Small bowel obstruction: Causes and management

Authors Richard A Hodin, MD Liliana Bordeianou, MD Section Editors David Soybel, MD Lawrence S Friedman, MD Deputy Editor Susan E Pories, MD, FACS

Last literature review version 17.3: September 2009 | This topic last updated: October 8, 2009 (More)

INTRODUCTION Small bowel obstruction (SBO) occurs when the normal flow of intestinal contents is interrupted. Postoperative adhesions are the most common cause of mechanical SBO, which cause extrinsic compression of the intestine. Malignant tumors or strictures of the small bowel can cause intrinsic blockage and are the second leading cause of SBO. Hernias cause extrinsic compression and are the third most common cause of SBO [1] . Intussusception, volvulus, Crohn's disease, and gallstones (gallstone ileus) account for only a small percentage of cases (show table 1).

This topic review will focus on the causes and treatment of SBO. The clinical manifestations and diagnosis of SBO are presented separately. (See "Small bowel obstruction: Clinical manifestations and diagnosis").

CAUSES OF OBSTRUCTION

Adhesions Postoperative adhesions cause the majority of small bowel obstructions. The risk of developing an obstruction after surgery from postoperative adhesions is estimated to be between 15 and 42 percent [2-6] . In a study of over 12,000 patients undergoing open lower abdominal surgery, 25 percent of readmissions for obstruction were in the first postoperative year, but obstruction continued to occur throughout the 10 year study period [2] .

Population based studies have shown that 24 percent of patients undergo surgery during their index admission [7] . Of those who underwent surgery, 38 percent had lysis of adhesions, 18 percent had lysis of adhesions with a small bowel resection, and the remainder had a hernia repair or a small bowel resection with a hernia repair [7] .

The risk of SBO due to adhesions depends in part upon the type of surgery being performed and the cause of the SBO. A study comparing open appendectomy to open cholecystectomy in a series of 567 patients showed that obstruction was significantly more common after appendectomy (10.7 versus 6.4 percent) [5] . However, the belief that lower intestinal and pelvic surgery lead to higher rates of postoperative small bowel obstructions than upper abdominal surgery has weak support in the literature. A study of patients who underwent colorectal cancer surgery found no difference in postoperative obstruction rates between those who required pelvic dissections as compared to those who did not [8] .

In fact, the etiology of postoperative small bowel adhesions may be multifactorial. The extent and the location of the dissection may be one important predictor of adhesion formation, but not the only one. For example, laparoscopic surgery appears to lead to a decrease in the frequency of postoperative adhesions, despite the fact that the procedures and dissection are similar to those done with the open approach [9] . The cause for the differences in the rates of postoperative adhesions between open and laparoscopic surgery is not clear.

Malignancy Malignant tumors are the second most common cause of SBO, accounting for about 20 percent of cases [1] . SBO has been described in as many as 42 percent of women with ovarian carcinoma and 28 percent of patients with colorectal carcinoma [10] . (See "Surgery for recurrent epithelial ovarian cancer" and see "Surgical management and palliation in patients who present with stage IV colorectal cancer").

Hernias Hernias are the third leading cause of intestinal obstruction and account for approximately 10 percent of all cases [1] . Ventral and inguinal hernias are most commonly represented, although internal hernias, femoral, obturator and parastomal hernias also occur.

Congenital and acquired internal hernias cause 0.6 to 5.8 percent of cases of SBO [11] . An obturator hernia occurs through the pelvic obturator canal, a rigid ring made up of the underside of the superior pubic ramus and the obturator fascia. It accounts for 0.2 to 0.4 percent of obstructions in the United States and is referred to as "little old ladies' hernia" because it is most common in emaciated older women. Obturator hernias have been associated with a mortality of 25 percent due to the difficulty in diagnosis and the population in which it occurs [12] .

