) may be

helpful.

Treatment

In case of doubt, early surgical intervention is to be preferred to a “wait and see”
policy. This rule is particularly true for previously healthy patients and those with
postoperative peritonitis. Caution is required in patients at high operative risk
because of co morbidity or advanced age.

Treatment consists of:

A- general care of the patient;

B- specific treatment of the cause;

C- peritoneal lavage when appropriate.

A-General care of the patient

1- Correction of circulating volume and electrolyte imbalance.
 Patients are frequently hypovolaemic with electrolyte disturbances. The

plasma volume must be restored and electrolyte concentrations corrected.
Central venous catheterization and pressure monitoring may be helpful,
particularly in patients with concurrent disease. Plasma protein depletion
may also need correction as the inflamed peritoneum leaks large amounts of

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protein. If the patient‟s recovery is delayed for more than 7-10 days,
intravenous nutrition is required.

2- Gastrointestinal decompression
 A nasogastric tube is passed into the stomach and aspirated. Intermittent

aspiration is maintained until the parplytic ileus has resolved. 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.

3- Antibiotic therapy
 Administration of antibiotics prevents the multiplication of bacteria and the

release of endotoxins. As the infection is usually a mixed one, initial
treatment with parenteral broad-spectrum antibiotics active against aerobic
and anaerobic bacteria should be given.

4- Correction of fluid loss

 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
faces 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.

5- Analgesia
 The patient should be nursed in the sitting-up position and must be relieved

of pain before and after operation. If appropriate expertise is available,
epidural infusion may provide excellent analgesia. Freedom from pain
allows early mobilization and adequate physiotherapy in the postoperative
period, which help to prevent basal pulmonary collapse, deep vein
thrombosis and pulmonary embolism.

6- Vital system support
 Special measures may be needed for cardiac, pulmonary and renal support,

especially if septic shock is present.

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B-Specific treatment of the cause

 If the cause of peritonitis is amenable to surgery, operation must be carried

out as soon as the patient is fit for anaesthesia. This is usually within a few
hours. In peritonitis caused by pancreatitis or salpingitis, or in cases of
primary peritonitis of streptococcal or pneumococcal origin, non-operative
treatment is preferred provided the diagnosis can be made with confidence.

C-Peritoneal lavage

 In operations for general peritonitis it is essential that, after the cause has

been dealt with, the whole peritoneal cavity is explored with the sucker and,
if necessary, mopped dry until all seropurulent exudates is removed. The use
of a large volume of saline (1-2 litters) containing dissolved antibiotic (e.g.
tetracycline) has been shown to be effective (Matheson) .

Summary box.

Management of peritonitis

o General care of patient:

  Correction of fluid and electrolyte imbalance.
  Insertion of nasogastric drainage tube.
  Broad – spectrum antibiotic therapy.
  Analgesia.
  Vital system support.

o Operative treatment of cause when appropriate with peritoneal

debridement/lavage.

Prognosis and complications

With modern treatment, diffuse peritonitis carries a mortality rate of about 10%.
The systemic and local complications are shown in Summary boxes.

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Summary boxes .

Systemic complications of peritonitis

o  Bacteraemic/endotoxic shock.
o  Bronchopneumonia/ respiratory failure.
o  Renal failure.
o  Bone marrow suppression .
o  Multisystem failure.

Summary boxes .

Abdominal complications of peritonitis

o  Adhesional small bowel obstruction.
o  Paralytic ileus.
o  Residual or recurrent abscess.
o  Portal pyaemia/liver abscess.

Acute intestinal abstruction due to peritoneal adhesions

 The usually gives central colicky abdominal pain with evidence of small

bowel gas and fluid levels sometimes confined to the proximal intestine on
radiography. 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 intestine on abdominal imaging. In
paralytic ileus, bowel sounds are reduced or absent.

Abdominal and pelvic abscesses

Abscess formation following local or diffuse peritonitis usually accupies one of the
situations shown in The symptoms and signs of a purulent collection may be vague

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and consist of nothing more than lassitude, anorexia and malaise; pyrexia (often
low – grade), tachycardia, leucocytosis, raised C-reactive protein and localised
tenderness are also common

Summary box .

