CHAPTER I

INTRODUCTION
Abdominal distress describes the state of the clinic due to emergency in the
abdominal cavity that usually arises suddenly with pain as the main complaint. This
situation requires immediate surgical intervention, for example: perforation, intra-
abdominal hemorrhage, infection, obstruction and gastrointestinal strangulation may
cause perforation resulting in contamination of the abdominal cavity by
gastrointestinal contents resulting in peritonitis.1,4
Inflammation of the peritoneum is a frequent and dangerous complication of
the spread of infection from the abdominal organs (eg appendicitis, salpingitis,
gastroduodenal ulceration), gastroduodenal ulcers, postoperative complications,
chemical irritation, or from penetrating abdominal wounds.4 Under normal
circumstances, the peritoneum is resistant to bacterial infections (in small
inoculation); continuous contamination, virulent bacteria, decreased resistance, and
the presence of foreign body or active digestive enzymes, are the factors that facilitate
the occurrence of peritonitis.8
Peritonitis is one of the most common causes of death in surgical patients with
mortality of 10-40%. Some researchers get this figure to reach 60% or even more than
60%. The decision to take surgery should be taken immediately because any delay
will lead to a disease that results in increased morbidity and mortality. The accuracy
of diagnosis and mitigation depends on the ability to perform anamnesis data analysis,
physical examination and investigation.1,8
In writing this reference will be discussed about the definition, etiology,
pathophysiology, clinical manifestations, management, complications and the
prognosis of peritonitis.

1
 CHAPTER II
LITERARY REVIEW

2.1 Definition
Peritonitis is an inflammation of the peritoneum (the serous membrane lining
the abdominal cavity and covering the abdominal viscera) is a dangerous
complication that can occur in both acute and chronic forms. This condition usually
occurs due to the spread of infection from the abdominal organs, gastrointestinal
perforations, or from penetrating injuries to the abdomen. The organisms that often
infect are organisms that live in the colon (in the case of appendix rupture) which
includes Escherichia coli or Bacteroides. Staphylococci and Streptococci often come
in from outside the peritoneal cavity.1,2

2.2 Anatomy & Physiology

The abdominal wall contains a complex structure of musculo-aponeurosis. At

the rear of this structure is attached to the upper spine in the ribs, and at the bottom of
the pelvic bone. This abdominal wall consists of various layers, from the inside out:
leather layer consisting of cutis and sub-cutis, sub-cutaneous fat and superficial facies
(facies skarpa), then the third abdominal wall muscle m. obliquus abdominis externa,
m. obliquus abdominis internus and m. transversum abdominis, and finally layers of
preperium and peritonium, the transversalis fascia, preperian and peritonium fats. The
muscle in the middle front consists of a pair of rectus abdominis muscles with its
fascia that are in the midline separated by linea alba.1, 2 The abdominal wall forms the
abdominal cavity that protects the contents of the abdominal cavity. The integrity of
the abdominal wall-muscle aponeurosis layer is essential to prevent a congenital,
acquired, or iatrogenic hernia. Another function of abdominal wall muscles is in
respiration also in the process of urination and defecation by elevating intra
abdominal pressure.2

2
 Gambar 1 : Anterior view of abdominal wall muscles and transverse view of abdominal

muscles11

Peritoneum is the largest serous membrane in the body. The peritoneum is

composed of two main parts, the parietal peritoneum, which lining the abdominal
cavity wall and is associated with the muscular fascia, and the visceral peritoneum,
which encompasses all the organs within the cavity. Peritoneum parietale has a
somatic and visceral component that allows the body to localize danger to the
abdomen, which leads to muscular defense and loose pain.1,2 The space that can exist
between these two layers is called peritoneal space or peritoneal cavity. The space
outside is called Spatium Extraperitoneale. In the peritoneal cavity there is a liquid
peritoneum that serves as a lubricant so that the tools can move without causing
significant friction. Excessive peritoneal fluid produced in certain disorders is called
ascites (hydroperitoneum).2 The peritoneal area is approximately 1.8 m2, equal to an
adult skin surface area. The function of the peritoneum is that half of its part has a
semipermiable basal membrane, which is useful for the diffusion of water,
electrolytes, macro, and micro cell. Peritoneum therefore has the ability to be used as
a dialysis medium that is peritoneal dialysis and absorbs brain fluid in peripheral
ventricular shunting operations in the case of hydrochepalus.3,4
Peritonium layer is divided into 3, namely:
1. The sheet that covers the intestinal wall, called the lamina visceralis (serosa
tunica).
2. The coat lining the inner abdominal wall is called the parietal lamina.
3.Lablets that connect the visceral lamina and lamina parietalis.

