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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.
Gazette visceralis lamina connecting the right and left parietal lamina sticking together and forming a duplex sheet called duplikatura. ventriculus and intestinal . Peritoneum is divided into three layers. In between the two cavities are entoderm which is enteron wall.1. Peritonitis is an inflammatory or suppurative response of the peritoneum caused by chemical irritation or bacterial invasion. Enteron abdominal region into the intestine. Duplikatura connects the intestine with walls of ventral and dorsal abdominal wall and can be seen as a tool hanger intestines called the mesentery. At the beginning. Ventrikulus high mesentery called mesogastrium ventrale and mesogastrium dorsale.CHAPTER II THEORY and DISCUSSION II. The peritoneum is the lamina lateral mesoderm that remain epithelial. Ventrale mesentery contained in the next caudal pars superior duodeni then disappeared. are united on the edge kaudalnya.Fascia that lines the abdominal wall is called the parietal lamina.DEFINITION Peritonitis is inflammation of the peritoneum which is wrapping perut. dorsal and ventral colon closer to each other. Second cavity mesoderm. Sheets left and right ventrale mesentery. 2. the mesoderm is the wall of a cavity that is coelom. namely: 1. which still exist.2 viscera in the cavity.Fascia visceralis and parietal lamina. At the time perkambangan and growth. so that the mesoderm then becomes peritoneum.Fascia that covered the walls of the intestine. Mesentery is divided into the mesentery and mesenteric ventrale dorsale. Thus in both ventral and dorsal colon there is a duplikatura. Lamina connecting 3. called the lamina visceralis (tunica serosa).
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. He is actually a continuation of the cecum. viscerale peritoneal adhesions in the peritoneum or mesentery parietale not perfect. Thus there are at flexura duodenojejenalis plica superior duodenal recess duodenal limit superior and limit inferior plica duodenal duodenal resesus inferior. it falls down sepulcher intestine and mesentery dorsale closer together parietale peritoneum. The transverse colon is intraperitoneal and have mounting tool called the transverse mesocolon. However. there are parts that do not have bowel tools hanger again. Because sepulcher intestine rotates. a fold of peritoneum due to the artery leading to the end of the processus vermiformis. In many places. Colon sigmoideum located intraperitoneally with a mesosigmoideum. Cavity called the cavum peritonei. The parts that still have the tool hanger is located inside the wall cavity formed by the peritoneum parietale. resulting in the notches between the colon (covered by peritoneum viscerale) and peritoneal parietale or between the mesentery and peritoneal parietale restricted folds.playback. and is now the so-called retroperitoneal dorsal peritoneum. After ductus omphaloentericus disappears. called intraperitoneal located. As a result of this attachment. Colon ascendens and colon descendens located retroperitoneal. Intestinal growing faster than the cavity so that the intestine had occurred twistingsepulcher sepulcher. Jejenum and ileum located intraperitoneally with a hanger mesentery. not all the happening places of attachment. cecum lies intraperitoneal due at the beginning of a bulge the walls of the intestines and does not have the tools. These relationships form a tube called the ductus omphaloentericus. Sepulcher intestine due to intestinal turned to the right by 270 ° with the axis ductus omphaloentericus and a. Enteron gut or in a place associated with the umbilicus and saccus vitellinus. thus: The duodenum is retroperitoneal. adhesions occur. In places viscerale peritoneum and mesentery dorsale approach dorsale peritoneum. superior mesenterica respectively in the ventral wall and the dorsal abdominal wall. Processus vermiformis located intraperitoneally with a hanger mesentery. The folds can also terjadfi because it runs the blood vessels. .