Clinical features of an abdominal/pelvic abscess

o  Malaise
o  Sweats with or without rigors.
o  Abdominal/pelvic (with or without shoulders tip) pain.
o  Anorexia and weight loss.
o  Symptoms from local irritation, e.g. hiccoughs (subphrenic), diarrhea and

mucus (pelvic).

o Swinging pyrexia.
o Localised abdominal tenderness/mass.

Later, a palpable mass may develop that should be monitored by marking out its
limits on the abdominal wall and meticulous daily examination. More commonly,
its course is monitored by repeat ultrasound or CT scanning. In most cases, with
the aid of antibiotic treatment, the abscess or mass gradually reduces in size until,
finally, it 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

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collection should be carried out by cautious blunt finger exploration to minimize
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 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 common after anastomostic leakage following colorectal surgery.
The most characteristic symptoms are diarrhea and the passage of mucus in the
stools. Rectal examination reveals a bulging of the anterior rectal wall, which,
when the abscess is ripe, becomes softly cystic. Left to nature, a proportion of these
abscesses burst into the rectum, after which the patient nearly always recovers
rapidly. If this does not occur, the abscess is definitely pointing into the rectum,
rectal drainage (Fig. 58.6) is employed. If any uncertainty exists, the presence of
pus should be confirmed by ultrasound or CT scanning with needle aspiration if
indicated. Laparotomy is almost never necessary. Rectal drainage of a pelvic
abscess is far preferable to suprapubic drainage, which risks exposing the general
peritoneal cavity to infection. Drainage tubes can also be inserted percutaneously
or via the vagina or rectum under ultrasound or CT guidance .

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Intraperitoneal abscess

Anatomy

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

Left subphrenic space

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

Left subhepatic space/lesser sac

The 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 subphrenic space

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

Right subhepatic space

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

Clinical features

The symptoms and signs of subphrenic infection are frequently non-specific and it
is well to remember the aphorism, “pus somewhere, pus nowhere else, under the
diaphragm”.

Symptoms

A common history is that, when some infective focus in the abdominal cavity has
been dealt with, the condition of the patient improves temporarily but, after an
interval of a few days or weeks, symptoms of toxaemia reappear. The condition of
the patient steadily, and often rapidly, deteriorates. Sweating, wasting and
anorexia are present. There is sometimes epigastric fullness and pain, or pain in
the shoulder on the affected side, because of irritation of sensory fibres in the
phrenic nerve, referred along the descending branches of the cervical plexus.
Persistent hiccoughs may be a presenting symptom.

Signs

A swinging pyrexia is usually present. If the abscess is anterior, abdominal
examination will reveal some tenderness, rigidity or even a palpable swelling.
Sometimes the liver is displaced downwards but more often it is fixed by adhesions.
Examination of the chest is important and, in the majority of cases, collapse of the
lung or evidence of basal effusion or even an empyema is found.

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Investigations

A number of the following investigations may be helpful:

o Blood tests usually show a leucocytosis and raised C-reactive protein.
o 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.

o Ultrasound or CT scanning is the investingation of choice and permits early

detection of subphrenic collections

o Radiolabelled white cell scanning may occasionally prove helpful when

other imaging techniques have failed.

Differential diagnosis

Pyelonephritis, amoebic abscess, pulmonary collapse and pleural empyema may
give rise to diagnostic difficulty.

Treatment

o The clinical course of suspected case is monitored, and blood tests and

imaging investigations are carried out at suitable intervals. If suppuration
seems probable, intervention is indicated. If skilled help is available it is
usually possible to insert a percutaneous drainage tube under ultrasound or
CT control. The same tube can be used to instill antibiotic solutions or
irrigate the abscess cavity. To pass an aspirating needle at the bedside
through the pleura and diaphragm invites potentially catastrophic spread of
the infection into the pleural cavity.

