Great notes on PERITONITIS

1. MSELEMA
PERITONITIS

2. Learning objectives
 Definition
 Etiology
 Classifications
 Pathophysiology
 Clinical presentation
 Differential diagnoses
 Workup
 Management
 Complications

3. DEFINITION
It is inflammation of the peritoneum (the
serous membrane which lines part of the
abdominal cavity and some of the viscera
it contains).
It is one of the most common causes of
surgical emergencies

4. AETIOLOGY
Bacterial [septic] peritonitis
Chemical [aseptic] peritonitis
Non bacterial infections

5. Bacterial [septic] peritonitis
 Is caused by introduction of bacterial infection
into the peritoneal cavity
 Perforation of a hollow viscus is the most
common cause of peritonitis.
 Examples include perforation of the stomach
(peptic ulcer, gastric carcinoma, of the
duodenum (peptic ulcer), intestine (e.g.
appendicitis, diverticulitis and anastomotic
leakage).
 In most cases of perforation of a hollow viscus,
mixed bacteria are isolated; the most common

6. Bacterial [septic] peritonitis
 Disruption of the peritoneum, even in the
absence of perforation of a hollow viscus, may
also cause infection simply by letting micro-
organisms into the peritoneal cavity.
 Examples include trauma, and surgical wounds,
drains
 Spontaneous bacterial peritonitis (SBP) is a
peculiar form of peritonitis occurring in the
absence of an obvious source of contamination.
 It occurs either in children, or in patients with
ascites.

7. Bacterial [septic] peritonitis
Systemic infections (such as
tuberculosis) may have a peritoneal
localisation.
Tansmural bacterial translocation e.g. IBD,
appendicitis, ischemic bowel
Female genital tract infection e.g. PID

8. 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

9. Chemical [aseptic] peritonitis
It is important to note that, while
these body fluids are sterile at first,
they frequently become infected
once they leak out of their organ,
leading to infectious peritonitis
within 24-48 hours.

10. Non-bacterial peritonitis
This is caused by non-bacterial
infections of the peritoneal cavity such
as:-
Fungal peritonitis
Viral peritonitis
Chlamydial peritonitis

11. CLASSIFICATIONS
Etiological classification
Pathological classification
Anatomical classification
Clinical classification

12. 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

13. Pathological classification
Primary peritonitis
Secondary peritonitis
Tertiary peritonitis

14. Primary peritonitis
 Spontaneous bacterial invasion of the peritoneal cavity
occurring in the absence of an apparent intra-abdominal
source of infection or pathology
 Commonly occurs in :-
 Infancy
 early childhood
 cirrhotic patients
 immunocompromised patients
 Usually caused by monomicrobial infection
predominantly Streptococcus pneumoniae

15. Secondary peritonitis
 Describes peritoneal infections resulting from
loss of integrity of GI tract:-
 GI perforation
 Anastomotic dehiscence
TYPHOID FEVER
 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

16. Tertiary peritonitis
 Represents the persistence or recurrence of
peritoneal infection following apparently
adequate therapy of SBPor Sp
 Tertiary peritonitis develops more frequently in:-
patients with significant preexisting co-morbid
conditions
immunocompromised patients
 Caused by GN and GP bacteria & Fungal
infection

17. Anatomical classification
Localized peritonitis
Diffuse or generalized peritonitis

18. 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

19. 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

20. 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

21. 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

22. Phase I: Absorption of contaminated
peritoneal fluid
 Involves absorption of contaminated
peritoneal fluid into systemic circulation
septicemia
 The resultant septicemia predominantly
involves gram negative facultative anaerobes
and is associated with high mortality

23. 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

24. 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
 TNF- produced by peritoneal mesothelial cells
stimulates the production of plasminogen activator –
inhibitor- 1 which inhibits degradation of fibrin [inhibits
fibrinolytic activity] ADHESIONS FORMATION

25. Clinical staging of peritonitis
The clinical features of peritonitis can
be conveniently described
pathohysiologically under 3 stages:-
Stage of peritonism /irritation
Stage of reaction
Stage of diffuse peritonitis

26. 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

27. 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

28. 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

29. CLINICAL PRESENTATION
History
Physical examination

30. History/symptoms
Abdominal pain
Anorexia
Nausea & Vomiting
Fever
Constipation

31. 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

32. Anorexia
Anorexia is frequently present and
may precede the development of
abdominal pain

33. Nausea & Vomiting
Vomiting may occur because of the
underlying visceral organ pathology (ie,
obstruction) or secondary to the
peritoneal irritation

34. Fever
 Fever with temperatures that can exceed
38°C is usually present, but patients with
severe sepsis may present with hypothermia

35. Constipation
Is usually present unless a pelvic
abscess develops which can cause
diarrhoea

36. Physical examination
General examination
Abdominal examination

37. General examination
Toxic with “facies hippocratica”
Febrile T>38'C
Tachycardia
Shallow breathing
Hypotension
Dehydration
Septic shock

38. 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

39. Peritonitis
Intestinal obstruction
Pancreatitis
Renal colicky
Appendicitis
Ruptured ectopic pregnancy
Pelvic inflammatory disease
Septic abortion
Cystitis

40. WORKUP
Laboratory studies
Imaging studies
Diagnostic procedures

41. Laboratory studies
CBC  leucocytosis
Serum creatinine & electrolytes
Aspirated peritoneal fluid for
microbiological & biochemical
examination
Grouping and cross-matching

42. Imaging studies
Plain chest & abdominal radiographs
Abdominal Ultrasound

43. Plain chest & abdominal radiographs
 They 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

44. 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

45. Diagnostic procedures
Peritoneal pus aspiration confirm the
diagnosis
Laparoscopy

46. MANAGEMENT
Principles of treatment
Modalities of treatment

47. 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

48. Modalities of treatment
Pre operative care/pre-referral
management
Surgical treatment

49. Pre-operative care/pre-referral
management
• Hb,grouping and cross matching
Oxygen therapy if available
Fluid resuscitation
Nasogastric decompression
NPO(Nothing per oral)
Antibiotics
Analgesics
Catheterization
Referral the patient for lapararomy

50. NB
 Amount of intravenous fluid administration
should be given with caution to patients with
cardiac insufficiency.
 Blood Transfusion may be indicated to some
patients depending on the status of anaemia.
 Surgery (laparotomy) is needed to perform a full
exploration and lavage of the peritoneum, as
well as to correct any gross anatomical damage
which may have caused peritonitis.
 This procedure is done at a referral hospital.
The exception is spontaneous bacterial

51. 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

52. 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

53. 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

54. 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

55. 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

56. Operative treatment
 Aimed at to correct the underlying cause
 Every attempt should be made to perform
operation as soon as possible

57. Intra-operative care
Surgical Incision
Correction of the underlying pathology
Peritoneal lavage
Drainage
Closure

58. Surgical Incision
Midline vertical incision
Transverse incision especially in children
< 2 years

59. Correction of the underlying pathology
This depends on the underlying
pathology

60. 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

61. 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

62. Closure
 Midline incision is closed as a single layer with
polypropylene or nylon taking generous bites
of tissues on either sides
 Transverse and para-median 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

63. Post-operative care
Intravenous fluids
Nasogastric aspiration
Antibiotics
Analgesics
Monitor:-
Temperature
PR
RR

64. COMPLICATIONS
 Paralytic ileus
 Septicemia and Septic shock
 Intrabdominal residue abscesses
 Intestinal obstruction due to peritoneal
adhesions
 Anemia