causing the building called epiploicae Appendices. Terkaudal close attachment part that runs trasversal transverse mesocolon. Ductus choledochus. Ventriculus because they rotate. thus curvatura major in minor curvatura the left and the right. menyilangi adjacent dorsal pars superior . Choledocus duct formed by the duct and ductus hepaticus communis cysticus. In the liver ventrale mesogastrium formed and evolved. Caudal section also occurs mesogastrium dorsale attachment to the transverse mesocolon and omentum called magi. Arteria hepatica propria. In the colon there sigmoideum intersigmoideum recess between the peritoneum and mesosigmoideum parietale. Ventriculus rotate the longitudinal axis. Thus mesogastrium dorsale attachment for an arc from left to right cranial caudal. Ligamentum teres hepatis sinistra the rest of the umbilical vein. entered in the fossa sagittalis sinistra hepatis and ends on ramus sinistra portae vein. Peritoneum covering the colon folds and unfolds out filled with fat. Lesser omentum attached to the fossa sagittalis sinistra dorsokranial and surrounds part portae hepatis. most mesogastrium dorsale approach perietale peritoneum and grow attached. walk through the ligament to kaudomedial. Pockets formed by him called omentalis stock. Then ventriculus play against the sagittal axis. hepatica propria in the second dorsal side of this building in the middle of running v. Autonomic nerve fibers. Lympha vessels. Mesogastrium ventrale attached to the ventral abdominal wall parietale peritoneum and the diaphragm. so that the cardia and pylorus move to the left to the right. extending from the umbilicus to the liver in the free edge of the ligament falciforme hepatis. portae. Liver evolved into caudal to the edge of the lesser omentum mesogastrium called or ligament hepatogastricum the next caudal edge freely called hepatoduodenale ligament. On the left runs a. Stratum circulare coli folds and unfolds so happens plica semilunaris.In the colon there descendens paracolici recess. In the free edge of the lesser omentum or ligament hepatoduodenale are: Vena portae. Falciforme ligament attached to the boundary between the lobe lobe dexter and sinister.
the lien and the peritoneum covering the diaphragm parietale. Part bursae omentalis terkranial called bursae omentalis superior recess. caput and corpus-located pancreatis retroperitoneal. second right sheet ligamentumtidak until the lien attached.duodeni up in the sulcus between the pars descendens duodeni and caput pancreatis duodeni major tributaries of the papillae. 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. Because most mesogastrium dorsale mesoduodenum and grow attached to the peritoneum parietale. In the mesentery and duodenum (mesoduodenum) and mesogastrium dorsale going and growing pancreas. Magi omentum is divided in two by a ligament precholienale lien. Into the hole called the foramen epiploicum omentalis stock (Winslowi) is limited: Cranial section by caudate processus Ventral section by lig. The part that does not grow is a continuation omentalis called bursae bursae omentalis inferior recess. especially to the left. but still within the cauda pancreatis greater amentum. The two sheets of folds that grow attached caudal section. Because there was a change in the location of the stock omentalis ventriculus. 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. . ligament gastrosplenic section between lien and ventriculus.hepatoduodenale Caudal section by pars superior duodeni Dorsal section by parietale peritoneum covering the inferior vena cava. Because the lien grow. while the sheet is attached to the left from the hilum surrounded lien.
Pain is felt like a stabbing or slashed. However. sigmoid colon. Thus incision or suturing of the intestine can be done without perceived by the patient. slick and slippery due to increased peritoneal fluid mengeluiarkan bit. or inflammatory processes. 6. As a result. Total peritoneal surface area of about 2 meters. pancreas. so that pain can arise due to the stimuli in the form of palpation. and parietal parts that lines the abdominal wall and fascia associated with muskularis. then the third abdominal wall muscles m. Fluid and electrolyte small can move both directions. ascending colon and descenden. sub-cutaneous fat and superficial facies (facies skarpa). jejenum. Molecules larger diaphragm cleared into mesothelium and lymphatic through stomata kecil. The transverse .Plain coated peritoneal mesothelium. pemuntaran ventriculus and intestine sepulcher going in the other direction.5 Organs located in the peritoneal cavity of gastric. The peritoneum is a single layer of cells on the basis fibroelastik mesoepitelial. m. Obliquus external abdominis. Divided into sections visceral. transverse colon. spleen. The state is called situs inversus. from outside to inside. and its activity is consistent with a semipermeable membrane. that covers the intestines and mesentery. the peritoneum can be likened to the stratum synoviale in joints.7 II. and at the bottom of the pelvis. Viserale peritoneum that surrounds the abdominal organs are innervated by the autonomic nervous system and is not sensitive to palpation or cutting. The peritoneum is a smooth easy movement of intra peritoneal tools to one another. duodenum. gallbladder fellea.ANATOMY Abdominal wall containing structures musculo-aponeurosis complex. and appendix (intraperitoneum). or excessive contraction of muscles causes ischemia eg colic or inflammation such as appendicitis. when performed organ pull or strain. Sometimes. kidney and ureter (retroperitoneum ). consisting of layers of skin and sub kutis kuitis.2. The abdominal wall consists of various layers. 4 Parietale peritoneum innervated by peripheral nerves. and patients can pinpoint the location of pain. Obliquus internus abdominis and m. the tools should be located on the right side to the left or vice versa. cecum. 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. Thus. ileum. then there will be pain. pressure. The back of the structure is attached to the upper spine to the ribs. liver.
