CHAPTER I

INTRODUCTION

Describe the state of emergency abdominal clinic due to gravity in the abdominal cavity

which usually occurs suddenly with pain as a chief complaint. This situation requires an

immediate response is often in the form of surgery, such as in perforation, intra-abdominal

hemorrhage, infection, obstruction and strangulation of the gut can lead to perforation which

resulted in contamination of the abdominal cavity by the contents of the gastrointestinal tract that

occurs peritonitis.

Inflammation of the peritoneum is a dangerous complication that often occurs due to

spread of infection from the abdominal organs (eg, appendicitis, salpingitis, perforated

gastroduodenal ulcers), gastrointestinal rupture, postoperative complications, chemical irritation,

or penetrating injuries abdomen.

In normal circumstances, the peritoneum resistant to bacterial infection (by inoculation of

small-scale); ongoing contamination, bacterial virulence, resistance decreases, and the presence

of foreign objects or active digestive enzymes, are all factors that facilitate the peritonitis.3

The decision to perform surgery should be taken because any delay will cause disease resulting

in increased morbidity and mortality. The accuracy of diagnosis and mitigation depends on the

ability to analyze data on medical history, physical examination and penunjang.3, 7

In writing Referat will be discussed on the handling of peritonitis. Peritonitis is attributed to the

abnormalities in the abdomen in the form of inflammation and penyulitnya, also by obstructive

ileus, ischemia and bleeding. Some disorders are caused by direct or indirect injuries resulting in

gastrointestinal perforation or perdarahan.

CHAPTER II

THEORY and DISCUSSION

II.1.DEFINITION

Peritonitis is inflammation of the peritoneum which is wrapping perut.2 viscera in the

cavity, Peritonitis is an inflammatory or suppurative response of the peritoneum caused by

chemical irritation or bacterial invasion.

The peritoneum is the lamina lateral mesoderm that remain epithelial. At the beginning,

the mesoderm is the wall of a cavity that is coelom. In between the two cavities are entoderm

which is enteron wall. Enteron abdominal region into the intestine. Second cavity mesoderm,

dorsal and ventral colon closer to each other, so that the mesoderm then becomes peritoneum.

Peritoneum is divided into three layers, namely:

1.Fascia that covered the walls of the intestine, called the lamina visceralis (tunica

serosa).

2.Fascia that lines the abdominal wall is called the parietal lamina.

Lamina connecting

3.Fascia visceralis and parietal lamina.

Gazette visceralis lamina connecting the right and left parietal lamina sticking together

and forming a duplex sheet called duplikatura. Thus in both ventral and dorsal colon there is a

duplikatura. Duplikatura connects the intestine with walls of ventral and dorsal abdominal wall

and can be seen as a tool hanger intestines called the mesentery. Mesentery is divided into the

mesentery and mesenteric ventrale dorsale. Ventrale mesentery contained in the next caudal pars

superior duodeni then disappeared. Sheets left and right ventrale mesentery, which still exist, are

united on the edge kaudalnya. Ventrikulus high mesentery called mesogastrium ventrale and

mesogastrium dorsale. At the time perkambangan and growth, ventriculus and intestinal

playback. Enteron gut or in a place associated with the umbilicus and saccus vitellinus. These

relationships form a tube called the ductus omphaloentericus.

Intestinal growing faster than the cavity so that the intestine had occurred twisting-

sepulcher sepulcher. Sepulcher intestine due to intestinal turned to the right by 270 ° with the

axis ductus omphaloentericus and a. superior mesenterica respectively in the ventral wall and the

dorsal abdominal wall. After ductus omphaloentericus disappears, it falls down sepulcher

intestine and mesentery dorsale closer together parietale peritoneum. Because sepulcher intestine

rotates, the colon adjacent to the oral (cranial) sepulcher move to the right and the next anal

(caudal) move to the left and both approach parietale peritoneum.