Other types of congenital internal hernias include paraduodenal, transmesenteric, and transomental hernias. Acquired internal hernias are often caused by failure to close mesenteric defects after bowel resection or by other artificially created foraminae through which small bowel can herniate. Diagnosis is rarely made preoperatively, as presentation is indistinguishable from other causes of mechanical small bowel obstruction. Computed tomography can be useful in suspected cases of obturator hernia [12] .

Operative therapy includes reduction of herniated small bowel with resection of non-viable segments. There is debate regarding closure of the obturator canal as the tissues are difficult to approximate and recurrence complicates only 0 to 10 percent of cases without canal closure [13] . Other internal hernia defects should be closed after reduction of herniated small bowel has been achieved.

Strictures Intraluminal stricture can be caused by a number of disorders including Crohn's disease, certain drugs such as enteric-coated potassium chloride solutions and NSAIDs, radiation therapy, ischemia, and tumors [14,15] . Resection is avoided to the extent possible in patients with Crohn's disease because of the likelihood of subsequent resection and short bowel syndrome. (See "Surgical management of inflammatory bowel disease"). Radiation therapy for abdominal malignancy can also cause stricture, especially in previously operated patients where adhesions may fix loops of small intestine within the field of radiation [16] . Because irradiated bowel heals poorly, operative treatment usually requires bypass [17] or resection, with at least one side of the anastomosis being performed with nonirradiated bowel [18] . (See "Gastrointestinal toxicity of radiation therapy"). Stricture can also result from

an episode of mesenteric ischemia. Because the ileocolic artery is the last branch of the superior mesenteric artery, the usual site of ischemic stricture in the small bowel is the distal ileum [19] . (See "Acute mesenteric ischemia").

Small intestinal tumors Intraluminal neoplasms such as carcinoid, small bowel carcinoma, and lymphoma can cause obstruction. Symptoms usually develop gradually and progressively. (See "Treatment of small bowel neoplasms").

Early postoperative obstruction Early postoperative bowel obstruction is defined as occurring within 30 days of the initial operation. The incidence is estimated to be 1 to 4 percent. The cause is almost always adhesions unless the index operation was laparoscopic. (See "Laparoscopic treatment" below).

Early postoperative obstruction and adynamic ileus can be distinguished clinically: Nearly all patients with early postoperative bowel obstruction have an initial period of return of bowel function and oral intake, which is then followed by nausea, vomiting, abdominal pain, and distention [20] . Patients with adynamic ileus do not experience postoperative period of return of bowel function. Early postoperative bowel obstruction and adynamic ileus can be differentiated radiologically (plain films or CT scan) since patients with obstruction have a predominance of small bowel gaseous distention and a paucity of air in the colon [21] .

Management has traditionally been conservative, ie, nonoperative, for the first 7 to 14 days after diagnosis, since about 90 percent will resolve spontaneously [22] . The soft, filmy adhesions that develop early after operation do not generally cause strangulation and usually undergo dissolution/reformation, thereby relieving the obstruction. Patients with signs or symptoms of strangulation should be operated on expeditiously.

In contrast, early postoperative obstruction after laparoscopy usually requires operative intervention. One study demonstrated that virtually all patients in their series with postlaparoscopic obstruction eventually needed reoperation. In all cases, the cause of obstruction was small bowel incarcerated in a peritoneal defect caused by trocar placement or peritoneal incision for herniorrhaphy [23] . However, the most likely cause of SBO after laparoscopy depends upon the procedure that was performed. SBO in the setting of simple laparoscopic cholecystectomy is almost always caused by a trocar site problem requiring surgical intervention. On the other

hand, in more complicated laparoscopic procedures, other causes of obstruction may be seen.

For example, following a laparoscopic gastric bypass to treat morbid obesity, patients may develop a "Petersen Hernia" through the defect created in the mesocolon through which the Roux limb passes. Frequently these hernias present with a closed loop small bowel obstruction and need surgery. They should be suspected when a gastric bypass patient presents with symptoms of SBO and a CT scan shows dilatation in both the pancreaticobiliary and alimentary limbs [24] .

