PERITONITIS

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 FORMAT
• Definition
• Etiology
• Classifications
• Pathophysiology
• Clinical presentation
• Workup
• Management
• Complications
• Prognosis
 DEFINITION
• Can be defined as inflammation of the serosal
membrane that lines the abdominal cavity
and the organs contained therein

• It is inflammation of the peritoneum

• It is one of the most common causes of

surgical emergencies
 AETIOLOGY
• Bacterial [septic] peritonitis
• Chemical [aseptic] peritonitis
• Non bacterial infections
 Bacterial [septic] peritonitis
• Is caused by introduction of bacterial infection
into the peritoneal cavity
• Route of infection
– GI perforation e.g. perforated PUD or
appendicitis
– Exogenous contamination e.g. drains, trauma,
open surgery
– Tansmural bacterial translocation e.g. IBD,
appendicitis, ischaemic bowel
– Female genital tract infection e.g. PID
– Haematogenous spread e.g. septicaemia
 Chemical [aseptic] peritonitis
• Chemical (sterile) peritonitis is caused by
introduction of chemically irritant
substances such as:-
– gastric acid e.g. perforated ulcer
– bile e.g. perforated gall bladder or a
lacerated liver
– Blood e.g. ruptured spleen or ectopic
pregnancy
– Urine e.g. ruptured urinary bladder
– Meconium peritonititis
 Non-bacterial peritonitis
• This is caused by non-bacterial infections of
the peritoneal cavity such as:-
– Fungal peritonitis
– Viral peritonitis
– Chlamydial peritonitis
 CLASSIFICATIONS
• Etiological classification
• Pathological classification
• Anatomical classification
• Clinical classification
 Etiological classification
• Bacterial [septic] peritonitis
– It is caused by introduction of bacterial
infection into the peritoneal cavity
• Chemical [aseptic] peritonitis
– It is caused by introduction of a chemically
irritating materials into the peritoneal cavity
• Non-bacterial peritonitis
– Caused by non-bacterial infection of the
peritoneal cavity
 Pathological classification
• Primary peritonitis
• Secondary peritonitis
• Tertiary peritonitis
 Primary peritonitis
• Refers to spontaneous bacterial invasion of the
peritoneal cavity
• Occurs in the absence of an apparent intra-
abdominal source of infection or pathology
• Occurs without loss of integrity of the GI tract
• Commonly occurs in infancy and early childhood,
in cirrhotic patients and immunocompromised
hosts
• It is a frequent complication of patients with
chronic ascites secondary to cirrhosis or nephrotic
syndrome
• Usually caused by monomicrobial infection
predominantly Streptococcus pneumoniae
 Secondary peritonitis
• Describes peritoneal infections secondary to
intraabdominal lesions, such as perforation of
the hollow viscus, bowel necrosis, nonbacterial
peritonitis, or penetrating infectious processes
• Results from loss of integrity of GI tract:-
– GI perforation
– Anastomotic dehiscence
– Infected pancreatic necrosis
• It is the most common form of peritonitis encountered in
clinical practice today
• Usually caused by polymicrobial infections mainly
aerobes and anaerobes e.g. E.coli and Bacteroides fragilis
 Tertiary peritonitis
• Represents the persistence or recurrence of
peritoneal infection following apparently
adequate therapy of SBP or SP
• Patients with tertiary peritonitis usually present
with an abscess with or without fistulization
• Tertiary peritonitis develops more frequently in
patients with significant preexisting comorbid
conditions and in patients who are
immunocompromised
• Caused by GN and GP bacteria & Fungal infection
 Anatomical classification
• Localized peritonitis
• Diffuse or generalized peritonitis
 Localized peritonitis
• Localized peritonitis refers to loculi of
infection, usually walled-off or contained
by adjacent organs
• Factors favoring localized peritonitis
include:-
– Anatomical factor compartmentalization of
peritoneal cavity
– Pathological factor omentum wall the inflamed
structures
– Surgical factor use of drain help to localize infection
 Diffuse or generalized peritonitis
• Diffuse or generalized peritonitis refers to
spread of infection to the entire peritoneal
cavity
• Factors favoring generalization
– Sudden visceral perforation
– Violent peristalsis
– Injudicious handling of localized collections
– Immunocompromised patient
– Children have small omentum
 Clinical classification
• Acute peritonitis
– Clinical presentation is of sudden onset with
abdominal pain associated with anorexia,
vomiting, fever and abdominal rebound tenderness
and rigidity
– E.g. bacterial peritonitis
• Chronic peritonitis
– Presents with gradual onset of abdominal pain,
low grade fever, abdominal findings and weight
loss
– E.g. TB peritonitis
 PATHOPHYSIOLOGY
• Peritonitis is thought to pass through three
phases:-
– Phase I: Absorption of contaminated peritoneal
fluid
– Phase II: Activation of immune system
– Phase III: Localization of infection by host
defenses
 Phase I: Absorption of contaminated
peritoneal fluid

