I.Identity Name: Mr..

S Age: 50 yr Gender: male Religion : Islam Occupation: Self Employed Address: Plumbon Date of admission: 23 - 10-2012 Date of inspection: 25 - 10-2012

II. Anamnesis (Autoanamnesis dated 25-04 - 2010) The main complaint: Abdominal pain Additional complaints: Defecation hard already 1 week, can not fart 1 week, nausea (+), urination no complaints

History of present illness Patients come to the hospital with complaints of pain Arjawinangun abdominal arteries radiating area towards the back.Pain is felt 5 days SMRs. And the pain is intermittent nor continuous. Also found nausea and vomiting, vomiting occurred twice. Patients also complain t o be flatus and bowel 1 week SMRs.Ien te pas Stomach bloating also.BAK patients LANC a r.Fever is not felt by the patient. History of the disease before Hypertension (-), DM (-)

III.Physical examination Status generalist General condition: Looks sick were Awareness: compos mentis Vital sign: Tension: 90/60 Pulse : 90 Respirasi: 28 x Temperature : 36,7 Head: normocephal Eyes: Conjuctiva not anemis and jaundice, isokor round pupil, light reflex + / + Thorax Cast: Inspection: ICTUS cordis is not visible Palpation: ICTUS cordis palpable Percussion: limit of normal heart Auscultation: BJ I-II regular, murmur -, gallop Pulmo: Inspection: hemitoraks movement of the right and left symmetric Palpation: vocal and tactile fremitus hemitoraks symmetrical right and left Percussion: resonant throughout the lung fields Auscultation: vesicular, rhonki - / -, wheezing - / Abdomen Inspection: Not seen any time Palpation: Tenderness + Percussion: Timpani
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Auskulltasi: Noisy intestine increased Genitals: no abnormalities Extremities: warm Akral, edema - / -

IV.Examination Support Routine blood Lab Hb: 6.4 RBC: 2.38 Leukocytes: 17.4 Platelets: 367 KGDS: 89 mg / dl Radiological examination image obtained ilues loka middle abdomen, and the picture does not look peritonitis V. Differential Diagnosis 1.Obstruction Ileus 2. Paralytic ileus
3. Acute Gastroenteritis 4. Acute Appendicitis