Trauma Traumatic small bowel obstruction caused by intramural hematoma results in nausea, vomiting, and upper abdominal tenderness. The duodenum is the most frequently involved segment of the bowel because it is fixed in the retroperitoneum and easily compressed between the abdominal wall and the vertebral column. A common cause is injury from a seat belt. (See "General approach to blunt abdominal trauma in adults").

The diagnosis can be established with an upper gastrointestinal series. Patients who do not present with peritonitis can be managed conservatively with nasogastric suction and total parenteral nutrition [25] . (See "Nutritional support in critically ill patients: Parenteral nutrition").

If obstruction persists longer than 14 days, some authors recommend surgery since irreversible intestinal fibrosis may have occurred [26] . If initial laparotomy is performed, the usual treatment is incision and drainage of the hematoma. Resection is rarely required. However, late fibrosis of the affected segment can occur and cause reobstruction due to gradual narrowing of the intestinal lumen [25] .

Intussusception Intussusception is an "internal prolapse" of the bowel, that leads to obstruction and compromise of mesenteric blood flow, with resultant inflammation and the potential for ischemia of the bowel wall [27] . This occurs when a mass or lead point in the bowel (intussusceptum) is pulled forward by normal peristalsis, with resultant invagination or telescoping of the bowel wall (intussuscipiens) (show picture 1) [28] .

Bowel intussusception is rare in adults, and accounts for 1 to 5 percent of bowel obstruction [27] . Adult intussusception commonly involves a distinct pathologic lead point, which is malignant in over half of the cases [11,27,29] . Pediatric intussusception is usually due to a benign etiology and can usually be managed with non-operative reduction. (See "Intussusception in children").

Intussusceptions can be classified by etiology (benign lesion [eg, polyps], malignant lesion, or idiopathic) or by location: Entero-enteric: Confined to the small bowel Colo-colic: Involving the large bowel only Ileo-colic: Prolapse of the terminal ileum within the ascending colon Ileo-cecal: The ileo-cecal valve is the leading point of intussusception

Symptoms are often chronic; intermittent abdominal pain is the most common presentation in adults. Other common symptoms are those associated with intermittent partial bowel obstruction and can include nausea, vomiting, melena, weight loss, fever, and constipation [28] .

Plain abdominal films show small bowel obstruction. The diagnosis is most often made with computed tomography (CT) [28] . A "target sign" may be seen on CT on perpendicular view, while the intussusception will appear as a sausage shaped mass when the CT beam is parallel to the longitudinal axis. The distended loop of bowel (intussuscipiens) has a thickened wall because it represents two layers of bowel. However, target signs are sometimes seen on CT scans of patients who do not have a clinical presentation indicative of bowel obstruction. In such cases, the finding is of little clinical significance and is probably related to normal peristalsis.

Because of the high percentage of associated malignancy, radiologic decompression is not appropriate in the adult population and surgical resection using appropriate oncologic techniques is recommended in most cases [27] . However, if a benign diagnosis has been established preoperatively or the patient is at risk for short bowel syndrome, a combined approach with limited intestinal resections and snare polypectomies is more appropriate.

An increased incidence of intussusception has been reported in patients with acquired immune deficiency syndrome (AIDS) [12,13,28] . This is due to the high incidence of infectious and neoplastic conditions of the bowel in AIDS patients, such

as lymphoid hyperplasia, Kaposi's sarcoma, and non-Hodgkin's lymphoma. (See "AIDS-related Kaposi's sarcoma: Clinical features and treatment").

Bezoars Gastrointestinal bezoars can be caused by high fiber dietary habits, poor dentition with resultant inability to properly chew food, and medications [30] . The usual therapy for obstruction due to gastrointestinal bezoar is laparotomy with enterotomy and removal of the offending bezoar. Endoscopy or gastrotomy can be used to remove or mince gastric bezoars at the time of surgery for bowel obstruction. Enzymatic digestion has also been used [30] . (See "Gastric bezoars").

