Peritonitis&Typhoid

7/27/2019 Peritonitis&Typhoid

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Peritonitis and Typhoid Perforation

Agus Nurtadwiyana, MD, FInaCS

Dept. of Sugery Hasan Sadikin Hospital

Bandung


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Peritoneal cavity

Mesothelium

Total area of peritoneum 1.8m2

Formed by a single layer of mesothelial cells

with an underlying supporting layer of highly

vascularized loose connective tissue

Microvili

Cuboidal and flattened cells


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Peritoneal cavity encompass the potential space

defined by the mesothelial serous membrane

and extends superiorly from the diaphragm tothe pelvis in its most caudad extent

Gap (stomata) between neighboring cuboidal

cells

Peritoneal cavity


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Anatomic locations of various intraperitoneal abscess


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Innervation

Visceral peritoneum

Parietal peritoneum


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Physiology


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Translymphatic clearance and

phagocytosis


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Typhus Abdominalis Phase


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Terminology

ACCP/SCCM Concensus Conference [1]

Systemic Inflammatory Response Syndrome (SIRS)

to a wide variety of severe clinical insults, manifested by two

of more of the following conditions Temp > 380C or < 360C

HR > 90 beats/min

RR > 20 breaths/min or PaCO2 < 32 mmHg WBC > 12000/mm3, or < 4000/mm3 or immature forms (band) > 10%

Sepsis

SIRS to a documented infection

Severe Sepsis / Severe SIRS Sepsis of SIRS associated with organ dysfunction,

hypoperfusion, hypotension but are not limited to lactic

acidosis, oliguria, or acute alteration in mental status

Bone DC, Balk RA, Cerra FG et al. Chest 101: 1644-1655, 1992


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Sepsis / SIRS induced hypotension BP < 90 mmHg or

Reduction of > 40 mmHg from baseline in the absence of

other causes of hypotension

Septic shock / SIRS shock

Subset of severe sepsis / SIRS

Hypotension despite fluid resuscitatioon

Presence of perfusion abnormalities

Multiple Organ Dysfunction Syndrome (MODS)

Presence of altered organ function

Homeostasis cannot be maintained without intervention

Terminology

ACCP/SCCM Concensus Conference [2]

Bone DC, Balk RA, Cerra FG et al. Chest 101: 1644-1655, 1992


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G-CSF

IFN-a

MMP

TGF-bXO

H2O2

HO

O2-

PAF TXA2

PGI2 LTB4

PGE2 Bradykinin

ICAM

VCAMELAM

Selectins

CD18/11

TNF-a

IL-1IL-6

IL-8

IL-10

Pro-inflammatory and anti-inflammatory mediators in sepsis

Cytokines Adhesion molecules

OthersAutocoidsOxygen Radicals

Endotoxin

Nitric

Oxide

Pro-inflammatory and

Anti-inflammatory Mediators


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Inflammatory Processes

Bacteremia

Fungemia

Viremia

Others

Trauma

BurnPancreatitis

Others

Adapted from Bone DC et al, 1992


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PERITONITIS

Introduction

Complex illness that requires coordinated effortsof timely surgical intervention, systemic antibiotic

therapy and supportive critical care management Peritonitis and its sequelae, intraabdominal

abscess frequently associated with activation of

SIRS and MODS Initial management of patients with peritonitis

can avoid subsequent evolution of MOF cascade


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Classification of Intraabdominal Infections

Clinical entity Examples

Primary Peritonitis

No apparent primary GI source

Hematogenous or lymphatic seedings

No disruption of GIT

Monomicrobial

Spontaneous peritonitis in children and

adults

Peritonitis in CAPD

Peritonitis in ascites secondary tohepatic cirrhosis

Secondary Peritonitis

Diffuse or localized (abscess) peritonitis

Originating from a defect in GIT

Usually polymicrobial

Perforation of GIT

Intestinal ischaemia

Perioperative contamination

Anastomotic leak

Abdominal trauma

Leakage from female genital tract


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Classification of Intraabdominal Infections

Clinical entity Examples

Tertiary Peritonitis

Persistent peritonitis with systemicspread in debilitated patients

Frequently attributable to resistent

gram-negative bacilli and yeasts

IAI did not respond to previousoperative efforts

Analogous to nosocomial infection

Modified from Smith J.M.B et al: Intra-abdominal Infections, 2000


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Acute Peritonitis


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Natural history of intraabdominal infection

Contamination

Dissemination

Inflammation

Abscess

Drainage

Tertiary Peritonitis

Resolution Death


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Diagnosis of Peritonitis

History Fever

Pain

Nausea

Physical examination Inspection and auscultation Palpation

Rectal and vaginal examination

Laboratory Tests Leucocytosis / leucopenia

Diff count


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Essential Surgical Principles in the