VI .Working Diagnosis Obstruction Ileus VII.Management Infusion Rl Cefotaxime

VIII. Prognosis

Ketorolac Ranitidine Dulcolax

Quo ad Vitam: Dubia ad Bonam Quo ad functionam: Dubia ad Bonam

Ileus Obstruction

Intestinal obstruction is abdominal surgical emergencies in a common and account for 60% - 70% of all cases of acute abdomen. Acute abdomen may be caused by abnormalities in the abdomen in the form of inflammation, and penyulitnya, obstructive ileus, ischemic, and hemorrhagic. Some disorders can be caused by direct or indirect injury resulting in perforation or gastrointestinal bleeding sa Luran. Ileus is a disruption passage of intestinal contents is a sign of acute intestinal obstruction requiring immediate aid or action. Ileus is two ileus obstruction and paralytic ileus. Barriers can be caused by the passage of intestinal obstruction or intestinal lumen by peristalsis disturbance. Bowel obstruction or ileus called obstruction (mechanical obstruction) for example, by strangulation, invagination or blockage in the intestinal lumen. Dynamic ileus can be caused by excess dynamic like spasms. Intestinal obstruction is a disorder in both peristalsis in the colon and small intestine. Mechanical obstruction may be due to a lesion in the intestinal wall, outside the gut and in the intestinal lumen. Bowel obstruction can be acute or chronic, partial or total. Chronic intestinal obstruction is usually about as a result of colon carcinoma. Most of the obstruction it affects the small intestine. Total obstruction of the small intestine is gravity that require early diagnosis and emergency surgery. Based on research conducted by Markogiannakis et al (in 2001 - 2002), found 60% of patients who were treated at Hippokration Hospital, Athens experienced ileus obstruction and average - average age around 16-98 years, with a sex ratio of more women than men - men. Embryology Intestinal primitive form since the fourth week of fetal development.Endodermal layer to form the epithelial lining of the digestive tract and splanchnic mesoderm around endermal form of muscular connective tissue and other intestinal lining. Unless the duodenum, where the primitive gut comes from the middle intestine. During the fourth week of fetal development, the length rises rapidly, herniation of intestine was happening until the umbilicus. Round the middle intestine has two branches namely cranial and caudal. Cranial branch evolved into the distal duodenum, and ileum proximal jejenum. While branch caudal to distal ileum, proximal two-thirds of the transverse colon. Bowel herniation was happening until the age of 10 weeks' gestation fetus, when the intestines back into the abdominal cavity. After turning a complete 270 from the starting point, the proximal portion jejenum back into
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the abdomen and occupies the left side of the abdomen with the next ring occupies the right. General Secretary of the last entry and its location in the right upper quadrant, although in the end the cecum will drop to its normal position in the right lower quadrant. Malrotation congenital intestinal anomalies can occur in this process. Phase embryology and levels of intestinal rotation 1.Intestine with superior mesenteric artery and vein in the mesentery would. Intestine after rotating 90 . Located in the proximal part of the right, distal to the left. 2. Duodenal next round dorsal a.mesenterika superior, while the cecum with spin in the ventral colon to the right. 3. Round continues, the cecum on the right is still down to the bottom right. Hindgut formed part transverse colon, descending colon and sigmoid were diperdarahi by a.mesenterika superior. 1. After a complete rotation (270 ) In embriologik, right colon from the middle intestine, whereas the left colon to the rectum comes from the hindgut. In the development of the disorder sometimes occurs embriologik embryonic gut rotation so that the right colon and cecum have a free mesentery. This situation facilitates the rotation or volvulus most common intestinal mesentery as can occur with long roots in the sigmoid colon with a narrow. ANATOMY The small intestine extends from pylorum to caecum length 270 cm to 290 cm. The small intestine is divided into duodenum, and ileum jejenum. The duodenum about 25 cm in length, from the pylorus to jejenum. Long jejenum 100-110 cm and a length of 150 -160 cm ileum. Separation duodenum and jejenum characterized by Treitz ligament. This ligament acts as a suspensory ligament. Kira - about two-fifths of the remaining small intestine is jejenum, and three-fifths are terminal ileum parts. Jejenum have great vascularity which are thicker than ileum. Appendix vermiformis appendix is a tube measuring around your little finger ileosekal located in the area, which is at the apex cecum. In microscopy, the intestinal wall is divided into four layers, namely serous layer, muscularis propria, and submucosa layers mucosal lining. Serous layer is the outermost layer that consists of the parietal peritoneum and visceralis and space that lies between the visceral and parietal layers called the peritoneal cavity. Muscularis propria layer consists of two layers
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of longitudinal muscle is a thin muscle layer and a thick layer of circular muscle. Ganglion cells derived from Myenterica plexus (Auerbach) that sits between the muscle layer and sends stimulation to the second layer. Submucosa layer consists of a layer of connective tissue fibroelastis that contains blood vessels and nerves. Mucosal layer is divided into 3 layers of muscularis mucosa, lamina propria and epithelial layer. Mucosal and submucosal layers form a circular layer called valvula koniventes (Lig.Kerckringi) that protrude into about 3 mm. Mesentery is a broad fold of peritoneum, which hangs like a fan jejenum and ileum from the posterior abdominal wall. Mayus omentum is a peritoneal lapisanganda mengantung of curvatura major stomach and goes down in front of the abdominal viscera. Omentum usually contain a lot of fat and lymph nodes that help protect against infection peritoneal cavity. Lesser omentum is a fold of peritoneum extending from curvatura minor stomach and upper duodenum to the liver, forming Hepatogastrikum ligament and ligament hepatoduodenale. Superior mesenteric artery branched from the aorta just below celiaca artery. These arteries mendarahi entire small intestine except duodenum diperdarahi by gastroduodenalis artery and superior pancreaticoduodenal artery branches. The blood is returned through the superior mesenteric vein, combined with the splenic vein to form the portal vein. Innervated intestine both branches of the autonomic nervous system. Stimulate the parasympathetic stimulation of secretory activity and movement, whereas sympathetic stimulation inhibits bowel movements. Sensory nerve fibers of the sympathetic system delivers pain, while the parasympathetic nerve fibers regulate intestinal reflexes. The large intestine is divided into caecum, colon and rectum. In the caecum and appendix ileosekal valves are attached to the end of the caecum. Caecum occupies approximately the first two or three inches of the colon. Kolon subdivided into ascending colon, transverse colon, and sigmoid descenden. The place where the colon to form a sharp turn to the right and left upper abdomen respectively called the hepatic flexure and the splenic flexure. Sigmoid colon from the iliac crest height and shape of an S-shaped curve Angled bottom while turning left sigmoid colon to the rectum together. The large intestine has four layers of morphologic like other parts of the intestine. Cecum, ascending colon and transverse colon to the right diperdarahi by the superior branch a.mesenterika a.ileokolika, a.kolika right and a.kolika media. The left transverse colon, colon descendens, sigmoid colon and rectum perdarahi largely by inferior a.mesenterika through
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a.kolika sinistra, a.sigmoid and a.hemoroidalis superior. Colonic veins run parallel to arteries. Kolon innervated by the sympathetic fibers from plexus n.splanknikus and presakralis and parasympathetic fibers derived from N.vagus. PHYSIOLOGY The small intestine has two main functions of digestion and absorption materials - nutrients, water, electrolytes and minerals. The process of digestion begins in the mouth and stomach by working ptialin, hydrochloric acid and pepsin to food intake. The process continues in the duodenum, especially by the action of the enzyme - enzymes that hydrolyze pancreatic carbohydrates, fats, and proteins into substances - substances that are more simple. The presence of bicarbonate in the pancreatic secretion help neutralize acids and provide an optimal pH for the enzyme - enzymes. Secretion of bile from the liver to help digestion by emulsifying fats thus providing more surface area for pancreatic lipase work. The digestion process is accomplished by a number of enzymes in the intestinal lymph (sukus enterikus). Many of the enzymes - enzymes present in brush border villi and assimilate substances - nutrients while absorbed. Segmental bowel movement will mix substances eaten with pancreatic secretions, hepatobiliar and intestinal secretions and peristaltic movements propel contents from one end to the other with a speed that is appropriate for optimal absorption and continuous supply of gastric contents. Absorption is the transfer of the final results of the digestion of carbohydrates, fats and proteins through the intestinal wall into the blood and lymph circulation to be used by the cells - the body's cells. In addition, water, electrolytes and vitamins are also absorbed. The movement of bowel function for the digestion and absorption of ingredients - food can run optimally. Bowel movement consists of: 1. Movement mixing (mixing) or segmenting movement that mixes food with enzymes the digestive enzymes to be easy to digest and is absorbed 2. Propulsif peristalsis movement or the push food to the large intestine. Contraction of the small intestine caused by the activity of intestinal smooth muscle consists of 2 layers of the longitudinal muscle layer and the circular muscle layer. Muscles that primarily contribute to the segmentation contractions to mix food is longitudinal muscle. When part distends the food, the intestinal wall to contract locally. Each contraction involves a segment of intestine approximately 1-4 cm. At the time the contract segment of the small