3
Visceral peritoneum is associated with parietale in the abdominal wall through a
duplicature called mesenterium.1,2,3
The peritoneal cavity in the male is completely covered but in women it has a
connection with the outside world through the uterine, uterine and vaginal tubes.
Spatium Extraperitoneale can be distinguished according to its location, in front
(spatum praepitoneale), behind (spatium retroperitoneale) and below (spatium
subperitoneale). Tools located within the peritoneal cavity are called intraperitoneale
sites, such as the stomach, jejunum, ileum, and spleen. While located behind the
peritoneum is called retroperitoneale as in the kidneys and pancreas.1,3,4
Omentum is a two layer of peritoneum that connects the stomach with other
viscera devices such as the liver (omentum minus), with transverse colon (omentum
majus), and with the spleen (omentum gastrosplenicum). The peritoneum of the small
intestine is called mesenterim, from appendix called mesoappendix of colon
transversum and sigmoideum called transverse mesocolon and sigmoideum.
Mesentery and omentum contain blood vessels and lymph nodes and nerves for the
corresponding viscera.2,3

Picture 2. Peritonium Structure 12

Peritoneum parietale is sensitive to pain, temperature, touch and pressure and

gets innervation from the segmental nerves that also supply the skin and muscles of

4
the outer side. Irritation of peritoneum parietale provides localized pain, but peritoneal
viscerale inseriada does not provide pain.1,2 Peritoneum viscerale is sensitive to strain
and tear but not sensitive to palpation, pressure or temperature.4,5
Abdominal wall bleeding comes from several directions. From the
craniodorsal obtained bleeding from a branch. Intercostalis VI - XII and a. superior
epigastric. From a caudal there is a. iliaca, a. superficial sircumflexa, a. external
pudenda, and a. inferior epigastric. The wealth of this vascularization allows the
incision of the abdomen horizontally and vertically without causing bleeding
disorders. 1, 2, 3 The innervation of the abdominal wall is segmentally segmented by
n.thorakalis VI - XII and n. lumbar. 2

2.3 Etiology
Peritoneal infection can be classified as:
 Primary peritonitis (sponataneous)
Caused by direct hematogenic invasion from peritoneal organs into the
peritoneal cavity itself. The most likely cause of primary peritonitis is
Spontaneous Bacterial Peritonitis (SBP) caused by chronic liver disease.
About 10-30% of cirrhosis patients with ascites will develop bacterial
peritonitis.
Caused by a hematogenous invasion of the peritoneal organ directly from the
peritoneal cavity. Many occur in patients: 3.4
- Hepatic cirrhosis with ascites
- Nephrosis
- SLE
- Bronkopnemonia and pulmonary tuberculosis
- Pyelonephritis
 Secondary peritonitis
Peritonitis following an acute infection or perforation of gastrointestinal
tractus or urinary tract. In general, a single organism will not cause fatal
peritonitis. The synergism of multiple organisms can aggravate the occurrence
of this infection. Anaerobic bacteria, especially Bacteroides species, can
increase the effect of aerobic bacteria in causing infection. 3,4,5
The most common cause of secondary peritonitis is perforative appendicitis,
perforative gaster, duodenal ulcer, perforative colon et causa diverticulitis,

5
 volvulus, cancer and strangulation of the intestines. Main differences of
secondary peritonitis is that the infective bacteria are most likely to be gram-
positive bacteria from upper gastrointestinal tract.
Caused by acute infection of intraperitoneal organs such as:
• Chemical Irritation: Perforation of the gaster, pancreas, gallbladder, liver,
lien, ruptured extra tubal pregnancy
• Bacterial irritation: Perforation of the colon, small intestine, appendix,
ovarian cysts rupture, rupture of the jelly and kidney.
• Penile wounds / trauma, which carry germs from outside inside
peritoneal cavity.

