Dayu Satriya Wibawa

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can be identified as
being :
1. Primary
2. Secondary
3. Tertiary

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• Patients does not have fundamental disease process within the
abdomen that is responsible for the developing infection

• Microbial pathogen has gained access by hematogenous or

lymphatic route

• Most common clinical scenario is patient with hepatic cirrhosis and

ascites

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Patient with primary biliary or enteric disease

Transmural tissue necrosis & perforation

Secondary contamination of the peritoneal sac

Common diseases: Perforated appendix, perforated

gastrointestinal tract malignancies, perforated peptic
ulcer, etc.
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• Patient with chronic fibrinopurulent peel & exudate across the
surface of the visceral and parietal peritoneum associated with
open wound
• Usually infected with hospital-acquired gram-negative organisms

• Required meticulous, daily wound management

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 Type Source of bacteria Pathogens Treatment & Comments

Primary Hematogenous or E. Coli, Antibiotics alone; must be

Lymphatic Klebsiella spp, sure of the diagnosis; no
“seeding” of Pneumococci anaerobes and not
peritoneal cavity polymicrobial infections
Secondary Perforation of Enteric gram- Surgical source control;
viscous or billiary negative drainage and debridement of
tract Obligate anaerobes peritoneal cavity; antibiotics
against pathogens
Tertiary Environment of Resistant gram- Mechanical debridement;
ICU or resistant negatives frequent reoperations;
colonization from meticulous wound care;
the host antimicrobial therapy

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HOST AGENT

ENVIRONMENT

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1. Mechanical clearance of
bacteria via lymphatics
2. Phagocytic killing of bacteria
by immune cells activation
3. Mechanical sequestration

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Bacteria commonly encountered in intraabdominal Infections
Facultative Obligate Anaerobes Facultative
Gram-negative Bacilli Gram-positive Cocci
Eschericia coli Bacteroides fagilis Enterococci
Klebsiella spp Bacteroides spp Staphylococcus spp
Proteus spp Fusobacterium spp Streptococcus spp
Enterobacter spp Clostridium spp
Morganella morganii Peptococcus spp
Pseudomonas Aeruginosa Lactobacillus spp

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1. Level of Gastrointestinal
Perforation
2. Virulence factor

3. Microbial synergy

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1. Adjuvant Substances
 Increase bacterial virulence
 Interfere with host defenses

Factor Effect
Blood Nutritive effect on bacterial growth,
Hgb toxic to WBC
Fibrin Impairs PMN chemotaxis, sequesters bacteria
Fluid Impairs phagocytosis, dilutes opsonin
Bile Lysis of host leucocytes
Urine Opsonin deficient
Chyle Opsonin deficient
Pancreatic Fluid Opsonin deficient
Platelets Impairs bacterial clearance, secondary to
physical obstruction

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2. Foreign Materials
 Impairs phagocytoses
 Induce inflammatory reaction

Macroscopic
Surgical drains
Suture material
Laparotomy sponges
Haemostatic pads/powders
Surgical clips
Prosthetic implants
Microscopic
Barium sulfate
Clothing fibers (introduced during
trauma)
Fecal material
Necrotic tissue
Talcum powder
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 Primarily based on clinical findings
 Appropriate history and the physical
finding of rebound tenderness fulfill the
necessary criteria for establishing
diagnoses
 Laboratory findings are extraordinarily nonspecific
 Imaging generally used for suspected abscess or perforation

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 The standard for acute bacterial peritonitis has four basics
components :

1. Source Control
2. Drainage & debridement
3. Antibiotics
4. Systemic supportive care

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 Carefully planned incision is the beginning

 Materials for aerobic & anaerobic culture of

fluid & infected tissue are obtained
immediately after the abdomen is opened
 Immediate evacuation of all purulent collection
is mandatory
 Contaminated or necrotic material is removed
 The primary disease is then treated

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Oriented toward covering Enteric Gram negative and
Obligate Anaerobes

3 STRATEGIES :
1. Triple-drug therapy
2. Double-drug combinations
3. Single antibiotic preparation

Generally it is desirable to use aggressive dosing strategies when

confronted with patients who have severe bacterial peritonitis

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1. Maximizing
tissue perfusion
2. Adequate oxygen
delivery
3. Nutritional
support

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