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o If an operative approach is necessary and a swelling can be detected in the

subcostal region or in the loin, an incision is made over the site of masimum
tenderness or over any area where oedema or reness is discovered. The
parietes usually form part of the abscess wall so that contamination of the
general peritoneal cavity is unlikely.

o If no swelling is apparent, the subphrenic spaces should be explored by

either an anterior subcostal approach or from behind after removal of the
outer part of the 12th rib according to the position of the abscess on
imaging. When the posterior approach, the pleura must not be opened and,
after the fibers of the diaphragm have been separated, a finger is inserted
beneath the diaphragm so as to explore the adjacent area. The aim with all
techniques of drainage is to avoid dissemination of pus into the peritoneal or
pleural cavities.

o When the cavity is reached, all of the fibrinous loculi must be broken down

with the finger and one or two drainage tubes must be fully inserted. These
drains are withdrawn gradually during the next 10 days and the closure of
the cavity is checked by sonograms or scanning. Appropriate antibiotics are
also given.

Special forms of peritonitis

Postoperative

o The patient is ill with raised pulse and peripheral circulatory failure.

Following an anastigmatic dehiscence, the general condition of a patient is
usually more serious than if the patient had suffered leakage from a
perforated peptic ulcer with no preceding operation. 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 attributed wrongly to
cardiopulmonary collapse, which is usually concomitant.

o Peritonitis follows abdominal operations more frequently than is realized.

The principles of treatment do not differ from those of peritonitis of other

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origin. Antibiotic therapy alone is inadequate; no antibiotic can stay the
onslaught of bacterial peritonitis caused by leakage from a suture line,
which must be dealt with by operation.

In patients on treatment with steroids

Pain is frequently slight or absent. Physical signs similarly vague and misleading.

In children

The diagnosis can be more diffuclt, particularly in the preschool child. Physical
signs should be elicited by a gentle, patient and sympathetic approach.

In patients with dementia

Such patients can be fractious and unable to give a reliable history. Abdominal
tenderness is usually well localised, but guarding and rigidity are less marked
because the abdominal muscles are often thin and weak.

Bile peritonitis

Unless there is reason to suspect that the biliary tract was damaged during
operation, it is improbable that bile as a cause of peritonitis will be thought of
until the abdomen has been opened. The common causes of bile peritonitis are
shown in Summary box.

Summary box .

Causes of bile peritonitis

o Perforated cholecysitits.
o Post cholecystectomy:

 Cystic duct stump leakage
 Leakage from an accessory duct in the gall bladder bed Bile duct

injury

 T-tube drain dislodgement (or tract rupture on removal)

o Following other operations/ procedures:

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  Leaking duodenal stump post gastrectomy
  Leaking biliary – enteric anastomosis
  Leakage around percutaneous placed biliary drains

o Following liver trauma

Unless the bile has extravasated slowly and the collection becomes shut off from
the general peritoneal cavity, there are signs of diffuse peritonitis. After a few
hours a tinge of jaundice is not unusual. Laparotomy (or laparoscopy) should be
undertaken with evacuation of the bile and peritoneal lavage. The source of bile
leakage should be identified. 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 should be drained as it is too oedematous
to repair, but sometimes it can be covered by a jejunal patch. The patient is often
jaundiced from absorption of peritoneal bile, but the surgeon must ensure that the
abdomen is not closed until any obstruction to a major bile duct has been either
excluded or relieved. Bile leaks after cholecystectomy or liver trauma may be dealt
with by percutaneous (ultrasound – guided) drainage and endoscopic biliary
stenting to reduce bile duct pressure. The drain is removed when dry and the stent
at 4-6 weeks.

Meconium peritonitis

Pneumococcal peritonitis

Primary pneumococcal peritonitis may complicate nephritic syndrome or cirrhosis
in children. Otherwise healthy children, particularly girls between 3 and 9 years of
age, may also be affected, and it is likely that the route of infection is sometimes
via the vagina and fallopian tubes. At other times, and always in males, the
infection is blood-borne and secondary to respiratory tract or middle ear disease.
The prevalence of pneumococcal peritonitis has declined greatly and the condition
is now rare.

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Clinical features

The onset is sudden and the earliest symptom is pain localised to the lower half of
the abdomen. The temperature is raised to 39 0 C or more and there is usually
frequent vomiting. After 24-48 hours, profuse diarrhoea is characteristic. There is
usually increased frequency of micturition. The last two symptoms are caused by
severe pelvic peritonitis. On examination, abdominal rigidity is usually bilateral
but is less than in most cases of acute appendicitis with peritonitis.