which stick together with the surrounding surface so as to limit the infection. Intercostalis VI . Pockets of pus (abscess) formed between fibrinous adhesions. bile.PATOFISOLOGI The initial reaction to invasion by bacteria peritoneum is a discharge of fibrinous exudate. The release of various .2 a. E. acquired. foreign body (talc. Mycobacterium Tuberculosa.Etiology Peritonitis can be caused by abnormalities in the abdomen such as inflammation and perforation penyulitnya appendicitis. KlebsiellaEnterobacter group. but it can persist as fibrous bands.abdominis. a. Wealth vascularization allows horizontal and vertical abdominal incision without causing interference perdarahan.3. sircumfleksa superficial. abdominal typhoid perforation.6 Innervation of the abdominal wall in segmental dipersyarafi by n.6 Abdominal wall to form the abdominal cavity that protects the contents of the abdominal cavity. it can lead to cell death.9 II. the fascia transversalis.6 II. From kraniodorsal acquired bleeding from aa branch. 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. superior epigastric.Bakterial: Bacteroides. Proteus. coli. streptococcus.4. From there a caudal. b. and external pudendal a. which later can lead to intestinal obstuksi.XII and a. lumbar I. and pancreas. blood. 2. Pneumococus.XII and n. Cause inflammation and fluid accumulation due to capillary membrane leak. The integrity of layers musculo-aponeurosis abdominal wall is very important to prevent congenital hernia occurs.thorakalis VI . Abdominal wall bleeding from several directions. preperitonial fat and peritoneum. iliaca a.Kimiawi: sap stomach. perforated peptic ulcers. Obstructive ileus and bleeding due to perforation of a hollow organ due to trauma abdomen. flour). or iatrogenic. inferior epigastric. If the fluid deficit is not corrected quickly and aggressively.3. and finally layered preperitonium and peritoneum. The attachment usually disappears when the infection disappear. Another function of the abdominal wall was breathing well on the process of urination and defecation with elevated intra-abdominal pressure. urine.
reduced peristaltic activity to arise paralytic ileus. Adhesions can form between the intestine arches that stretch and can interfere with the recovery of bowel movement and cause intestinal obstruction. the input that does not exist. Ileus Ileus may be as simple as intestinal obstruction that is not accompanied pinched blood vessels and can be total or partial. Edema caused by capillary permeability organs are rising. it can arise generalized peritonitis.mediators. ileal perforation in typhoid fever usually occurs in patients who have a fever for more than 2 weeks accompanied by headache. Hypovolemia increases with an increase in temperature. circulatory disorders and oliguria. on stangulasi ileus accompanied pinched blood vessel obstruction causing ischemia. Typhi that enter the human body through the mouth from contaminated food and water. Lost fluids and electrolytes into the intestinal lumen. further increasing intra abdominal pressures. 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. and malaise followed by . but it soon failed so happens hypovolemia. 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. intestine then becomes Atoni and stretch. Trapping fluid in peritoneal cavity and intestinal lumen. shock. cough. If infected material is widespread on the surface of the peritoneum or when the infection spreads. 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. can start hiperinflamatorius response. 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. Because the body tries to compensate by way of retention of fluid and electrolytes by the kidneys. such as interleukins. Abdominal typhus is an acute infectious intestinal disease caused by the bacteria S. making a full effort into breathing difficult and causing decreased perfusion. and vomiting. resulting in dehydration. With the development of generalized peritonitis. 5 The organs in the peritoneal cavity including abdominal wall had edema. Tachycardia initially increase cardiac output. so as to bring to the further development of the failure of many organs. Some germs destroyed by stomach acid. waste products also accumulate.
