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Clinical sciense

Disusun Oleh :
session
Ira Tanti Sartika 10100110115015
PERITONITIS

Kartini 10100110115060
Preseptor :
Ira tanti sartika/10100115015
Hj. Liza Nursanti
dr., Sp.B., M.Kes., Fina CS
Kartini/12100115060
Program Profesi Dokter
SMF Ilmu Bedah
Pembimbing
:Hj. Liza
Nursanti,
dr.,
Fakultas
Kedokteran
UNIBSA
RS AL-Islam
Sp. B., M. Kes., FINACS
SMF ilmu bedah
RS AL-ISLAM BANDUNG
2017

Peritoneum
The peritoneum is the
largest and most complex
serous membrane in the
body.
This parietal layer of the
peritoneum reflects onto
the
abdominal
visceral
organs to form the visceral
peritoneum.
It
thereby
creates a potential space
between the 2 layers (ie,
the peritoneal cavity).
Normally, the amount of
peritoneal fluid present is

Peritonitis
Called intra-abdominal infection
Definition : Microbial contamination of the
peritoneal cavity
Classified according to etiology :
Primary microbial peritonitis
Secondary microbial peritonitis
Tertiary microbial peritonitis

SBP occurs in both children


and adults and is a well-known
The overall incidence of
and ominous complication of
cirrhosis.[5]Of patients with
peritoneal infection and
cirrhosis who have SBP, 70%
abscess is difficult to
are Child-Pugh class C. In
establish and varies with
these patients, the
the underlying abdominal
development of SBP is
disease processes.
associated with a poor longEpidemiolo term prognosis.

gy

In patients with ascites,


the prevalence may be
as high as 18%.

Two peak ages for SBP are


characteristic in children:
one in the neonatal period
and the other at age 5
years.

Etiology
The etiology of disease depends on the type, as well
as location, of peritonitis, as follows:

Primary
peritonitis

Secondary
peritonitis

Chemical
peritonitis

Tertiary
peritonitis

Peritoneal
abscess

Pathophysiology Of Peritonitis

Primary Microbial Peritonitis


Occurs when microbes invade the normally sterile
confines
of
the
peritoneal
cavity
via
hematogenous dissemination from a distant
source of infection or direct inoculation
More common :
Patients who retain large amounts of peritoneal
fluid due to ascites,
Individuals who are being treated for renal
failure via peritoneal dialysis
These infections invariably are monomicrobial
and rarely require surgical intervention

Primary Microbial Peritonitis


The diagnosis :
The diagnosis is established based on a patient
who has ascites for medical reasons
Physical examination that reveals diffuse
tenderness and guarding without localized findings
Roentgenograms : absence of pneumoperitoneum
on abdominal flat plate and upright
Paracentesis the presence of more than 100
WBCs/mL, and microbes with a single morphology
on Gram's stain
Patients receiving peritoneal dialysis : the
presence of gram-positive organisms

Primary Microbial Peritonitis


In patients without this risk factor organisms can
include E. coli, K. pneumoniae, pneumococci, and
others, although many different pathogens can be
causative
Treatment :
Treatment consists of administration of an
antibiotic to which the organism is sensitive;
often 14 to 21 days of therapy are required.
Removal of indwelling devices (e.g., peritoneal
dialysis catheter or peritoneovenous shunt) may
be required for effective therapy of recurrent
infections.

Secondary Microbial Peritonitis


Occurs subsequent to contamination of the peritoneal cavity
due to perforation or severe inflammation and infection of an
intra-abdominal organ
Examples : appendicitis, perforation of any portion of the GI
tract, or diverticulitis
Treatment :
effective therapy requires source control to resect or
repair the diseased organ; dbridement of necrotic,
infected tissue and debris; and administration of
antimicrobial agents directed against aerobes and
anaerobes1
This type of antibiotic regimen should be chosen
because in most patients the precise diagnosis cannot
be established until exploratory laparotomy is
performed, and the most morbid form of this disease
process is colonic perforation, due to the large number

Secondary Microbial Peritonitis


A combination of agents or single agents with a broad
spectrum of activity can be used for this purpose; conversion
of a parenteral to an oral regimen when the patient's ileus
resolves will provide results similar to those achieved with IV
antibiotics2
Effective source control and antibiotic therapy is associated
with low failure rates and a mortality rate of approximately 5
to 6%; inability to control the source of infection leads to
mortality greater than 40%3
The response rate to effective source control and use of
appropriate antibiotics has remained approximately 70 to
90% over the past several decades4,5
Patients in whom standard therapy fails develop an intraabdominal abscess, leakage from a GI anastomosis leading
to postoperative peritonitis, or tertiary (persistent) peritonitis

Secondary Microbial Peritonitis

The latter is a poorly understood entity that is more


common in immunosuppressed patients in whom
peritoneal host defenses do not effectively clear or
sequester the initial secondary microbial peritoneal
infection
Today, the vast majority of such abscesses can be
effectively
diagnosed
via
abdominal
computed
tomographic (CT) imaging techniques and drained
percutaneously
Surgical intervention is reserved for those individuals
who harbor multiple abscesses, those with abscesses in
proximity to vital structures such that percutaneous
drainage would be hazardous, and those in whom an
ongoing source of contamination (e.g., enteric leak) is
identified