In places viscerale peritoneum and mesentery dorsale approach dorsale peritoneum, adhesions

occur. However, not all the happening places of attachment. As a result of this attachment, there

are parts that do not have bowel tools hanger again, and is now the so-called retroperitoneal

dorsal peritoneum. The parts that still have the tool hanger is located inside the wall cavity

formed by the peritoneum parietale, called intraperitoneal located. Cavity called the cavum

peritonei, thus:

The duodenum is retroperitoneal; Jejenum and ileum located intraperitoneally with a

hanger mesentery; Colon ascendens and colon descendens located retroperitoneal;

The transverse colon is intraperitoneal and have mounting tool called the transverse mesocolon;

Colon sigmoideum located intraperitoneally with a mesosigmoideum; cecum lies intraperitoneal

due at the beginning of a bulge the walls of the intestines and does not have the tools. Processus

vermiformis located intraperitoneally with a hanger mesentery, a fold of peritoneum due to the

artery leading to the end of the processus vermiformis. He is actually a continuation of the

cecum.

In many places, viscerale peritoneal adhesions in the peritoneum or mesentery parietale

not perfect, resulting in the notches between the colon (covered by peritoneum viscerale) and

peritoneal parietale or between the mesentery and peritoneal parietale restricted folds. The folds

can also terjadfi because it runs the blood vessels. Thus there are at flexura duodenojejenalis

plica superior duodenal recess duodenal limit superior and limit inferior plica duodenal duodenal

resesus inferior.

In the colon there descendens paracolici recess. In the colon there sigmoideum

intersigmoideum recess between the peritoneum and mesosigmoideum parietale.

Stratum circulare coli folds and unfolds so happens plica semilunaris. Peritoneum covering the

colon folds and unfolds out filled with fat, causing the building called epiploicae Appendices.

Ventriculus rotate the longitudinal axis, thus curvatura major in minor curvatura the left and the

right. Then ventriculus play against the sagittal axis, so that the cardia and pylorus move to the

left to the right. Ventriculus because they rotate, most mesogastrium dorsale approach perietale

peritoneum and grow attached. Thus mesogastrium dorsale attachment for an arc from left to

right cranial caudal. Terkaudal close attachment part that runs trasversal transverse mesocolon.

Caudal section also occurs mesogastrium dorsale attachment to the transverse mesocolon and

omentum called magi. Pockets formed by him called omentalis stock.

Mesogastrium ventrale attached to the ventral abdominal wall parietale peritoneum and the

diaphragm. In the liver ventrale mesogastrium formed and evolved. Liver evolved into caudal to

the edge of the lesser omentum mesogastrium called or ligament hepatogastricum the next caudal

edge freely called hepatoduodenale ligament. Falciforme ligament attached to the boundary

between the lobe lobe dexter and sinister. Lesser omentum attached to the fossa sagittalis sinistra

dorsokranial and surrounds part portae hepatis. Ligamentum teres hepatis sinistra the rest of the

umbilical vein, extending from the umbilicus to the liver in the free edge of the ligament

falciforme hepatis, entered in the fossa sagittalis sinistra hepatis and ends on ramus sinistra

portae vein.

In the free edge of the lesser omentum or ligament hepatoduodenale are:

- Vena portae;

- Arteria hepatica propria;

- Ductus choledochus;

- Autonomic nerve fibers;

- Lympha vessels.

On the left runs a. hepatica propria in the second dorsal side of this building in the middle

of running v. portae. Choledocus duct formed by the duct and ductus hepaticus communis

cysticus, walk through the ligament to kaudomedial, menyilangi adjacent dorsal pars superior

duodeni up in the sulcus between the pars descendens duodeni and caput pancreatis duodeni

major tributaries of the papillae.

In the mesentery and duodenum (mesoduodenum) and mesogastrium dorsale going and

growing pancreas. Because most mesogastrium dorsale mesoduodenum and grow attached to the

peritoneum parietale, caput and corpus-located pancreatis retroperitoneal, but still within the

cauda pancreatis greater amentum.