stricture due to fibrosis and neoplasms. sepsis when the intra peritonial hollow organs. this will reduce the complaints for a while until it happens peritonitis bakteria. Then spread throughout the abdomen causes pain all over the abdomen in early perforation. Obstruction causes mucus produced mucosal dam experience.1 In appendicitis usually is usually caused by a blockage of the lumen of the appendix by hyperplasia of lymphoid follicles. This pain arises suddenly. the pain in the shoulder show excitability peritonium be mengenceran stimulates acid salt.4 Perforation of peptic ulcer characterized by stimulation of peritoneum which began in the epigastrium and extends throughout the peritoneum caused by generalized peritonitis. fekalit. Perforation of the stomach and duodenum front causing acute peritonitis. ranging from the nature of gastric chemistry until the colon that contains feces. especially felt in the epigastric region due to stimulation of peritoneum by stomach acid. Patients who experience severe pain perforation looks like being stabbed in the stomach. diapedesis bacteria.abdominal pain. 7 . no bacterial infection. foreign body. sometimes called phase phase chemical peritonitis. no early symptoms because microorganisms need time to breed new after 24 hours of onset of symptoms of acute abdomen because stimulation peritonium. the longer the mucus is more and more. 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. causing perforation and peritonitis eventually lead to both local and general.1. and the general state of decline due to toksemia. tenderness.7 In both abdominal trauma and abdominal penetrating trauma blunt abdominal trauma can lead to peritonitis. mucosal ulceration. defans muscular. but the elasticity of the wall of the appendix has limitations that led to increased intraluminal pressure and impede lymph flow resulting in edema. 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. Peritonial stimuli arising in accordance with the contents of the hollow organs. Chemical stimulus onset fastest and slowest feces. When perforation occurs at the top. and bile or pancreatic enzymes.
Perforation of the organs in the abdomen. systemic lupus erythematosus. c. a single organism will not cause a fatal peritonitis. intraabdominal malignancy. especially Bacteroides species. . such as appendicitis.Peritonitis acute bacterial secondary (supurativa) Peritonitis which follows an acute infection or gastrointestinal perforation tractusi or urinary tract.Spesifik: eg Tuberculosis 2.II. Besides an extensive and long-contamination of bacteria also can aggravate peritonitis.Wound / trauma penetration. Coli. . chronic renal failure. non-tuberculosis pneumonia an Tonsillitis. Bakterii anaerobes.Peritonitis tertiary. Sreptococus or Pneumococus. b.Non specific: for example. namely: 1.CLASSIFICATION Based on the pathogenesis of peritonitis can be classified as follows: a.Peritonitis primary bacterial . and splenectomy. usually E.5. immunosuppression. Germs can be derived from: . and hepatic cirrhosis with ascites. High-risk groups are patients with nephrotic syndrome. which carry germs from the outside into the peritoneal cavity. can magnify the effect of aerobic bacteria causing the infection.Complications of the inflammatory process intra-abdominal organs. The reason is monomikrobial. for example: . perforation of the intestine so that the feces out of the colon. Primary bacterial peritonitis is divided into two. Risk factors that contribute to this is the presence of malnutrition peritonitis. Synergism of multiple organisms can aggravate this infection. such as peritonitis caused by chemicals. In general. Peritonitis is bacterial contamination haematogenously the peritoneal cavity and found no focus of infection in the abdomen.
pancreatic lymph.Talc peritonitis .. d.Peritonitis Other forms of peritonitis: . Peritonitis is caused by direct irritants.Hiperlipidemik peritonitis . such sepertii bile. lymph gastric. and urine.Aseptic / sterile peritonitis .Peritonitis caused by fungi -Peritonitis source of the bacteria that can not be found.Granulomatous peritonitis .
Pain is a subjective form of pain with movement such as walking. When bacterial peritonitis has occurred. and abdominal distention. 1. abdominal tenderness and rigidity of the local. the pain being spread throughout the abdomen. DIAGNOSIS Diagnosis of peritonitis can be enforced by the clinical. hypotension.1. fever. abdominal distension. and neurogenic). severe peritonitis and types of organisms responsible. Peritonitis can be local. laboratory and X-Ray.1 This stimulation causes pain on any movement that causes a shift in the peritoneum peritoneum. and classical bowel weakened or disappeared . Decreased bowel peristalsis is lost due to temporary paralysis usus. vomiting. weakness. Clinical features that are common in the presence of primary bacterial peritonitis. moderate granulomatous peritonitis .a sign stimulus peritoneum.CLINICAL The presence of blood or fluid in the peritoneum cavity will give a sign . diffuse or general. weight loss. abdominal pain. the patient's body temperature will rise and occurs tachycardia. Stimulation peritonium defans cause tenderness and muscular. Lots of pain if the pain is driven as palpation. breathing. pain and loose bowel press decreased or disappeared. coughing. or tests lainnya. psoas tests. and then gradually spread from the focus of infection. the pain at first because the main cause. The clinical features depend on the extent of peritonitis. tenderness loose. liver dullness may disappear due to the free air under the diaphragm. In addition to pain.CHAPTER III CLINICAL DIAGNOSIS III. fever. and the patient was lethargic and syok.3 Chronic bacterial peritonitis (tuberculous) gives an overview of the clinical presence of night sweats. septic. severe. While the clinical picture in secondary bacterial peritonitis is the existence of acute abdominal pain. and in patients with perforation (eg perforated ulcer). or the public. spread. Clinical features for non bacterial peritonitis with acute bacterial peritonitis. appendicitis). In other situations (eg. shock (hypovolemic. Pain is a sudden.. patients usually exhibit other signs and symptoms are nausea. or straining.
