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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
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