In the adjacent ventral cauda greater amentum pancreatis lien form and grow towards the

left so that it is covered in large part by greater amentum left sheet. Magi omentum is divided in

two by a ligament precholienale lien, the lien and the peritoneum covering the diaphragm

parietale, ligament gastrosplenic section between lien and ventriculus. Because the lien grow,

especially to the left, second right sheet ligamentumtidak until the lien attached, while the sheet

is attached to the left from the hilum surrounded lien.

Because there was a change in the location of the stock omentalis ventriculus. Into the hole

called the foramen epiploicum omentalis stock (Winslowi) is limited:

- Cranial section by caudate processus

- Ventral section by lig.hepatoduodenale

- Caudal section by pars superior duodeni

- Dorsal section by parietale peritoneum covering the inferior vena cava.

- Stock omentalis own restricted:

- Cranial section by hepatic caudate lobe

- Ventral section by the lesser omentum and ventriculus Caudal section by

mesocolontransversum and transverse colon

Dorsal section by parietale peritoneum covering the caput and corpus pancreatic

On the left by a greater amentum with pancreatic cauda and lien

Magi omentum attached to the caudal colon tansversum cover of next vental intestine as a

curtain to then fold into the cranial direction and attached to major curvatura ventriculi. The two

sheets of folds that grow attached caudal section. The part that does not grow is a continuation

omentalis called bursae bursae omentalis inferior recess. Part bursae omentalis terkranial called

bursae omentalis superior recess.

Plain coated peritoneal mesothelium, slick and slippery due to increased peritoneal fluid

mengeluiarkan bit. Thus, the peritoneum can be likened to the stratum synoviale in joints. The

peritoneum is a smooth easy movement of intra peritoneal tools to one another. Sometimes,

pemuntaran ventriculus and intestine sepulcher going in the other direction. As a result, the tools

should be located on the right side to the left or vice versa. The state is called situs inversus.

The peritoneum is a single layer of cells on the basis fibroelastik mesoepitelial. Divided into

sections visceral, that covers the intestines and mesentery, and parietal parts that lines the

abdominal wall and fascia associated with muskularis.

Viserale peritoneum that surrounds the abdominal organs are innervated by the

autonomic nervous system and is not sensitive to palpation or cutting. Thus incision or suturing

of the intestine can be done without perceived by the patient. However, when performed organ

pull or strain, or excessive contraction of muscles causes ischemia eg colic or inflammation such

as appendicitis, then there will be pain. Patients who merasaka visceral pain usually can not

pinpoint the location of the pain that he usually uses his hand to assign it to all areas of pain. 4

Parietale peritoneum innervated by peripheral nerves, so that pain can arise due to the stimuli in

the form of palpation, pressure, or inflammatory processes. Pain is felt like a stabbing or slashed,

and patients can pinpoint the location of pain.

Total peritoneal surface area of about 2 meters, and its activity is consistent with a semi-

permeable membrane. Fluid and electrolyte small can move both directions. Molecules larger

diaphragm cleared into mesothelium and lymphatic through stomata kecil.5

Organs located in the peritoneal cavity of gastric, liver, gallbladder fellea, spleen, ileum,

jejenum, transverse colon, sigmoid colon, cecum, and appendix (intraperitoneum), pancreas,

duodenum, ascending colon and descenden, kidney and ureter (retroperitoneum ). 6.7

II.2.ANATOMY

Abdominal wall containing structures musculo-aponeurosis complex. The back of the

structure is attached to the upper spine to the ribs, and at the bottom of the pelvis. The abdominal

wall consists of various layers, from outside to inside, consisting of layers of skin and sub kutis

kuitis, sub-cutaneous fat and superficial facies (facies skarpa), then the third abdominal wall

muscles m. Obliquus external abdominis, m. Obliquus internus abdominis and m. The transverse

abdominis, and finally layered preperitonium and peritoneum, the fascia transversalis,

preperitonial fat and peritoneum. Muscles on the front of the center consists of a pair of the

rectus abdominis muscle with fascianya which are separated by the midline linea alba.6

Abdominal wall to form the abdominal cavity that protects the contents of the abdominal cavity.