Gallstone ileus Gallstones cause 1 to 2 percent of small bowel obstructions and usually affects older patients. "Gallstone ileus" results from erosion and fistulization between the biliary and intestinal tracts, with the most common form being cholecystoduodenal fistula. Other possible entry sites include stomach, jejunum, ileum, and colon. Gallstones can also fistulize to the duodenum from the distal common bile duct [31] . (See "Gallstone ileus").

Radiographic signs include aberrantly located gallstones, pneumobilia, and bowel obstruction. Only one-half of the patients with gallstone ileus in one series had the diagnosis made preoperatively. The most common site of obstruction is the terminal ileum, and obstructing gallstones are reported to be 2.5 cm or larger in most series. Mortality rates are reported from 12 to 27 percent [32] .

Surgical treatment for gallstone ileus in patients with significant comorbidities consists of enterolithotomy alone (open or laparoscopic) during the acute episode. Cholecystectomy and fistula takedown should be performed after the patient has recovered from the acute episode [33,34] .

A one-stage procedure for gallstone ileus should be reserved for young, fit and low risk patients.

INITIAL MANAGEMENT The primary goals in the initial management of patients with SBO are to determine: The degree of volume depletion and metabolic derangement The severity, cause, extent and location of the obstruction Whether nonoperative management can be considered The need for and timing of operative intervention

Adequate intravenous access should be obtained for fluid resuscitation. Suspected impending or ongoing strangulation, with ischemia of an isolated segment of small bowel, warrants operative intervention as soon as possible, whereas other situations may permit a period of safe observation prior to surgery. Even if strangulation is suspected and operative intervention is planned, it may be necessary to resuscitate the patient in an intensive care unit, which can help to prevent hypotension upon the induction of anesthesia. (See "Maintenance and replacement fluid therapy in adults").

A Foley catheter should be placed to monitor urine output, and crystalloid solution (usually Lactated Ringer's), should be given until the patient makes urine or is clinically euvolemic. If necessary, a central venous catheter or Swan-Ganz catheter can be inserted to aid in fluid management, particularly in patients with history of congestive heart failure. (See "Indications for and complications of central venous catheters").

The phrase "never let the sun rise or set on a small bowel obstruction" has long been a cardinal rule of general surgeons. To prevent strangulation of the intestine and its attendant morbidity and mortality, it has been recommended that obstructed patients should be observed for no longer than 12 to 24 hours, after which time, if no improvement is shown, the patient should be brought to surgery.

Prompt surgical intervention is warranted in patients with obstruction in which there is no prior history of abdominal surgery (so-called "de novo" obstruction) or cases in which closed-loop obstruction or strangulation are strongly suspected. Radiologic demonstration of mesenteric ischemia or closed-loop obstruction in any patient should also prompt surgical intervention. (See "Small bowel obstruction: Clinical manifestations and diagnosis").

NONOPERATIVE MANAGEMENT Nonoperative management with nasogastric suction and intravenous fluids can sometimes be successful in patients with partial SBO [1,7,35] . This includes patients with partial SBO due to metastatic intraabdominal malignancy, recurrent adhesive obstruction, obstructing radiation enteritis, or during the early postoperative period. (See "Small bowel obstruction: Clinical manifestations and diagnosis").

Safe nonoperative management of small bowel obstruction requires that small bowel strangulation be ruled out to the extent possible. Mortality for patients with gangrenous strangulated obstruction is substantially higher than for patients with simple mechanical obstruction relieved within 24 hours (4.5 to 31 versus approximately 1 percent) [36] .

Frequent clinical reassessments of the patient are required to ensure that there are no developing signs of strangulation. If there is concern that the patient has increasing pain, distension and persistent high NG output, surgical exploration should be considered.

It is difficult to accurately predict strangulation preoperatively [37,38] . In one study, experienced clinicians were wrong more than one-half of the time for preoperative diagnoses of strangulation or no strangulation in patients eventually found to have gangrenous bowel [38] .