if the cause is a disturbance passage intestine (ileus) obstructive then on plain abdominal radiological 3 positions available are: 1. fever and signs of peritonitis who turned up 2 weeks after surgery.Backs (supine). Peritoneal biopsy percutaneous or laparoscopic tuberculomas show characteristic granulomas. c. 2. small intestine and large intestine dilated.3 Prior to the peritonitis. with a horizontal beam. Picture obtained by the dilation of intestinal obstruction in the proximal region. namely: 1.LLD. thickening dnding intestine. presence or absence of propagation. to see the fluid level and the possibility of bowel perforation.Sleep.2 Radiological Radiological examination is the investigation for consideration in estimating a patient with an acute abdomen. III. In tuberculosa peritonitis peritoneal fluid contains a lot of protein (more than 3 gram/100 ml) and many lymphocytes. preperitonial fat. X-Ray Ileus is a discovery that is not typical of peritonitis. Of water fluid level can be expected passage of intestinal disorders. b. increased hematocrit and metabolic acidosis. identified with the culture of the tubercle bacillus. Free air can be seen in cases of perforation. 3.laboratory test In laboratory tests found the lekositosis. if possible. the rays of the vertical projection of anteroposterior (AP). and is the basis of culture results obtained before diagnosis. Shooting should be made using the film cassette that can cover the entire abdomen and its walls. with a horizontal beam projection AP. such as fish spines picture (Herring bone appearance). Need to set the size of the tape and the film size 35 x 43 cm. When water is short-fluid level layout means there ileus .Skewed to the left (left lateral decubitus = LLD).Or half sitting or standing.showed clinical severe abdominal pain. 2. In plain abdominal peritonitis done three positions. to see the distribution of the intestine. AP projection.
Intestinal general.Sitting or standing. and blurring the abdominal cavity.air fluid level . Radiological obtained the water fluid level and step ladder appearance. . 3. On the allegation whether due to peptic ulcer perforation. . air fluid levels. So radiological in obstructive ileus is a partial bowel distension.high.2 In the case of peritonitis due to bleeding.Lie. So radiological peritonitis is a vagueness in the abdominal cavity.term possibility of interference in the colon.LLD. preperitonial fat and psoas line disappears. Picture will be clearer in the USG (ultrasonography) . the images are not clear on plain abdomen. the main radiological signs are: 1. If prolonged ileus obstructive ileus can be paralitik. It is located between the heart of the abdominal wall or the pelvis to the abdominal wall. where a thorough bowel dilation that sometimes . free water obtained subdiafragma crescent (semilunair shadow). moderate if the long . and the presence of free air or intra subdiafragma peritoneal. got free water peritonial intra abdominal highest. obtained preperitonial fat disappears.Herring bone appearance The difference with obstructive ileus: intestinal dilation fluid thoroughly so the water level was short . 2. While in paralytic ileus radiological obtained as follows: . 3. psoas line disappeared.term (colon) due to colon lumen diameter wider than the small intestine.Half sitting or standing. ruptured appendix or for any other reason.short (small intestine) and long . Peritonitis due to perforation of the radiological picture can be seen on plain abdominal examination 3 positions. The picture obtained is the infra-diaphragmatic free air and water fluid level.sometimes difficult to distinguish between hugely dilated intestinum tenue or intestinum crassum. and herring bone appearance.