The integrity of layers musculo-aponeurosis abdominal wall is very important to prevent

congenital hernia occurs, acquired, or iatrogenic. Another function of the abdominal wall was

breathing well on the process of urination and defecation with elevated intra-abdominal pressure.

Abdominal wall bleeding from several directions. From kraniodorsal acquired bleeding from aa

branch. Intercostalis VI - XII and a. superior epigastric. From there a caudal. iliaca a.

sircumfleksa superficial, a. and external pudendal a. inferior epigastric. Wealth vascularization

allows horizontal and vertical abdominal incision without causing interference perdarahan.6

Innervation of the abdominal wall in segmental dipersyarafi by n.thorakalis VI - XII and n.

lumbar I.6

II.3.Etiology

Peritonitis can be caused by abnormalities in the abdomen such as inflammation and

perforation penyulitnya appendicitis, perforated peptic ulcers, abdominal typhoid perforation.

Obstructive ileus and bleeding due to perforation of a hollow organ due to trauma abdomen.2

a.Bakterial: Bacteroides, E. coli, streptococcus, Pneumococus, Proteus, Klebsiella-

Enterobacter group, Mycobacterium Tuberculosa.

b.Kimiawi: sap stomach, and pancreas, bile, blood, urine, foreign body (talc, flour). 2,3,9

II.4.PATOFISOLOGI

The initial reaction to invasion by bacteria peritoneum is a discharge of fibrinous exudate.

Pockets of pus (abscess) formed between fibrinous adhesions, which stick together with the

surrounding surface so as to limit the infection. The attachment usually disappears when the

infection disappear, but it can persist as fibrous bands, which later can lead to intestinal obstuksi.

Cause inflammation and fluid accumulation due to capillary membrane leak. If the fluid

deficit is not corrected quickly and aggressively, it can lead to cell death. The release of various

mediators, such as interleukins, can start hiperinflamatorius response, so as to bring to the further

development of the failure of many organs. Because the body tries to compensate by way of

retention of fluid and electrolytes by the kidneys, waste products also accumulate. Tachycardia

initially increase cardiac output, but it soon failed so happens hypovolemia. 5

The organs in the peritoneal cavity including abdominal wall had edema. Edema caused by

capillary permeability organs are rising. The collection of fluid in the peritoneal cavity and

intestinal lumens and edema around the intra peritoneal organs and abdominal wall edema

including retroperitoneal tissue causing hypovolemia. Hypovolemia increases with an increase in

temperature, the input that does not exist, and vomiting.

Trapping fluid in peritoneal cavity and intestinal lumen, further increasing intra

abdominal pressures, making a full effort into breathing difficult and causing decreased

perfusion. If infected material is widespread on the surface of the peritoneum or when the

infection spreads, it can arise generalized peritonitis. With the development of generalized

peritonitis, reduced peristaltic activity to arise paralytic ileus; intestine then becomes Atoni and

stretch. Lost fluids and electrolytes into the intestinal lumen, resulting in dehydration, shock,

circulatory disorders and oliguria. Adhesions can form between the intestine arches that stretch

and can interfere with the recovery of bowel movement and cause intestinal obstruction. 1

Long intestinal blockage or obstruction in the intestines can cause ileus due to mechanical

disruption (blockage) then an increase in intestinal peristalsis in an effort to overcome these

barriers. Ileus Ileus may be as simple as intestinal obstruction that is not accompanied pinched

blood vessels and can be total or partial, on stangulasi ileus accompanied pinched blood vessel

obstruction causing ischemia, which ends with necrosis or gangrene and perforation of the

intestine and eventually occur due to the spread of bacteria on the abdominal cavity so it can

happen peritonitis.