intestine that undergo relaxation, other segments will soon start contractions, and so on. When the small intestine relaxes, the food will be returned to its original position. This movement is repeated continuously so the food will be mixed with digestive enzymes and make contact with the intestinal mucosa and subsequent absorption occurs. Segmentation contractions lasted because of the slow wave which is the basic electric rhythm (BER) of the gastrointestinal smooth muscle. The process of segmentation contraction lasts 8 to 12 times / min in the duodenum and about 7 times / min in the ileum. Peristalsis in the small intestine to push food toward the colon with a speed of 0.5 to 2 cm / sec, which is faster in the proximal than the distal. Peristalsis is very weak and usually disappear after takes approximately 3 to 5 cm Setting the frequency and strength of the movement segmentation mainly governed by the slow wave that produces the action potential caused by the presence of cells - pace maker cells found in the intestinal wall, where the activity of the cell - the cell is affected by the nervous and hormonal systems. Peristaltic activity will increase after eating. This is largely due to the entry of food into the duodenum, causing peristaltic reflex that will spread to the intestinal wall. In addition, the hormone gastrin, CCK, serotonin, and insulin also increase bowel movements. Instead sekretin and inhibit glucagon bowel movements. Upon reaching the ileocaecal valve, food sometimes - sometimes blocked for several hours until someone eating again. At the moment, the increased activity of the peristaltic reflex gastrileal and push food through the colon leading to the ileocaecal valve. Food was settled for a time in the area ileum by the ileocaecal sphincter function so that the food can be absorbed in this area. Ileocaecal valve serves to prevent the food back from the caecum into the ileum. Ileocaecal sphincter function regulated by a feedback mechanism. When the pressure in the caecum increases resulting in dilation, the ileocaecal sphincter contraction increases and ileum peristalsis is reduced thereby slowing the emptying of the ileum. If there is inflammation of the caecum or the appendix the ileocaecal sphincter spasm will experience, and the ileum will experience paralysis so pengosonga ileum severely hampered. Etiology The cause of obstruction in the small intestine can be divided into three, namely extraluminal obstruction, intrinsic obstruction and intraluminal obstruction. Extraluminal obstruction such
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as adhesion, hernia, carcinoma and abscess. Intrinsic obstruction of the intestinal wall as the primary tumor. And as enteroliths intraluminal obstruction, gallstones and foreign bodies. The cause can be seen in the table below. 6