Repeat CT scans may be helpful to detect early signs of bowel ischemia such as thickening of the small bowel wall and/or mesentery, air in the bowel wall, or ascitic fluid. There is little role for repeated plain abdominal films, given that such x-rays can only detect the latest stage of obstruction (ie, perforation with free air).

Nasogastric tube The management of nasogastric (NG) tubes in the setting of a small bowel obstruction remains a matter of clinical judgment and may differ from patient to patient. In patients with complete or high-grade small bowel obstruction, placement of a nasogastric tube can decompress the distended stomach and improve patient comfort.

A soft 14 French, well lubricated NG tube works well and should be placed with the patient in the upright sitting position. An NG tube of this size has a better chance of sumping and suctioning intestinal contents efficiently than a smaller tube. It is helpful to provide the patient with a cup of water and a straw, and to take advantage of the patient's own swallowing mechanism to pass the tube into the esophagus and then into the stomach. Excessive gagging along with the inability to speak suggests that the tube may be within the trachea, and should therefore be withdrawn and replaced.

Ideally, the tip of the tube should placed into the most dependent portion of the stomach. Instillation of air while listening over the epigastrium is not an accurate way to ensure that the tube is in proper position since the air may be heard even if the tip of tube is in too far or not far enough. Aspiration of gastric contents through the tube indicates that the tip lies within the gastrointestinal tract. As an alternative, the tube can be flushed with 20 to 30 cc of warm water and then an attempt made to suck the water back into the tube with a large syringe. If most of the instilled water can be retrieved, the tube is likely in the proper position. If the fluid cannot be drawn back, the tube should be readjusted and the test repeated [39] .

Ideal tube positioning should be documented with a plain x-ray [40] . Once the NG tube is in its proper position, it should be taped to the nose securely, but care should be taken not to push the tube up against the nares too tightly with the tape as this can cause pressure necrosis [41] . The NG tube should then be placed on intermittent low wall suction.

Many patients experience discomfort related to the gag reflex, which will almost always pass within 24 to 48 hours. Several small randomized trials have shown that instillation of local anesthetic sprays (eg, preservative free lidocaine spray, 4 percent delivered by single dose atomizer to the nose and pharynx) into the oropharynx can help alleviate some of the gag reflex and discomfort associated with the placement of an NG tube [42] .

The development of new chest pain suggestive of acid reflux in a patient with a newly placed nasogastric tube may indicate the development of esophagitis and the nasogastric tube should ideally be removed. For patients who still require an NG tube, suppression of gastric acid secretion to decrease the acidity of the material that refluxes into the esophagus is helpful. (See "Medical management of gastroesophageal reflux disease in adults").

The amount of output from the NG tube should be carefully documented to help with clinical judgments regarding the progression or resolution of the obstruction, and the requirement for intravenous hydration. Nasogastric losses can be replaced with intravenous normal saline plus KCL (30 to 40 meq/L). (See "Maintenance and replacement fluid therapy in adults").

Resolution of a small bowel obstruction is generally accompanied by a decrease in abdominal distension, the passage of flatus and/or stool per rectum, and a decrease in the volume of nasogastric tube output. In cases where the obstruction is clearly resolved, the nasogastric tube can be simply removed and the diet advanced as tolerated. In cases where the resolution of the obstruction is not so clear, the tube can be clamped for periods of four hours at a time and residuals checked. If the residuals are less than 100 cc after four hours and the patient is not nauseated, the tube can usually be safely removed as this indicates that most of the gastric contents are emptying normally.

Long decompression tubes A variety of long decompression tubes (such as the Miller-Abbott tube) were used in the past in an attempt to decompress the bowel and avoid the need for surgery. The tubes were weighted with a mercury-filled balloon and passed into the stomach, after which the patient was placed into the right lateral decubitus position so that peristalsis would carry the tube beyond the pylorus and into the more distal jejunum. Several trials comparing standard NG tubes and long tubes found no significant difference in the percentage of patients ultimately requiring surgical intervention [35,43] . Furthermore, the long tubes often do not pass into the small intestine, and sometimes form knots, rendering them difficult to remove. Thus, long tubes are now used rarely.