Management of Peritonitis

( Mortality Dropped 80% 30% )

Immediate operation where possible

Elimination of the source of infection Removal of exudate

No medicines administered into peritoneal cavity

Drains not normally used

Martin Kirschner 1926, Hau 1998


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Management of Acute Peritonitis

1. Initial operation to control primary source ofbacterial contamination

2. Supportive care to maintain systemic

oxygenation and hemodynamics3. Antimicrobial therapy to assist the

inflammatory response in microbial control

4. Careful post-operative clinical surveillance forevidence of residual undrained infection thatmay require second intervention


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Management of Severe Bacterial

Infection and Sepsis

Source Control

Nutrition / MetabolicSupport

Resuscitation &

Physiologic Support


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Source Control

Nutrition / Metabolic

Support Resuscitation &Physiologic Support

1. Remove / Treat Infection

2. Remove / Treat Inflammation

3. Remove Dead Tissue4. Stabilization Injured Tissue

5. Restore Microcirculation

1. Minimize flow-dependent

oxygen consumption

2. Minimize flow-dependent

lactate clearance

1. Achieve Nitrogen Balance

2. Avoid Calorie Overload

3. Avoid Long-Chain Fat Overload

4. Appropriate vitamins, Minerals,Trace Elements


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Treatment of Peritonitis

Type of

Peritonitis

Pathogens Treatment

Primary E.coli, Klebsiella sp,

pneumococci

Antibiotics alone

Must be sure of the diagnosis

No anaerobs and not a

polymicrobial infection

Secondary Enteric gram-negatives

and obilgate anaerobs

Surgical source control

Drainage and debridement of

peritoneal cavity

Antibiotics against pathogens

Tertiary Resistant gram-negatives(e.g Pseudomonas sp)

enterococci, Candida sp

Mechanical debridement

Frequent reoperations

Meticulous wound care

Antimicrobial therapy

Donald E.Fry : Peritonitis: Management of the Patient with SIRS and MODS,2000

Antibiotics Choices for Treatment of Ac te Bacterial


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Antibiotics Choices for Treatment of Acute Bacterial

Peritonitis Supported by Randomized Clinical Trials

Therapy Dosage Comments

Single Agent

Cefoxitin 1-2g q4-6h Short half-life (45 min)

Low toxicity

Cefotetan 1-2g q12h Longer half-life (3.5h)

Low toxicity

Ceftizoxime 2g q8-12h Excellent gr(-)

Controversial anaerobic

Ampicillin/Sulbactam 3g q6h Short half-life (1h)

Ticarcillin/Clavulanate 3.1g q4-6h Short half-life (1h)

Piperacillin/Tazobactam 3.375g q6h Short half-life (1h)Excellent comprehensive coverage

Imipenem/Cilastatin 0.5g q6h Short half-life (1h)

Excellent coverage

Meropenem 1g q8h Short half-life

Excellent coverage


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Therapy Dosage Comments

Combinations

Aerobic & Anaerobic drugs

Aerobic Choices

Gentamycin 1-2mg/kg q8h Nephrotoxicity, unpredictable

pharmacology, excellent gr(-) coverage

Tobramycin 1-2mg/kg q8h Same as gentamycin

Amikacin 5mg/kg q8h Same as gentamycin

Aztreonam 2g q8-12h Low toxicity, gr(-) coverage suspect

Ciprofloxacin 750mg q12h Low toxicity

Anaerobic ChoicesClindamycin 600-900mg q6h Expensive. Adds gr(+) coverage

Metronidazole 500mg q6h Inexpensive, strictly anaerobic

coverage

Donald E.Fry : MOF, 2000


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Correlation of APACHE-II Score with Mortality in Intraabdominal Infection

( Wittmann et.al 1996 )

0

10

20

30

40

50

60

70

80

90

100

Mortality(%)

0 5 10 15 20 25 30 35

APACHE-II Score


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Conclusions (1)

Peritonitis represents a complex diseaseprocess that requires precise judgement as towhen operation is to be performed and what

operative proceduresApplication of source control with drainage and

debridement are paramount for patient recovery

Administration of systemic antibiotics againstenteric gram-negative rods and obligateanaerobs of human colon is important adjunctivemeasures


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Conclusions (2)

Antibiotic therapy is best executed withaggressive dosing and at earliest possible time

When an abscess or tertiary peritonitis evolve, it

is unlikely that systemic antibiotic therapy is ofprimary value; rather, mechanical elimination ofpus and exudate are the major feature ofsuccessful management

Future developments that aid in augmenting thehost responsiveness will add to the establishedarmamentarium in the management of peritonitis


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Thank

You

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Peritonitis&Typhoid