Causes of Obstruction Ileus Lesions extrinsic to the bowel wall (postoperative) Hernia (inguinal, Adhesions

femoral, umbilical) Neoplasms Intraabdominal abscess

Intraluminal obstruction Gallstone Enterolith

Lesions intrinsic to the intestinal wall cyst) Inflammation (Crohn's Congenital (Malrotation,

Disease, Diverticulitis) Neoplasms Traumatic Intusepsi

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Adhesion, inkarserata hernia and colon malignancies most frequently cause obstruction. on adhesion, onset occurs arrived - arrived with complaints of abdominal bloating and abdominal pain.Of the 60% of cases of ileus obstruction in the USA, which is the most common cause adhesion gynecologic surgery, appendectomy and colorectal resection. Ileus due to adhesion is generally not accompanied by strangulation. Adhesion is generally derived from the peritoneal cavity due to local or generalized peritonitis or postoperatively. Adhesions can form adhesions may be in the form of single or multiple. Pathophysiology Patofisiologik events that occur after bowel obstruction is the same, regardless of whether the obstruction was caused by a mechanical or functional causes. The main difference is the mechanical obstruction (ileus obstruction) the peristaltic first - then a strong first intermittent and then disappeared. While in paralytic ileus, peristalsis from the beginning is not there. Patofisiologik changes in bowel obstruction can be seen in the table below. Patofisiologik mechanical bowel obstruction associated with changes in the function of the intestine, where an increase in intraluminal pressure. If there is obstruction the proximal part of the intestine distends and containing gas, fluid and electrolytes. If there is an increase in intraluminal pressure, hypersecretion will increase when the intestinal absorption capacity decreases, resulting in a substantial loss of volume and progressive systemic. Initially, peristalsis in the proximal colon increased to fight the resistance. The ongoing peristaltic activity causing rupture, where the frequency depends on the site of obstruction. If the obstruction persists and an increase in intraluminal pressure, the proximal part of the intestine will not contract properly and bowel become disorganized and lost. Increased intraluminal pressure and the presence of vascular distension caused disruption especially venous stasis. Intestinal wall into edema and bacterial translocation occurs to the blood vessels. Toxin production caused by the translocation of bacteria causing systemic symptoms. Local effect stretching the colon is due to ischemic necrosis with absorption of toxins of bacteria into the peritoneal cavity and systemic circulation. In simple mechanical obstruction, barrier passage appears without vascular and neurologic disturbances. Food and liquids are ingested, intestinal secretions and air would gather in large numbers if obstruksinya complete. Proximal part of the intestine distends and the distal collapse. Secretory function and decreased intestinal absorption of mucous membranes and intestinal wall edema and congestion becomes. Severe intestinal distension
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by itself on a continuous - continuous and progressive will disrupt peristalsis and mucosal secretory function and increase the risk of dehydration, ischemia, necrosis, perfo constellation, peritonitis and death. Strangulated obstruction, usually originated from venous obstruction, which is then followed by occlusion of the artery, causing a rapid ischemic bowel wall. Edema and necrosis of the intestine, accelerate intestinal become gangrene and perforation. DIAGNOSIS