Secondary Microbial Peritonitis

The necessity of antimicrobial agent therapy and precise


guidelines that dictate duration of catheter drainage
have not been established

A short course (3 to 7 days) of antibiotics that possess


aerobic and anaerobic activity seems reasonable, and
most practitioners leave the drainage catheter in situ
until it is clear that cavity collapse has occurred, output is
less than 10 to 20 mL/d, no evidence of an ongoing
source of contamination is present, and the patient's
clinical condition has improved

Common cause Secondary peritonitis

Common cause Secondary peritonitis

Tertiary peritonitis
Tertiary peritonitis develops more frequently in
immunocompromised patients and in persons
with
significant
preexisting
comorbid
conditions.
Although rarely observed in uncomplicated
peritoneal infections, the incidence of tertiary
peritonitis in patients requiring ICU admission
for severe abdominal infections may be as high
as 50-74%.

Treatment
The general principles guiding the treatment of
infections are 4-fold:
Control the infectious source
Eliminate bacteria and toxins
Maintain organ system function
Control the inflammatory
process

Treatment
The treatment of peritonitis is multidisciplinary,
with complementary application of medical,
operative, and nonoperative interventions.
Medical support includes the following:
Intensive care
with
Systemic
hemodynamic,
antibiotic
pulmonary,
therapy
and renal
support
Nutrition and
metabolic
support

Inflammatory
response
modulation
therapy

Microbiology of Primary, Secondary, and


Tertiary Peritonitis

Microbiology of Primary, Secondary, and Tertiary


Peritonitis

Microbiology of Primary, Secondary, and Tertiary


Peritonitis

Chemical peritonitis

Chemical (sterile) peritonitis may be caused by irritants


such as bile, blood, barium, or other substances or by
transmural inflammation of visceral organs (eg, Crohn
disease) without bacterial inoculation of the peritoneal
cavity.

Clinical signs and symptoms are indistinguishable from


those of SP or peritoneal abscess, and the diagnostic and
therapeutic approach should be the same.

Peritonealabscess

Peritoneal abscess describes the formation of an infected


fluid collection encapsulated by fibrinous exudate,
omentum, and/or adjacent visceral organs.
The overwhelming majority of abscesses occur
subsequent to secondary peritonitis.
Abscess formation may be a complication of surgery.
The incidence of abscess formation after abdominal
surgery is less than 1-2%, even when the operation is
performed for an acute inflammatory process.

Prognosis
Over the past decade, the combination of better
antibiotic therapy, more aggressive intensive care, and
earlier diagnosis and therapy with a combination of
operative and percutaneous techniques have led to a
significant reduction in morbidity and mortality related to
intra-abdominal sepsis.

Daftar pustaka
1. Solomkin JS, Mazuski JE, Baron EJ, et al: Infectious Diseases Society of America: Guidelines for the
selection of anti-infective agents for complicated intra-abdominal infections. Clin Infect Dis 37:997,
2003. [PubMed: 14523762]
2. Solomkin JS, Reinhart HH, Dellinger EP, et al: Results of a randomized trial comparing sequential
intravenous/oral treatment with ciprofloxacin plus metronidazole to imipenem/cilastatin for intraabdominal infections. The Intra-Abdominal Infection Study Group. Ann Surg 223:303, 1996. [PubMed:
8604912]
3. Solomkin JS, Dellinger EP, Christou NV, et al: Results of a multicenter trial comparing
imipenem/cilastatin to tobramycin/clindamycin for intra-abdominal infections. Ann Surg 212:58,
1990.
4. Solomkin JS, Meakins JL Jr., Allo MD, et al: Antibiotic trials in intra-abdominal infections: A critical
evaluation of study design and outcome reporting. Ann Surg 200:29, 1984. [PubMed: 6375597]
5. Solomkin JS, Yellin AE, Rotstein OD, et al: Protocol 017 Study Group. Ertapenem versus
piperacillin/tazobactam in the treatment of complicated intra-abdominal infections: Results of a
double-blind, randomized comparative phase III trial. Ann Surg 237:235, 2003. [PubMed: 12560782]
6. Evans HL, Raymond DP, Pelletier SJ, et al: Tertiary peritonitis is not an independent predictor of
mortality in surgical patients with intra-abdominal infection. Surg Infect 2:255, 2001. [PubMed:
12593701]
7. Lamme V, Mahler CW, van Ruler O, et al: Clinical predictors of ongoing infection in secondary
peritonitis: Systematic review. World J Surg 30:2170, 2006. [PubMed: 17102920]
8. Brian J daley, MD, MBA, dkk. Peritonitis and abdominal sepsis.
http://emedicine.medscape.com/article/180234-overview#a5 dikutip tanggal 11 Oktober 2016

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