Abdominal typhus is an acute infectious intestinal disease caused by the bacteria S. Typhi

that enter the human body through the mouth from contaminated food and water. Some germs

destroyed by stomach acid, some into keusus smooth and achieve plaque peyeri lymphoid tissue

in the terminal ileum that experienced bleeding complications in this place hypertrophy and

intestinal perforation may occur, ileal perforation in typhoid fever usually occurs in patients who

have a fever for more than 2 weeks accompanied by headache, cough, and malaise followed by

abdominal pain, tenderness, defans muscular, and the general state of decline due to toksemia.4

Perforation of peptic ulcer characterized by stimulation of peritoneum which began in the

epigastrium and extends throughout the peritoneum caused by generalized peritonitis.

Perforation of the stomach and duodenum front causing acute peritonitis. Patients who

experience severe pain perforation looks like being stabbed in the stomach. This pain arises

suddenly, especially felt in the epigastric region due to stimulation of peritoneum by stomach

acid, and bile or pancreatic enzymes. Then spread throughout the abdomen causes pain all over

the abdomen in early perforation, no bacterial infection, sometimes called phase phase chemical

peritonitis, the pain in the shoulder show excitability peritonium be mengenceran stimulates acid

salt, this will reduce the complaints for a while until it happens peritonitis bakteria.1

In appendicitis usually is usually caused by a blockage of the lumen of the appendix by

hyperplasia of lymphoid follicles, fekalit, foreign body, stricture due to fibrosis and neoplasms.

Obstruction causes mucus produced mucosal dam experience, the longer the mucus is more and

more, but the elasticity of the wall of the appendix has limitations that led to increased

intraluminal pressure and impede lymph flow resulting in edema, diapedesis bacteria, mucosal

ulceration, and venous obstruction that edema increases then the flow impaired arterial wall

infarction appendix will be followed by necrosis or gangrene of the appendix wall, causing

perforation and peritonitis eventually lead to both local and general.7

In both abdominal trauma and abdominal penetrating trauma blunt abdominal trauma can lead to

peritonitis, sepsis when the intra peritonial hollow organs. Peritonial stimuli arising in

accordance with the contents of the hollow organs, ranging from the nature of gastric chemistry

until the colon that contains feces. Chemical stimulus onset fastest and slowest feces. When

perforation occurs at the top, such as the stomach region will occur immediately after the trauma

and stimulation will occur while the symptoms of severe peritonitis when the bottom such as

colon, no early symptoms because microorganisms need time to breed new after 24 hours of

onset of symptoms of acute abdomen because stimulation peritonium.1, 7

II.5.CLASSIFICATION

Based on the pathogenesis of peritonitis can be classified as follows:

a.Peritonitis primary bacterial , Peritonitis is bacterial contamination haematogenously the

peritoneal cavity and found no focus of infection in the abdomen. The reason is monomikrobial,

usually E. Coli, Sreptococus or Pneumococus. Primary bacterial peritonitis is divided into two,

namely:

1.Spesifik: eg Tuberculosis

2.Non specific: for example, non-tuberculosis pneumonia an Tonsillitis.

Risk factors that contribute to this is the presence of malnutrition peritonitis, intra-

abdominal malignancy, immunosuppression, and splenectomy. High-risk groups are

patients with nephrotic syndrome, chronic renal failure, systemic lupus erythematosus,

and hepatic cirrhosis with ascites.

b.Peritonitis acute bacterial secondary (supurativa) Peritonitis which follows an acute infection

or gastrointestinal perforation tractusi or urinary tract. In general, a single organism will not

cause a fatal peritonitis. Synergism of multiple organisms can aggravate this infection. Bakterii

anaerobes, especially Bacteroides species, can magnify the effect of aerobic bacteria causing the

infection. Besides an extensive and long-contamination of bacteria also can aggravate peritonitis.