Region of
Etiology
origin
Boerhaave syndrome
Oesophagus Malignancy
Trauma (mostly penetrating)
Peptic ulcer perforation
Malignancy (eg, adenocarcinoma, lymphoma, gastrointestinal
Stomach
stromal tumor)
Trauma (mostly penetrating)
Peptic ulcer perforation
Duodenum
Trauma (blunt and penetrating)
Cholecystitis
Stone perforation from gallbladder (ie, gallstone ileus) or
common duct
Biliary tract
Malignancy
Choledochal cyst (rare)
Trauma (mostly penetrating)
Pancreatitis (eg, alcohol, drugs, gallstones)
Pancreas
Trauma (blunt and penetrating)
Ischemic bowel
Incarcerated hernia (internal and external)
Closed loop obstruction
Small
Crohn disease
bowel
Malignancy (rare)
Meckel diverticulum
Trauma (mostly penetrating)
Ischemic bowel
Diverti
Large culitis
bowel and MalignancyUlcerative colitis and Crohn disease
appendix Appendicitis
Colonic volvulus
Trauma (mostly penetrating)

6
 Pelvic inflammatory disease (eg, salpingo-oophoritis, tubo-
Uterus,
ovarian abscess, ovarian cyst)
salpinx, and
Malignancy (rare)
ovaries
Trauma (uncommon)
Table 1 Etiology of Secondary Peritonitis

 Tertiary peritonitis
Peritonitis with inadequate therapy, superinfective of bacteria, and post-
operative infection are classified as tertiary peritonitis. Inadequately treated
peritonitis, superinfection of germs, and consequent previous surgery. 2.3

2.4 Patophysiology

The initial reaction of the peritoneum to invasion by bacteria is the release of a

fibrinous exudate. The pus pockets (abscesses) are formed between fibrinous
attachments, which adhere together with the surrounding surface to limit infection.
Attachment usually disappears when the infection disappears, but can persist as
fibrous bands, which may later lead to intestinal obstruction.2
Inflammation causes fluid accumulation because capillaries and membranes
leak. If the fluid deficit is not corrected rapidly and aggressively, it can lead to cell
death. The release of various mediators, such as interleukins, can initiate a hyper
inflammatory response, thereby leading to subsequent development of multiple organ
failures. Because the body tries to compensate by means of fluid retention and
electrolytes by the kidneys, the waste products also accumulate. Tachycardia initially
increases cardiac output, but this soon fails as soon as hypovolemia occurs.2,5
The organs inside the peritoneal cavity and the abdominal wall itself then
become edema, which is caused by elevation of capillary vessel permeability of these
organs. The collection of fluids in the peritoneal cavity and intestinal lumen and the
edema of all the intra peritoneal organs and abdominal wall edema including
retroperitoneal tissue leads to hypovolemia. Hypovolemia increases with temperature
rise, reduced food intake, and vomiting.2
The Trapped fluid in the peritoneal cavity and intestinal lumen, further
increases intra-abdominal pressure, making full breathing effort difficult and leading
to decreased perfusion. If the infecting material is widespread on the peritoneal
surface or when the infection spreads, general peritonitis may develop. With the
development of general peritonitis, peristaltic activity decreases until paralytic ileus

7
develops; The gut then becomes atony and stretches. Liquids and electrolytes are lost
into the intestinal lumen, resulting in dehydration, shock, circulatory disorders and
oliguria. Attachment may be formed between intersecting bowls and may interfere
with the restoration of bowel movements and result in intestinal obstruction.1,2,4
Old obstruction of the intestine or intestinal obstruction can cause ileus due to
mechanical disturbance (blockage) then there is an increase in intestinal peristalsis as
an attempt to overcome obstacles. This ileus may be a simple ileus that is an intestinal
obstruction that is not accompanied by a vertebral artery and may be total or partial,
in obstruction of ileus, accompanied by pinched blood vessels resulting in ischemia
which will end with necrosis or gangrene and eventually bowel perforation occurs and
due to bacterial spread abdominal cavity so that peritonitis can occur.5
Typhus abdominalis is an acute infection of the small intestine caused by S.
typhi germs that enter the human body through the mouth from eating and
contaminated water. Some germs are destroyed by stomach acid, some go into fine
and reach lymphoid plaque Payer tissue in hypertrophic terminal ileum where
bleeding complications and intestinal perforation occur, ileal perforation of typhoid
usually occurs in patients with fever for approximately 2 weeks accompanied by
headache, cough and malaise followed by abdominal pain, tenderness, muscular
defense, and generalized degenerative conditions due to toxemia.4,6
The typical peptic ulcer perforation is characterized by the peritoneal
stimulation that begins in the epigastrium and extends throughout the peritoneum, due
to generalized peritonitis. Perforation of the stomach and the front duodenum causes
acute peritonitis. Patients who experience this perforation experience great pain as
being stabbed in the stomach. This sudden pain arises especially in the epigastric
region due to peritoneal stimulation by stomach acid, bile and / or pancreatic
enzymes. Then spread throughout the abdomen causing pain throughout the abdomen
at the beginning of perforation, there is no bacterial infection, sometimes this phase is
called the phase of chemical peritonitis, the pain in the shoulder shows the stimulation
of peritonium in the form of dilution of salt acid that stimulates, this will reduce the
complaint for a while until then peritonitis bacteria.2,3
In appendicitis, peritonitis is caused by obstruction of the appendix lumen by
hyperplasia of the lymphoid follicle, fecal matter, foreign body, stricture due to
fibrosis and neoplasm. The obstruction causes the mucus produced by the mucosa to
have a dam, the longer the mucus increases, but the elasticity of the appendix wall has