Clinical Symptoms

The main symptoms of ileus obstruction include colicky abdominal pain, nausea, vomiting, abdominal distension and can not defecate (obstipasi). Nausea and vomiting are common in high obstruction lies. When the location of the obstruction in the distal part of the dominant symptom is abdominal pain. Abdominal distention occurs when obstruction persists and the proximal part of the intestine becomes very dilated. Obstruction of the small intestine causing symptoms such as abdominal pain around the umbilicus or the epigastrium. Patients with partial obstruction may develop diarrhea. Sometimes - sometimes dilatation of the bowel can be palpated. Obstruction of the colon usually have a milder clinical symptoms than small bowel obstruction. Generally, symptoms of constipation ended obstipasi and abdominal distension.Vomiting is rare. In the proximal small bowel obstruction symptoms are usually vomiting. Abdominal pain is intermittent or variable and colic with the up and down pattern. If the obstruction is located in the middle or high location of the small intestine (ileum and proximal part jejenum) it is constant pain / settle. At this early stage, normal vital signs. Along with the loss of fluid and electrolytes, dehydration will occur with clinical manifestations of tachycardia and postural hypotension. Body temperature is usually normal but sometimes - sometimes can be increased. From the physical examination found the presence of fever, tachycardia, hypotension, and severe symptoms of dehydration. Fever indicates obstruction strangulate. On examination of the abdomen seemed distended abdomen obtained and peristaltic increases (sound Borborigmi). In the advanced stage where the obstruction continues, peristaltic will weaken and disappear. The presence of blood in feces mixed toucher rectal examination can be suspected of malignancy and intusepsi.

Examination Support
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Laboratory Laboratory tests have limited value in establishing the diagnosis, but it helps provide an assessment of the severity and assist in resuscitation. In the early stages, it was found that normal laboratory results. Subsequently found any hemoconcentration, leukocytosis and abnormal electrolyte values. Increased serum amylase is often obtained. Leukocytosis indicate ischemic or strangulated, but only occurs in 38% - 50% compared to 27% of strangulation obstruction - 44% in non Strangulated obstruction. Increased hematocrit can occur in dehydration. Moreover, it can be found electrolyte disturbance. Blood gas analysis may be impaired, with metabolic alkalosis when severe vomiting, and metabolic acidosis when there is a sign - a sign of shock, dehydration and ketosis. Radiological Dilatation of the colon with the picture "step ladder" and "water fluid levels" in plain abdomen can be concluded that the presence of an obstruction. Plain abdomen have a higher sensitivity of 66% in small bowel obstruction, whereas sensitivity of 84% in colonic obstruction. In plain abdominal match picture "step ladder and air fluid levels" especially at the distal obstruction. In the colon may not seem gas. If stangulasi and necrosis occurs, it will be a picture of a regular muosa loss and the presence of gas in the intestinal wall. Free air on upright thoracic photo showed a bowel perforation. The use of contrast is not recommended because it can cause peritonitis due to perforation. CT scans sometimes - sometimes used for diagnosis in small bowel obstruction to identify patients with complete obstruction and bowel obstruction is suspected abscess or malignancy. COMPLICATIONS Complications that can arise such as bowel perforation, sepsis, shock-dehydration, abscesses, pneumonia, aspiration of the vomit and died. Diagnosis APPEAL Ileus may be caused by processes in intraabdominal and retroperitoneal, including ischemic bowel, ureteric colic, pelvic fractures and after abdominal surgery. In case of paralytic ileus, pain is usually not too heavy and more constant.