Germs can be derived from:

- Wound / trauma penetration, which carry germs from the outside into the

peritoneal cavity.

- Perforation of the organs in the abdomen, such as peritonitis caused by chemicals,

perforation of the intestine so that the feces out of the colon.

- Complications of the inflammatory process intra-abdominal organs, such as

appendicitis.

c.Peritonitis tertiary, for example:

- Peritonitis caused by fungi

-Peritonitis source of the bacteria that can not be found.

Peritonitis is caused by direct irritants, such sepertii bile, lymph gastric, pancreatic lymph,

and urine.

d.Peritonitis Other forms of peritonitis:

- Aseptic / sterile peritonitis

- Granulomatous peritonitis

- Hiperlipidemik peritonitis

- Talc peritonitis

CHAPTER III

CLINICAL DIAGNOSIS

III.1.CLINICAL

The presence of blood or fluid in the peritoneum cavity will give a sign - a sign stimulus

peritoneum. Stimulation peritonium defans cause tenderness and muscular, liver dullness may

disappear due to the free air under the diaphragm. Decreased bowel peristalsis is lost due to

temporary paralysis usus. When bacterial peritonitis has occurred, the patient's body temperature

will rise and occurs tachycardia, hypotension, and the patient was lethargic and syok.1

This stimulation causes pain on any movement that causes a shift in the peritoneum peritoneum.

Pain is a subjective form of pain with movement such as walking, breathing, coughing, or

straining. Lots of pain if the pain is driven as palpation, tenderness loose, psoas tests, or tests

lainnya..

DIAGNOSIS

Diagnosis of peritonitis can be enforced by the clinical, laboratory and X-Ray. The

clinical features depend on the extent of peritonitis, severe peritonitis and types of organisms

responsible. Peritonitis can be local, spread, or the public. Clinical features that are common in

the presence of primary bacterial peritonitis, abdominal pain, fever, pain and loose bowel press

decreased or disappeared. While the clinical picture in secondary bacterial peritonitis is the

existence of acute abdominal pain. Pain is a sudden, severe, and in patients with perforation (eg

perforated ulcer), the pain being spread throughout the abdomen. In other situations (eg,

appendicitis), the pain at first because the main cause, and then gradually spread from the focus

of infection. In addition to pain, patients usually exhibit other signs and symptoms are nausea,

vomiting, shock (hypovolemic, septic, and neurogenic), fever, abdominal distension, abdominal

tenderness and rigidity of the local, diffuse or general, and classical bowel weakened or

disappeared . Clinical features for non bacterial peritonitis with acute bacterial peritonitis. 1.3

Chronic bacterial peritonitis (tuberculous) gives an overview of the clinical presence of night

sweats, weakness, weight loss, and abdominal distention; moderate granulomatous peritonitis

showed clinical severe abdominal pain, fever and signs of peritonitis who turned up 2 weeks

after surgery.

b.laboratory test

In laboratory tests found the lekositosis, increased hematocrit and metabolic acidosis.

In tuberculosa peritonitis peritoneal fluid contains a lot of protein (more than 3 gram/100 ml) and

many lymphocytes; identified with the culture of the tubercle bacillus. Peritoneal biopsy

percutaneous or laparoscopic tuberculomas show characteristic granulomas, and is the basis of

culture results obtained before diagnosis.

c. X-Ray

Ileus is a discovery that is not typical of peritonitis; small intestine and large intestine dilated.

Free air can be seen in cases of perforation.

III.2 Radiological

Radiological examination is the investigation for consideration in estimating a patient

with an acute abdomen. In plain abdominal peritonitis done three positions, namely:

1.Backs (supine), the rays of the vertical projection of anteroposterior (AP).

2.Or half sitting or standing, if possible, with a horizontal beam projection AP.