8
limitations leading to increased intraluminal pressure and inhibiting lymphatic flow
resulting in edema, bacterial diapedesis, mucosal ulceration and venous obstruction so
that the edema increases later flow disrupted artery will cause an appendix wall
infarction followed by necrosis or gangrene of the wall resulting in perforation and
eventually result in peritonitis both local and general.2.5
In abdominal trauma both abdominal penetrating trauma and abdominal blunt
trauma can result in peritonitis up to sepsis when it comes to organs with intra-
peritoneal hollow. Peritoneal pain rises in accordance with the contents of the hollow
organ, ranging from gastric chemicals to colon containing feces. The fastest onset is
by chemical stimuli and the slowest is by feces. When perforation occurs at the top,
for example, the area of the stomach there will be stimulation immediately after
trauma and will occur symptoms of severe peritonitis whereas if the bottom as a
colon, at first there is no symptom because microorganisms need time to breed new
after 24 hours acute symptoms occur abdomen because of the peritoneal
stimulation.2,4,8

Types of peritonitis:
• Aseptic Peritonitis.
Occurred about 20% of all cases of peritonitis in Indonesia, and usually secondary to
perforated gastric or duodenal ulcers. Sterile peritonitis may develop into bacterial
peritonitis within a few hours following transmigration from microorganisms (eg
from the gut)
• Biliary peritonitis
Relatively rare from sterile peritonitis and can be caused from:
 Iatrogenic (cystic duct ligation during cholesistectomy)
 Acute cholecystitis
 Trauma
 Idiopathic

Other forms of sterile peritonitis, there are 4 causes:

1. Pancreatic fluid
For example from acute pancreatitis, trauma. Pancreatitis may be due to a laparotomy
diagnostic process in patients who have not increased serum amylase.

9
2. Blood.
For example, ovarian cyst rupture, a ruptured aortic aneurysm.
3. Urine
For example intraperitoneal rupture of the bladder.
4. Meconium
Is a sterile mixture of epithelial, mucin, salt,, fat, and biliary cells which are formed
when the fetus begins to swallow the amniotic fluid. Meconium peritonitis develops
slowly in intra-uterine life or in the perinatal period when meconium enters the
peritoneal cavity through inestablished perforation.

• TB peritonitis
Usually occurs in immigrants or immune-compromised patients. Spreads to the
peritoneum through:
1. Directly through lymphatic nodules, ileocaecal region or pyosalping TB.
2. Through blood (blood-borne) infection from pulmonary tuberculosis.
The event may be acute (such as peritonitis in general), and chronic (more specific
onset, with abdominal pain, fever, weight loss, night sweats, abdominal mass).
Macroscopic, there are 4 forms of this disease: ascitic, encysted, plastic, or purulent.
Treatment is based on anti-TB therapy, coupled with laparotomy (if indicated) for
intra-abdominal complications.
• Chlamydial Peritonitis
Fitz Hugh Curtis syndrome can cause pelvic inflammation and is described by right
hipochondrium pain, pyrexia, and hepatic rub.
• Drugs and foreign objects.
In the use of isoniazid, practolol, and intraperitoneal chemotherapy can cause acute
peritonitis. Powder and starch can stimulate the development of granulomata foreign
matter when they meet in the peritoneal cavity (eg surgical gloves).