• Involves rapid absorption of contaminated

peritoneal fluid into systemic circulation
septicemia
• The resultant septicemia predominantly
involves gram negative facultative anaerobes
and is associated with high mortality
Phase II: Activation of immune system
• This involves activation of immune system as
they encounter contaminated peritoneal fluid
• Activation of complement system is a first line
event in peritonitis and involve innate and
acquired immunity
• Peritoneal mesothelial cells secrete pro-
inflammatory mediators which act
synergistically with complement to increase
opsonization and phagocytosis
Phase III: Localization of infection by host
defenses
• Is an attempt by host defenses to localize infection
via production of fibrinous exudates that traps
microbes within its matrix and promotes local
phagocytic effector mechanisms
• It also serves to promote the development of
abscesses
• The plasminogen-activating activity generated by
peritoneal mesothelial cells determines whether
the fibrin produced is lysed or organized into
fibrous adhesions
• TNF- produced by peritoneal mesothelial cells
stimulates the production of plasminogen
activator –inhibitor- 1 which inhibits degradation
of fibrin [inhibits fibrinolytic activity]
ADHESIONS FORMATION
 CLINICAL PRESENTATION
• Stages of clinical features
• History
• Physical examination
 Stages of clinical features

• The clinical features of peritonitis can be

conveniently described under 3 stages:-
– Stage of peritonism /irritation
– Stage of reaction
– Stage of diffuse peritonitis
 Stage I: Stage of peritonism /irritation
• This is due to irritation of peritoneum caused
by perforation or inflamed viscous near about
• The pain is more severe and is made worse by
breathing and movement
• First experienced at the site of the lesion and
gradually spread allover the abdomen
• Two important features for diagnosis at this
stage:-
– Sudden onset of abdominal pain
– Presence of muscle guarding and rebound
tenderness
 Stage II: Stage of reaction
• At this stage irritant fluid becomes diluted
with the peritoneal exudates
• The intensity of symptoms  although the fire
is still burning under the ashes
• The patient feel comfortable
• Muscle rigidity and rebound tenderness 
• There is obliteration of liver dullness and
appearance of shifting dullness at this stage
• Erect abdominal x-ray will reveal gas under
the diaphragm in 70% of cases
Stage III: Stage of diffuse peritonitis
• At this stage the patient has gone a step further
towards the grave
• The pinched and anxious face, sunken eyes and
hollow cheeks [the so called faces hippocritica ] is
quite characteristic of this condition
• There is persistent vomiting, abdominal
distention and board-like rigidity of the
abdomen
• The abdomen becomes silent and increasingly
distended
• The pulse rate rises and become low in volume
• The patient finally collapses into
unconsciousness
 History/symptoms
• Abdominal pain
• Anorexia
• Nausea & Vomiting
• Fever
• Constipation
 Abdominal pain
• Most common symptom