3.Skewed to the left (left lateral decubitus = LLD), with a horizontal beam, AP projection.

Shooting should be made using the film cassette that can cover the entire abdomen and its

walls. Need to set the size of the tape and the film size 35 x 43 cm.3

Prior to the peritonitis, if the cause is a disturbance passage intestine (ileus) obstructive then on

plain abdominal radiological 3 positions available are:

1.Sleep, to see the distribution of the intestine, preperitonial fat, presence or absence of

propagation. Picture obtained by the dilation of intestinal obstruction in the proximal region,

thickening dnding intestine, such as fish spines picture (Herring bone appearance),

2.LLD, to see the fluid level and the possibility of bowel perforation. Of water fluid level can be

expected passage of intestinal disorders. When water is short-fluid level layout means there ileus

high, moderate if the long - term possibility of interference in the colon. The picture obtained is

the infra-diaphragmatic free air and water fluid level.

3.Half sitting or standing. Radiological obtained the water fluid level and step ladder appearance.

So radiological in obstructive ileus is a partial bowel distension, air fluid levels, and herring bone

appearance. While in paralytic ileus radiological obtained as follows:

- Intestinal general, where a thorough bowel dilation that sometimes - sometimes difficult

to distinguish between hugely dilated intestinum tenue or intestinum crassum.

- air fluid level

- Herring bone appearance

The difference with obstructive ileus: intestinal dilation fluid thoroughly so the water

level was short - short (small intestine) and long - term (colon) due to colon lumen diameter

wider than the small intestine. If prolonged ileus obstructive ileus can be paralitik.2

In the case of peritonitis due to bleeding, the images are not clear on plain abdomen. Picture will

be clearer in the USG (ultrasonography) .

Peritonitis due to perforation of the radiological picture can be seen on plain abdominal

examination 3 positions. On the allegation whether due to peptic ulcer perforation, ruptured

appendix or for any other reason, the main radiological signs are:

1.Lie, obtained preperitonial fat disappears, psoas line disappeared, and blurring the

abdominal cavity.

2.Sitting or standing, free water obtained subdiafragma crescent (semilunair shadow).

3.LLD, got free water peritonial intra abdominal highest. It is located between the heart

of the abdominal wall or the pelvis to the abdominal wall.

So radiological peritonitis is a vagueness in the abdominal cavity, preperitonial fat and

psoas line disappears, and the presence of free air or intra subdiafragma peritoneal.

III.3.THERAPY

The general principle is replacement therapy lost fluids and electrolytes intravenously

performed, appropriate antibiotics, gastrointestinal decompression by nasogastric suction and

intestinal disposal of septic focus (appendix, etc.) or other inflammatory causes, if possible drain

the pus out and act- pain relief measures. Great resuscitation with isotonic saline solution is

important. Returns intravascular volume improve tissue perfusion and delivery of oxygen,

nutrients, and defense mechanisms. Urine output of central venous pressure, and blood pressure

should be monitored to assess the adequacy of resuscitation.

Antibiotic therapy should be administered as soon as the diagnosis of bacterial peritonitis

was made. Broad-spectrum antibiotics are given empirically, and then changed its kind after

culture results come out. Antibiotic selection based on which organisms are suspected to be the

cause. Broad-spectrum antibiotics are also additional surgical drainage. Must be available a

sufficient dose during surgery, because bacteremia will develop during the operation. 5.11

Disposal of septic focus or other inflammatory performed by laparotomy surgery. Incision is

selected vertical incision middle underlined that generate access to the entire abdomen and easily

opened and closed. If localized peritonitis, an incision above the intended sites of inflammation.

