PERITONITIS

Prepared by
Dr brian c mawalla
 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

 Theclinical 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
 Anorexiais 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
 Feverwith 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”
0
 Febrile T>38 C
 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, highcost, 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 infact the preoperative preparation
of the patient which include:-
◦ Oxygen therapy
◦ Fluid resuscitation
◦ Nasogastric decompression
◦ Antibiotics
◦ Steroids
◦ Analgesics
 Oxygen therapy
 Is vitalfor 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

 Everyattempt 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 useof 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
 MWISHO

ASANTEN SANA KWA

KUNISIKILIZA