• May be localized or diffuse
• Sudden or gradual onset
• Initially, the pain is often dull and poorly
localized (visceral peritoneum) and then
progresses to steady, severe, and more
localized pain (parietal peritoneum)
• May be referred to the ipsilateral shoulder tip
if the diaphragmatic peritoneum is involved
 Anorexia
• Anorexia is frequently present and may
precede the development of abdominal pain
 Nausea & Vomiting
• Vomiting may occur because of the
underlying visceral organ pathology (ie,
obstruction) or secondary to the peritoneal
irritation
 Fever
• Fever with temperatures that can exceed
38°C is usually present, but patients with
severe sepsis may present with hypothermia
 Constipation
• Is usually present unless a pelvic abscess
develops which can cause diarrhoea
 Physical examination
• General examination
• Abdominal examination
 General examination
• Toxic with “facies hippocratica”
• Febrile T>380C
• Tachycardia
• Shallow breathing
• Hypotension
• Dehydration
• Septic shock
 Abdominal examination
• Distended abdomen
• Failure of the abdomen to move with
respiration
• Tenderness; initially localized  generalized
• Muscle guarding / rigidity
• Rebound tenderness
• Decreased or no bowel sound
• PR and PV also important to rule out Pelvic
abscess /peritonitis
 WORKUP
• Laboratory studies
• Imaging studies
• Diagnostic procedures
 Laboratory studies
• CBC  leucocytosis
• Serum creatinine & electrolytes
• Aspirated peritoneal fluid for microbiological
& biochemical examination
• Arterial blood gas
• Grouping and cross-matching
 Imaging studies
• Plain chest & abdominal radiographs
• Abdominal Ultrasound
• CT scan of the abdomen and pelvis
• MRI
• Contrast studies
Plain chest & abdominal radiographs
• Plain films of the abdomen (eg, supine, erect,
and lateral decubitus positions) are often the
first imaging studies obtained in patients
presenting with peritonitis
• Erect films are useful for identifying free air
under the diaphragm (most often on the right)
as an indication of a perforated viscus
• Distended bowel loops may indicate associated
intestinal obstruction
 Abdominal Ultrasound
• Abdominal Ultrasonography may detect
peritoneal abscesses and increased amounts
of peritoneal fluid (ascites)
• It is operator dependent and does not detect
peritoneal fluid < 100mls
CT scan of the abdomen and pelvis
• Computed tomography (CT) scans of the
abdomen and pelvis remain the diagnostic study
of choice for peritoneal abscess and the related
visceral pathology
• CT scan is indicated in all cases where the
diagnosis cannot be established on clinical
grounds and findings on abdominal plain films
• CT scans can detect small quantities of fluid,
areas of inflammation, and other GI tract
pathology, with sensitivities that approach 100%
• Peritoneal abscesses and other fluid collections
may be aspirated for diagnosis and drained under
CT guidance
 Magnetic resonance imaging
• Magnetic resonance imaging is an emerging
imaging modality for the diagnosis of
suspected intra-abdominal abscesses