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Obstipasi and distention of abdomen showed a large bowel obstruction. Vomiting is infrequent and non-colicky pain. Diagnosis can be established based on the results of x-ray photo showing the obstruction dilatation of the proximal colon. Small bowel obstruction can be confused with acute gastroenteritis, acute appendicitis and acute pancreatitis. Strangulation obstruction have a complaint similar to acute pancreatitis, ischemic enteritis or mesenteric vascular obstruction associated with venous thrombosis. Ileus obstruction should be distinguished from paralytic ileus. MANAGEMENT Basic treatment of obstructive ileus is a correction of electrolyte and fluid balance, eliminating stretching and vomiting with decompression, overcoming peritonitis and shock if present, and remove the obstruction to improve the viability and bowel function returned to normal Partial obstruction can be managed conservatively as long as there defecation and flatus. Decompression by nasogastric tube successfully in 90% of patients. Operative action can be sealed ukan obstruction exactly ten though partial.In obstruks i partial repeat difficult to determine whether or not operative action. Total small bowel obstruction treated with operative action after preparation.Surgery is sometimes difficult to do because kemungkainan rid of strangulation obstruction, especially with the possibility of complications and death in stranguasi. Surgeons must remain alert to the signs and symptoms improved after resuscitation without exception. Surgery should not be decided quickly, in some cases, such as partial obstruction, postoperative obstruction, patients with a history of surgery for obstruction, patients with radiation therapy, inflammation of the intestines and abdominal carcinoma.Some of these cases took first thought. Therapy is usually much nonoperatif selected patients. Pharmacological Medications - broad-spectrum antibiotics can be administered as a prophylactic. Antiemetic may be given to reduce the symptoms of nausea and vomiting.

Operative Preparation

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Time to dilakuakan bergatung opertif action on the state of the patient. The risk of strangulation to be considered despite the abnormal state of the fluid and electrolyte and the need to evaluate the systemic disease. 1. Nasograstik tube. Nasogastric tube in pairs to reduce vomiting, meghindari occurrence of aspiration, and to reduce the amount of air in the lumen of the gut that makes abdominal distention. 2. Resusiatasi fluid and electrolyte In resuscitation to note is overseeing signs - vital signs, dehydration and shock.Patients who develop ileus obstruction dehydrated and balance disorders ektrolit that needs to be given intravenous fluids such as Ringer's lactate. Response to therapy can be seen by monitoring signs - vital signs and the amount of urine to leak. Lack of fluid and electrolyte depends on the type and duration of obstruction. Hemoconcentration that occurs in longstanding obstruction that can not be simply corrected with dextrose solution alone. Loss of isotonic fluids should be initiated with intravenous isotonic saline solution. Gastrointestinal fluid loss is the cause of acid-base balance disorders, and the lack of mechanisms to correct this imbalance neuroendrokin, then we need to correct first. Examination of serum electrolytes and blood gas analysis may help to decide which elektrotit therapy should be given. Patients can not be operated if uncorrected hypokalemia. The amount of fluid and electrolytes needed to be estimated for each patient. Clinical features and association with systemic diseases also need to be monitored. Patients should be provided with strangulation obstruction or blood plasma. Antibiotics should be given if strangulation is suspected.

Operation The operation is performed after rehydration and nasogastric decompression to prevent secondary sepsis. The operation begins with a laparotomy was followed by surgical techniques that are tailored to the results of exploration during laparotomy. Here are some condition or consideration for surgery.

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Situations necessitating emergent operation Incarcerated, strangulated hernias Peritonitis Pneumatosis cystoides intestinalis Pneumoperitoneum Suspected or proven intestinal strangulation Closed-loop obstruction Nonsigmoid colonic volvulus Sigmoid volvulus associated with toxicity or peritoneal signs Complete bowel obstruction Situations necessitating urgent operation Progressive bowel obstruction at any time after nonoperative measures are started Failure to improve with conservative therapy within 24A "48 hr Early postoperative technical Complications Situations in roomates Usually delayed operation is safe Immediate postoperative obstruction