Surgery technique used to control contamination depends on the location and nature of

pathologic gastrointestinal tract. In general, a continuous peritoneal contamination can be

prevented by closing, mengeksklusi, or a perforated viscus mereseksi. 11th

Lavase peritoneum performed on the diffuse peritonitis, which is using crystalloid solution

(saline). Agar tidak terjadi penyebaran infeksi ketempat yang tidak terkontaminasi maka dapat

diberikan antibiotika ( misal sefalosporin ) atau antiseptik (misal povidon iodine) pada cairan

irigasi. Bila peritonitisnya terlokalisasi, sebaiknya tidak dilakukan lavase peritoneum, karena

tindakan ini akan dapat menyebabkan bakteria menyebar ketempat lain. 2.3

Drainase (pengaliran) pada peritonitis umum tidak dianjurkan, karena pipa drain itu dengan

segera akan terisolasi/terpisah dari cavum peritoneum, dan dapat menjadi tempat masuk bagi

kontaminan eksogen. Drainase berguna pada keadaan dimana terjadi kontaminasi yang terus-

menerus (misal fistula) dan diindikasikan untuk peritonitis terlokalisasi yang tidak dapat

direseksi.

III.4.DIFFERENTIAL DIAGNOSIS

The differential diagnosis of peritonitis is appendicitis, pancreatitis, gastroenteritis,

cholecystitis, salpingitis, ruptured ectopic pregnancy, etc..

III.5. KOMPLIKASI

Complication can occur in acute secondary bacterial peritonitis, where complication can

be divided into early and advanced complication, :

a. septicemia and septic syok, hipovolemik shock. Intra abdominal sepsis that can not be

controlled with multi-system failure residua intraperitoneal portal pyemia abcess.

(hepatic absess)

b. Advanced complication intestinal obstruction

III.6..Prognosis

The prognosis for peritonitis is both local and lightweight is fine, while the general

prognosis of peritonitis is lethal due to virulen of organism.

CHAPTER IV

CONCLUSION

Peritonitis is inflammation of the peritoneum which is wrapping the viscera in the

abdominal cavity. The peritoneum is a thin, clear membrane covering the abdominal organs and

the abdominal wall. Peritonitis are localized only in the pelvic cavity called pelvioperitonitis.

The cause of peritonitis include: the spread of infection from an infected abdominal

organs, pelvic inflammatory disease in women who are still active in sexual activity, infection of

the uterus and fallopian tubes, abnormal liver or heart failure, peritonitis can occur after a

surgery, peritoneal dialysis (treatment fails kidney), irritation without an infection.

Patofisologi peritoneum peritonitis was the initial reaction to bacterial invasion is the

release of fibrinous exudate. Formed pockets of pus (abscess) among fibrinous adhesions, which

stick together with the surrounding surface so as to limit the infection. The attachment usually

disappears when the infection disappear, but it can be settled as fibrinous bands, which later can

cause intestinal obstruction. The general principles of therapy in peritonitis are:  

Replacement of lost fluids and electrolytes made intravenously.

b)       Antibiotic therapy plays a very important role in the treatment of puerperal infection.

c)       Analgesic therapy given to treat pain.

d)      Surgery include infection of the material and correct the cause.

We as a nurse in addressing the problem of peritonitis in the community can provide a

variety of ways to prevent peritonitis and expected student / i can provide nursing care to clients

experiencing particularly peritonitis in accordance with what is learned.

List Pustaka

1.Silvia A. Price. , 2006. Pathophysiology Clinical Concepts Disease Processes, ECG; Jakarta

2.NANDA Nursing Diagnosis 2005-2006 Prima Medika: Jakarta

3.Wim de Jong. , 2005. Textbook of Surgery. EGC. Jakarta

4.Peritonitis, http://www.medikastore.com/med/peritonitis_pyk.php?dktg=7&UID 200 705.

5.System Gastroenterohepatology lectures, Makassar: 2005

6.Subanada, Supadmi, Aryasa, and Sudaryat. , 2007. Some Abnormalities Actions Requiring

7.Gastrointestinal Surgery. In: Capita Selekta Gastroenterology Children. Jakarta: CV Sagung

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