Differential diagnosis

A leucocytosis of 30 000µ 1-1 (30 X 109 1-1) or more with approximately 90%
polymorphs suggests pneumococcal peritonitis rather than appendicitis. Even so, it
is often impossible to exclude perforated appendicitis. The other condition that
can be difficult to differentiate from primary pneumococcal peritonitis in its early
stage is basal pneumonia. An unduly high respiratory rate and the absence of
abdominal rigidity are the most important signs supporting the diagnosis of
pneumonia, which is usually confirmed by a chest radiograph.

Treatment

o After starting antibiotic therapy and correcting dehydration and electrolyte

imbalance, early surgery is required unless spontaneous infection of pre-
existing ascites is strongly suspected, in which case a diagnostic peritoneal
tap is useful. Laparotomy or laparoscopy may be used. Should the exudates
be odourless and sticky, the diagnosis of pneumococcal peritonitis
practically certain, but it is essential to careful exploration to exclude other
pathology. Assuming that no other cause for the peritonitis is discovered,
some of the exudates is aspirated and sent to the laboratory for microscopy,
culture and sensitivity tests. Thorough peritoneal lavage is carried out and
the incision closed. Antibiotic and fluid replacement therapy are continued.
Nasogastric suction drainage is essential. Recovery is usual.

o Other organisms are known to cause some cases of primary pneumococcal

peritonitis, the peritoneal in children, including Haemophilus, other
streptococci and a few Gram – negative bacteria. Underlying pathology (

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

Idiopathic streptococcal and staphylococcal peritonitis in adults

Idiopathic streptococcal and staphylococcal peritonitis in adults is fortunately
rare. In streptococcal peritonitis, the peritoneal exudates is odourless and thin,
contains some flecks of fibrin and may be blood- stained. In these circumstances
pus is removed by suction, the abdomen closed with drainage and non-operative
treatment of peritonitis performed. The use of intravaginal tampons has led to an
increased incidence of Staphylococcus aureus infections: these can be associated
with “toxic shock syndrome” and disseminated intravascular coagulopathy.

Familial Mediterranean Fever (periodic peritonitis)

o Familial Mediterranean fever (periodic peritonitis) is characterized by

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

o Usually, children are affected but it is not rare for the disease to make its

first appearance in early adult life, with cases in women outnumbering those
in men by two one. Exceptionally the disease becomes manifest in patients
over 40 years of age. At operation, which may be necessary to exclude other
cases but should be avoided if possible, the peritoneum – particularly in the
vicinity of the spleen the gall bladder- is inflamed. There is no evidence that

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the interior of these organs is abnormal. Colchincine therapy is used during
attacks and to prevent recurrent attacks.

Starch peritonitis

Like talc, starch powder has found disfavor as a surgical glove lubricant. In a few
starch-sensitive

Tuberculous Peritonitis

Acute tuberculous peritonitis

Tuberculous peritonitis sometimes has an onset that so closely resembles acute
peritonitis that the abdomen is opened. Straw-coloured fluid escapes and tubercles
are seen scattered over the peritoneum and greater omentum. Early tubercles are
grayish 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 the diseased omentum is removed for histological confirmation of the
diagnosis and the wound closed without drainage.

Chronic tuberculous peritonitis

The condition presents with abdominal pain (90% of cases), fever (60%), loss of
weight (60%), ascites (60%), night sweats (37%) and abdominal mass (26%)
(Summary box).

Summary box .

Tuberculous peritonitis

o Acute and chronic forms.
o Abdominal pain, sweats, malaise and weight loss are frequent.

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o Caseating peritoneal nodules are common – distinguish from metastatic

carcinoma and fat necrosis of pancreatitis.

o Ascites common, may be loculated.
o Intestinal obstruction may respond to anti-tuberculous treatment without

surgery.

Origin of the infection

Infection originates from:

o tuberculous mesenteric lymph nodes;

o tuberculosis of the ileocaecal region;

o a tuberculous pyosalpinx;

o blood-borne infection from pulmonary tuberculosis, usually the “military”

but occasionally the “cavitating” form.

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Acute Peritonitis Dr. Basim Rassam

19-11-2015