But in strangulation obstruction, toxic effects to make the operation should be performed. Standard in inguinal incision can be performed in patients with a femoral hernia and inkaserata ingunalis. Adesiolisis laparaskopi dilakuakan can also in some patients with the utmost care. operative procedures on the cause of obstruction. On the obstruction on the adhesion should be adhesiolisi, obstruction of the tumor resection can be performed, and obstruction because alineum corpus should be disposed enterotomi. Gangreneus intestine should be resected, but it is difficult to determine whether the gut is still viable or not. Loop soaked with warm saline solution and see color, pulsation mesentrikanya and peristaltiknya a few minutes later. The use of intraoperative Doppler ultrasound is a method to see whether or not the part is still viable bowel obstruction. Florosein qualitative test can help, 1000mg florosein in injected into a peripheral vein for 30-60 minutes which will be seen in ultraviolet light (Wood's lamp). If the results were non-viable resection end-to-end anastomosis is the safest. Ekstirpasi obstructive lesions can not be performed in patients with carcinoma or radiation injury. Anastomosis of the proximal small bowel obstruction distal to the obstruction of the
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small intestine or colon (baypass) is probably the best procedure for these patients. Sometimes adhesion occurs very thick so it does not do the separation and dialkukan anastomosis can not be perfect. Long decompression with tube or tube gastrotomi jejunostomi and pemeberian makana via parenteral be menjadaikan spontaneous healing for several weeks. Decompression on the massive bowel dilatation facilitate abdominal closure and reduction of postoperative healing period. Decompression done by entering the long tube through oral or by needle aspiration of the intestinal wall. To prevent adhesion formation by sewing uncontrolled bowel loops that fit together menjadiakan can not show success. Another Prossedur by entering through a long tube or jejunostomi gastrotomi enough for 10 days is recommended. Pencegahn adhesion to hyaluronic acid bioabsorbable barrier methylcellulose proven effective in lowering the incidence and forms dahesi reopeatif. Generally known 4 types (way) surgery is done on the obstruction ileus. (A) Correction simple (simple correction). This is a simple surgery to rid the intestines of tongs, for example in non-strangulated hernia incarcerata, tongs by streng / adhesion or mild volvulus. (B) Measures operative by-pass. Creating a new gut "through" the colon is clogged, eg intralurninal tumors, Crohn's disease, and so on. (C) Make entero-cutaneous fistula in the proximal part of the obstruction, for example at an advanced stage Ca. (D) Perform a clogged bowel resection and anastomosis make ends intestinal lumen to maintain the continuity of the intestine, for example in carcinomacolon, invagination, Strangulated, and so on. In some obstruction ileus, sometimes done gradually operative action, either because the disease itself or because of an infected person, such as the Ca obstructive sigmoid, first performed a colostomy only, later on bowel resection and anastomosis. Prognosis Strangulated obstruction without mortality was 5% to 8% as long as the operation can be done immediately. Delay in performing surgery or in case of strangulation or other complications will increase the mortality to about 35% or 40%. The prognosis is good if the diagnosis and the action is fast.
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REFERENCES

1. Sjamsuhidajat r, De Jong W. Textbook of Surgery. Edition 2. Jakarta: EGC, 2003. 2. Wilson LM, Lester LB. Small intestine and colon. In: Price SA, Wilson LM, editor. Pathophysiology clinical concepts of disease processes. Translation: dr.Peter Grace. Jakarta: EGC; 1995. Hal.389 - 412. 3. Evers BM. Small intestine. In: Townsend CM, Beauchamp RD, Evers BM, Mttox KL, editors. Sabiston textbook of surgery. The biological basis of modern surgical practice. 17 th ed.Philadelphia: Elsevier Saunders; 2004. p.1323 - 1342. 4. Siregar H, Yusuf I, Sinrang AW, Gani AA. Gastrp-intestinal physiology. Ed.1. Ujungpandang: Fac. Unhas Medicine; 1995. 5. K. Yates Bowel obstruction. In: Cameron P, Jelinek G, Kelly AM, Murray L, Brown AFT, Heyworth T, editors. Textbook of adult emergency medicine. 2 nd ed.New York: Churchill Livingstone; 2004. p.306-9. 6. Naude GP. Gastrointestinal failure in the ICU. In: Bongard FS, Sue DY, editors. A lange medical book Current critical care diagnosis and treatment. 2 nd ed.New York: McGraw-Hill; 2003. p. 383-88.

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