2.5 Clinical Manifestation

The presence of blood or fluid in the peritonium cavity will provide signs of
peritonium stimulation. Stimulation of the peritonium causes tenderness and muscular
deformity, the liver can disappear from free air under the diaphragm. Bowel
peristalsis decreases until lost due to intestinal paralysis.4

10
 When there has been bacterial peritonitis, the patient's body temperature will
rise and tachycardia, hypotension and patient appear lethargic and shock.4 This
stimulation causes pain in every movement that causes peritoneal shift within the
peritonium. Subjective pain is painful when the patient moves like bumoing on the
road, breathing, coughing, or straining. Objective pain is painful when moved like a
palpation, loose tenderness, psoas test, or other tests.

2.6 Diagnosis
 Physical Examination
On physical examination, it should be noted the general condition, face, pulse,
breathing, body temperature, and patient lying attitude, before performing an
abdominal examination. Symptoms and signs of dehydration, bleeding, shock, and
infection or sepsis also needs attention.1
On physical examination, patients with peritonitis, the condition is generally not
good. Fever with temperature> 380C usually occurs. Patients with severe sepsis
will show symptoms of hypothermia. Tachycardia is caused by the release of
inflammatory mediators and intravascular hypovolemia caused by nausea,
vomitting, fever, large fluid loss from the abdominal cavity. With progressive
dehydration progressing, the patient may become more hypotensive. This can lead
to reduced urine production, and with severe peritonitis may result in septic
shock.8
Inspection: The examiner observes whether any former scar tissue indicates the
possibility of adhesion, a bulging abdomen with an intestinal image or bowel
movement caused by a disruption of the passage. In peritonitis usually will be
found belly bulge and tense or distended.1,2
Auscultation: Conducted to assess whether there is a decrease in bowel sounds.
Patients with general peritonitis, bowel sounds will weaken or disappear
altogether, this is due to peritoneal paralysis that causes the intestine paralytic /
immobilized (paralytic ileus). Whereas in local peritonitis bowel sounds can
sound normal.3.7
Palpation: The parietal peritoneum is innervated by highly sensitive somatic and
visceral nerves. The antitruous part of the peritoneum parietal is the most
sensitive. Palpation should always be performed in other parts of the abdomen that
are not complained of pain. It is useful as a comparison between the non-painful

11
part and the pain. Tenderness and muscular deformity (rigidity) suggest an
inflammatory process that affects peritoneum parietal (somatic pain). Pure defense
are the process of muscle reflex will be felt on inspiration and expiration in the
form of muscle contraction reaction to stimulus pressure.3,5
Abdominal wall muscles show reflexive muscular defense to protect inflamed
parts and avoid local movement or pressure.1.5
Percussion: Tapping pain indicates the irritation of the peritoneum. The presence
of free air or free liquids can also be determined by percussion through the
examination of liver and shifting dullness. In patients with peritonitis, liver
deafness disappears, and hypertrophy abdominal percussion due to the free air.7,8
In patients with abdominal pain complaints should generally be done rectal
examination and vaginal examination to help the diagnosis.1.7 Diffused pain in the
peritoneal folds of the Douglas cavity provides less information on pure
peritonitis; pain on one side suggests malformations in the pelvic area, such as
appendicitis, abscess, or adnexitis. Pain in all directions shows general peritonitis.
Anal shapes can also distinguish between intestinal obstruction with intestinal
paralysis, because the paralysis found widening ampoules, while the bowel
obstruction of the bowel usually collapses. Vaginal examination adds information
to possible abnormalities in the genitals in women.1,2
 Radiologic Examination
Radiological examination is the investigation for consideration in estimating
patients with acute abdomen. In peritonitis, a plain abdominal 3 positions are
taken, namely: 5.8
1.Supine, supine, rays from vertical direction with anteroposterior projection
(AP).
2. Sit or half-sit or stand where possible, with horizontal AP projection rays.
3. Left to left (left lateral decubitus = LLD), with horizontal light, AP projection.
The radiological features of peritonitis are: visible blur of the abdominal cavity,
preperitonial fat and psoas line disappear, and the presence of subdial or
peritoneal free air.2,8
 Laboratory Examination
1. Complete Blood, usually found leukocytosis, increased hematocrit