11th Lavase peritoneum performed on the diffuse peritonitis. Agar tidak terjadi penyebaran infeksi ketempat yang tidak terkontaminasi maka dapat diberikan antibiotika ( misal sefalosporin ) atau antiseptik (misal povidon iodine) pada cairan irigasi. etc. If localized peritonitis.11 Disposal of septic focus or other inflammatory performed by laparotomy surgery. and defense mechanisms. Antibiotic therapy should be administered as soon as the diagnosis of bacterial peritonitis was made. an incision above the intended sites of inflammation. Great resuscitation with isotonic saline solution is important. and blood pressure should be monitored to assess the adequacy of resuscitation. Broad-spectrum antibiotics are also additional surgical drainage. Bila peritonitisnya terlokalisasi. Urine output of central venous pressure. gastrointestinal decompression by nasogastric suction and intestinal disposal of septic focus (appendix. or a perforated viscus mereseksi. which is using crystalloid solution (saline).III. Returns intravascular volume improve tissue perfusion and delivery of oxygen. appropriate antibiotics.THERAPY The general principle is replacement therapy lost fluids and electrolytes intravenously performed.3. Incision is selected vertical incision middle underlined that generate access to the entire abdomen and easily opened and closed. Must be available a sufficient dose during surgery. . Antibiotic selection based on which organisms are suspected to be the cause. a continuous peritoneal contamination can be prevented by closing. nutrients. because bacteremia will develop during the operation.pain relief measures. sebaiknya tidak dilakukan lavase peritoneum. Surgery technique used to control contamination depends on the location and nature of pathologic gastrointestinal tract. karena tindakan ini akan dapat menyebabkan bakteria menyebar ketempat lain. Broad-spectrum antibiotics are given empirically. karena pipa drain itu dengan segera akan terisolasi/terpisah dari cavum peritoneum. dan dapat menjadi tempat masuk bagi kontaminan eksogen. 5. and then changed its kind after culture results come out.) or other inflammatory causes. In general. Drainase berguna pada keadaan dimana terjadi kontaminasi yang terusmenerus (misal fistula) dan diindikasikan untuk peritonitis terlokalisasi yang tidak dapat direseksi. 2. mengeksklusi.3 Drainase (pengaliran) pada peritonitis umum tidak dianjurkan. if possible drain the pus out and act.
ruptured ectopic pregnancy. etc. III. KOMPLIKASI Complication can occur in acute secondary bacterial peritonitis.III. cholecystitis.Prognosis The prognosis for peritonitis is both local and lightweight is fine. gastroenteritis. .6. Advanced complication intestinal obstruction III.DIFFERENTIAL DIAGNOSIS The differential diagnosis of peritonitis is appendicitis. septicemia and septic syok.5.(hepatic absess) b. where complication can be divided into early and advanced complication.. Intra abdominal sepsis that can not be controlled with multi-system failure residua intraperitoneal portal pyemia abcess. hipovolemik shock. while the general prognosis of peritonitis is lethal due to virulen of organism. : a..4. salpingitis. pancreatitis.
clear membrane covering the abdominal organs and the abdominal wall. infection of the uterus and fallopian tubes. which stick together with the surrounding surface so as to limit the infection. abnormal liver or heart failure. Formed pockets of pus (abscess) among fibrinous adhesions. but it can be settled as fibrinous bands. irritation without an infection. The peritoneum is a thin. 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. The general principles of therapy in peritonitis are: Replacement of lost fluids and electrolytes made intravenously. peritonitis can occur after a surgery. The attachment usually disappears when the infection disappear. peritoneal dialysis (treatment fails kidney). Patofisologi peritoneum peritonitis was the initial reaction to bacterial invasion is the release of fibrinous exudate. b) c) Antibiotic therapy plays a very important role in the treatment of puerperal infection. Peritonitis are localized only in the pelvic cavity called pelvioperitonitis. pelvic inflammatory disease in women who are still active in sexual activity. .CHAPTER IV CONCLUSION Peritonitis is inflammation of the peritoneum which is wrapping the viscera in the abdominal cavity. The cause of peritonitis include: the spread of infection from an infected abdominal organs. which later can cause intestinal obstruction. d) Surgery include infection of the material and correct the cause. Analgesic therapy given to treat pain.
In: Capita Selekta Gastroenterology Children. Makassar: 2005 6. Price.Subanada.Silvia A. Jakarta 2. Aryasa. 5.php?dktg=7&UID 200 705. .List Pustaka 1.NANDA Nursing Diagnosis 2005-2006 Prima Medika: Jakarta 3. and Sudaryat. http://www.Wim de Jong. Some Abnormalities Actions Requiring 7. . Pathophysiology Clinical Concepts Disease Processes. Textbook of Surgery. 2006. Jakarta 4.Peritonitis. EGC. . 2007. 2005. Jakarta: CV Sagung Seto .com/med/peritonitis_pyk.Gastrointestinal Surgery. ECG.System Gastroenterohepatology lectures. Supadmi.medikastore.
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