• Limited availability, high cost, as well as long

requestion time currently limit its usefulness
as a diagnostic tool in acute peritoneal
infections, particularly for patients who are
critically
 Contrast studies
• Conventional contrast studies are reserved
for specific indications in the setting of
suspected peritonitis or peritoneal abscess
 Diagnostic procedures
• Peritoneal pus aspiration confirm the diagnosis
• Laparoscopy
 MANAGEMENT
• Principles of treatment
• Modalities of treatment
 Principles of treatment
• The general principles guiding the treatment
of intra-abdominal infections are 4-fold:-
– To control the infectious source
– To eliminate bacteria and toxins
– To maintain organ system function
– To control the inflammatory process
 Modalities of treatment
• Conservative
• Surgical treatment
 Conservative treatment
• This in fact the preoperative preparation of
the patient which include:-
– Oxygen therapy
– Fluid resuscitation
– Nasogastric decompression
– Antibiotics
– Steroids
– Analgesics
 Oxygen therapy
• Is vital for all septic shocked patients
• It is administered at the rate of 5l/min to help
the response to the increased metabolic
demand of peritonitis
• Hypoxia can be monitored by:-
– Pulse oximetry
– Measurement of arterial blood gases
 Fluid resuscitation
• Is initially with crystalloid i.v., the volume
being dependent on the degree of shock and
dehydration
• Electrolytes replacement may be required
• The patient should be catheterized in order to
monitor the hourly output of urine
• Monitoring of CVP and the use of inotropes
may be required in severe sepsis or in patients
with co-morbidity
 Nasogastric decompression
• Decompression is performed by NGT to
evacuate the stomach and reduce
accumulation of additional air in the
paralyzed bowel
• NGT alleviates vomiting and abdominal
distension and reduces the risk of aspiration
pneumonia
• Oral feeding is absolutely prohibited till the
bowel sounds, rebound tenderness and rigidity
disappear
 Antibiotics
• Early and appropriate use of antibiotics is
crucial in reducing mortality in patients with
peritonitis
• Antibiotics prevents multiplication of bacteria
and release of endotoxins
• Should be broad-spectrum to cover aerobes
and anaerobes both GN & GP bacteria
• Should be given intravenously
• A 3rd generation cephalosporin,
aminoglycosides and metranidazole is a
common primary strategy
 Steroids

• Recent clinical studies have shown that large

doses of steroids reduce the mortality risk in
suppurative peritonitis
 Analgesics
• The patient should be relieved of pain before
and after operation
• Once the diagnosis has been made, analgesics
must be given and continued postoperatively
• Freedom from pain allows early mobilization
and adequate physiotherapy in the
postoperative period
• Early postoperative mobilization and
physiotherapy prevents basal pulmonary
collapse, DVT and pulmonary embolism
 Operative treatment
• Aimed at to correct the underlying cause

• Every attempt should be made to perform

operation as soon as possible
 Preoperative care
• As for conservative treatment above
 Intra-operative care
• Surgical Incision
• Correction of the underlying pathology
• Peritoneal larvage
• Drainage
• Closure
 Surgical Incision
• Midline vertical incision
• Transverse incision especially in children < 2
years
• Right para-median
 Correction of the underlying pathology
• This depends on the underlying pathology
 Peritoneal lavage
• All peritoneal pus, pseudo -membranes, loosely
adherent fibrins and other exudates should be
completely removed
• Contents of any localized collections or
abscesses should be completely evacuated
• This is called debridement of exudates or
peritoneal debridement
• This is followed by irrigation with warm
normal saline of all parts of the peritoneal
cavity
 Drainage
• The use of drain in generalized peritonitis is
of no benefit because:-
– It interferes with peritoneal defense
mechanism
– It provides access for exogenous bacterial
contamination
• Drain use is of great help in cases of localized
peritoneal fluid collections
 Closure
• Midline incision is closed as a single layer with
polypropylene or nylon taking generous bites
of tissues on either sides
• Transverse and paramedian incisions are
closed in the usual fashion
• The skin and subcutaneous layers of the
wound should be left open
• Delayed primary closure of the skin can be
performed after 4-5 days if the wound remains
healthy
 Post-operative care
• Intravenous fluids
• Nasogastric aspiration
• Antibiotics
• Analgesics
• Monitor:-
– Temperature
– PR
– RR
– Blood gases
 COMPLICATIONS
• Paralytic ileus
• Septic shock
• Intrabdominal residue abscesses
• Intestinal obstruction due to peritoneal
adhesions
• Tertiary peritonitis
 PROGNOSIS
• Predictors of severity include
– Age
– Sex [F>M]
– Peritonitis scoring systems
• APACHE II Score [acute phys and chronic health
score]
• Simplified physiology score
• Sepsis Severity score
• The Mannheim Peritonitis Index score
– Tertiary peritonitis
– Sepsis of upper GI origin
– Failure to clear the source of infection