12
 2. BGA, indicates metabolic acidosis, where carbon dioxide levels are caused by
hyperventilation.
3. In TB peritonitis, peritoneal fluid contains many proteins (more than 3 grams /
100 ml) and many lymphocytes; tubercle bacilli identified with culture.
Perinoneum per cutaneous or laparoscopic peritoneal biopsy shows typical
tuberculoma granuloma, and is a diagnostic basis before the culture results are
obtained.2,10

 Differential Diagnosis
The differential diagnosis of peritonitis are: appendicitis, pancreatitis,
gastroenteritis, cholecystitis, salpingitis, and impaired ectopic pregnancy.4

2.7 Treatment
 Conservative
The general principle of treatment is to rest the gastrointestinal tract by: 9
- Satisfy the patient
- Gastrointestinal decompression by nasogastric or intestinal suction
- Substitute for lost electrolyte fluid intravenously
- Provision of appropriate antibiotics
- Disposal of septic focus (appendix) or cause of other inflammation
1. Giving oxygen
It is vital for all patients with shock. Hypoxia can be monitored by pulse oximetry
or BGA.4
2. Fluid resuscitation
Usually with crystalloid, its volume is based on the degree of shock and
dehydration. Replacement of electrolytes (usually potassium) is usually required.
The patient should be catheterized to monitor the output of urine every hour.
Monitoring of central venous pressure and inotropic use should be used in patients
with sepsis or comorbid patients. Hypovolemia occurs because large amounts of
fluid and electrolytes move from the intestinal lumen into the peritoneal cavity
and lower the crypt into the vascular space.4,9
3. Analgesic
Intravenous opiate analgesics are used and may be needed antiemetics.4

13
4. Antibiotics
Must be broad spectrum, which concerns both aerobic and anaerobic, given
intravenously. Cephalosporin III generation and metronidazole are primary
strategies. For patients receiving peritonitis in the hospital (eg by anastomose
leak) or who are currently receiving intensive care, second-line therapy is
recommended either Meropenem or a combination of Piperacillin and
Tazobactam. Antifungal therapy should also be considered to protect against
possible exposure to Candida species. 4.5
 Definitive
Surgery
1. Laparotomy
Usually performed upper or lower midline incision depending on the inferred
location. The goal is: 9.10
- To eliminate the peritonitis causation
- To control the origin of sepsis by removing inflammatory or ischemic organs (or
perforated viscous closure).
- Peritoneal lavage
Controlling the primary source of sepsis is very important. Re-laparotomy plays
an important role in the treatment of patients with secondary peritonitis, which,
after primary laparotomy, worsens or sepsis develops. Re-operation can be done
as needed. A planned re-laparotomy is usually made by opening the abdominal
wall with a synthetic scalpel to prevent evisceration.
However, studies show that five year survival rates in hospitals and long-term, are
higher in re-laparotomy than in the planned re-laparotomy. Examination is
supported by CT scan. Keep in mind that not all sepsis patients are laparotomized,
but also require mechanical ventilation, antimicrobial, and organ support.
Addressing the problem and control of sepsis during surgery is very important
because most surgeries result in increased morbidity and mortality.
2. Laparoscopy
The theory that the risk of malignancy in hypercalcemia and septic shock in
absorption of carbon dioxide and endotoxins through inflamed peritoneum has not
been proven. However, laparoscopy is effective in the treatment of acute

14
 appendicitis and perforation of duodenal ulceration. Laparoscopy may be used in
cases of colonic perforation, but the conversion rate to laparotomy is greater.
Shock and ileus are contraindicated in laparoscopy.9
3. Drainage
Effectively used in localized sites, but quickly attached to the wall so that it often
fails to reach the peritoneal cavity. There are many occasions that allow the use of
drain as prophylaxis after laparotomy.

Picture 3. Drainage treatment of Peritonitis

2.8 Complication
1. Shock Sepsis1,10
Patients need intensive treatment in ICU
2. Intraabdominal abscess or persistent abdominal sepsis. 10.11
In signs of sepsis (pyrexia, leukocytosis), examination should include CT with
luminal contrast (especially if there is in-situ anastomosis). Re-laparotomy is required
when there is generalized peritonitis. Percutaneous drainage with the best antibiotic
option is a therapy in a localized setting. Antibiotic therapy is adapted to the culture
drawn from the drainage. Abdominal sepsis results in a mortality of 30-60%. Factors
affecting mortality rates are:
-Age
- Chronic illness

15
- Women
- Sepsis in upper gastrointestinal area
- Failure to get rid of sepsis sources.
3. Adhesion
May cause intestinal or volvulus obstruction.

2.9 Prognosis
The prognosis for local and mild peritonitis is good, whereas in general peritonitis the
prognosis is lethal due to virulent organism.1

16
 CHAPTER III
CONCLUSION
Peritonitis is an inflammation of the peritoneum (the serous membrane lining
the abdominal cavity and covering the abdominal viscera) is a dangerous
complication that can occur in both acute and chronic forms. This condition usually
occurs due to the spread of infection from abdominal organs, gastrointestinal
perforations, or from penetrating abdominal injuries.1,2
The presence of blood or fluid in the peritoneal cavity will provide signs of
peritoneal stimulation. Peritoneal stimulation causes tenderness and muscular
deformities, the liver can disappear from free air under the diaphragm. Bowel
peristalsis decreases until lost due to intestinal paralysis.4 The decision to take surgery
should be taken immediately because any delay will lead to a disease that results in
increased morbidity and mortality. The accuracy of diagnosis and mitigation depends
on the ability to perform an analysis of history data, physical examination and
investigation.
Management of peritonitis are: gastrointestinal decompression by nasogastric
or intestinal suction, fluid replacement and electrolytes lost intravenously, appropriate
antibiotics, and removal from the focus of infection of the abdominal organs. The
prognosis for local peritonitis is good, whereas for general peritonitis is bad.

17
 BIBLIOGRAPHY
1. Wim de jong, Sjamsuhidayat.R. 2011 Buku ajar Ilmu Bedah. Edisi 3. Jakarta :
EGC.
2. Schwartz, Shires, Spencer. 2000.Peritonitis dan Abses Intraabdomen dalam
Intisari Prinsip – Prinsip Ilmu Bedah. Edisi 6. Jakarta : EGC. Hal 489 – 493
3. Schrock. T. R.. 2000.Peritonitis dan Massa abdominal dalam Ilmu Bedah,
Ed.7, alih bahasa dr. Petrus Lukmanto, EGC, Jakarta.
4. Arief M, Suprohaita, Wahyu.I.K, Wieiek S, 2000, Bedah Digestif, dalam
Kapita Selekta Kedokteran, Ed:3; Jilid: 2; p 302-321, Media Aesculapius
FKUI, Jakarta.
5. Wim de jong, Sjamsuhidayat.R, 1997.Gawat Abdomen, dalam Buku ajar
Ilmu Bedah; 221-239, EGC, Jakarta.
6. Price, Sylvia. 2005.Patofisiologi Konsep Klinis Proses-Proses Penyakit. Edisi

6. Jakarta : EGC.

7. Philips Thorek, Surgical Diagnosis,Toronto University of Illnois College of

Medicine,third edition,1997, Toronto.
8. Rasad S, Kartoleksono S, Ekayuda I.1999.Abdomen Akut, dalam Radiologi
Diagnostik, Hal 256-257, Gaya Baru, Jakarta.
9. Rotstein. O. D., Simmins. R. L., 1997, Peritonitis dan Abses Intra-abdomen
dalam Terapi Bedah Mutakhir, Jilid 2, Ed.4, alih bahasa dr. Widjaja Kusuma,
Binarupa Aksara, Jakarta
10. Rosalyn Carson-De Witt MD, Peritonitis Health Article,
http://www.css/healthlinestyles.v1.01.css
11. Putz R & Pabst R. 2007. Atlas Anatomi Manusia:Sobotta, jilid.2.Jakarta
:EGC
12. http://www.google.co.id/imgres?q=peritoneum+anatomy&hl=en&biw=1024
&bih=456&tbm=isch&tbnid=kVlqe7wt9F-
yUM:&imgrefurl=http://www.radiologyassistant.nl/en/p4a252c5303035/perit
oneum-and-mesentery-part-i-anatomy.html&docid=__fv5Xl60-
q7gM&imgurl=http://www.radiologyassistant.nl/data/bin/a5097979750a1d_o
verzicht.jpg&w=500&h=503&ei=dgxHUZCqDY7zrQfbv4DQBw&zoom=1

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&sa=X&ved=0CHAQhBwwCA&ved=1t:3588,r:8,s:0,i:112&iact=rc&dur=24
50&page=1&tbnh=176&tbnw=175&start=0&ndsp=10&tx=88&ty=117

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