Water soluble contrast Hypertonic water soluble contrast agents (eg, Gastrografin) can be used for both diagnostic and therapeutic purposes in the setting of partial small bowel obstruction [44] . Gastrografin is a radio-opaque, water-soluble hypertonic liquid contrast agent given orally or through an NG tube.

For diagnostic purposes, Gastrografin can be used in conjunction with a CT scan to reassess the bowel for signs of strangulation.

Gastrografin draws fluid into the lumen due to its hypertonic constitution. The fluid shifts decrease intestinal wall edema and stimulate intestinal peristalsis, thereby improving bowel function and decreasing length of stay. A randomized trial of 76 patients with partial SBO found that patients who received Gastrografin were significantly more likely to avoid surgery (82 versus 45 percent) [45] . Patients who received gastrografin also had significantly more rapid resolution of symptoms and a shorter length of hospital stay. Others have also shown earlier improvement in symptoms and shorter hospital stays, but there have been inconsistent reports as to whether gastrografin reduces the rate of surgical intervention [46-48] .

The amount of Gastrografin to be administered generally ranges from 7.5 mL over 30 minutes to 22.5 mL over a course of 2 hours. This dose can be repeated if it is ineffective, with the caveat that use of more than a total of 100 mL of Gastrografin has not been studied [49] .

Abdominal radiographs should be performed no later than 24 hours after administration of the Gastrografin. In general, failure of the contrast to reach the colon 24 hours later should influence, but not dictate, the decision to operate. The time allowed for non-operative resolution following instillation of Gastrografin is a matter of clinical judgment in these patients. If there is concern that the patient has increasing pain, distension and persistent high NG output, surgical exploration should be considered.

OPERATIVE MANAGEMENT The timing of surgical intervention requires careful consideration. Approximately one-quarter of patients admitted for small bowel obstruction will require operation. Patients suspected of having complete or closedloop obstruction with fever, leukocytosis, tachycardia, metabolic acidosis, continuous pain or peritonitis warrant prompt exploration [44] .

Patients with copious emesis resulting from more proximal obstruction, obstruction lasting several days, or obstruction causing large-volume intraluminal fluid sequestration may have severe metabolic acidosis, volume depletion, and electrolyte abnormalities, and may need some degree of resuscitation prior to operation.

The nature of the obstruction determines the type and extent of surgery. Incarcerated inguinal hernias causing obstruction can usually be treated through an inguinal incision even if bowel resection is required. Operative treatment of most other types of small bowel obstruction requires laparotomy or laparoscopy for exploration. However, the etiology of the obstruction cannot always be determined preoperatively.

Laparoscopic treatment The indications for laparoscopy continue to expand as surgeons become more comfortable with laparoscopic techniques and procedures. Several retrospective series of patients treated laparoscopically for small bowel

obstruction have now been published [50-53] . Patients without intraabdominal malignancy, inflammatory bowel disease, or more than one previous laparotomy for bowel obstruction are candidates for consideration of the laparoscopic approach. The best candidates for consideration of laparoscopic management include those with mild abdominal distention, proximal obstruction, partial obstruction and anticipated single band obstruction [44] . Successful laparoscopic lysis of adhesions requires skilled surgeons and careful selection of patients [54] .

Success rates are in the range of 60 to 80 percent, and complications are rare but include iatrogenic perforation of the distended bowel, usually from trocar placement. Most authors recommend that the initial trocar be placed via the open technique in an area of the abdomen not previously incised. The left upper quadrant is a suitable substitute location if the midline is not available. Subsequent trocars are placed under direct vision, and some authors recommend that the infraumbilical region be cleared of adhesions and a port placed there for camera insertion. Care is taken to use atraumatic grasping instruments to run the bowel so as to avoid perforation. An electric table will allow the patient to be tilted aggressively to the side and placed into the Trendelenburg and reverse Trendelenburg positions; this will allow the distended bowel to fall away from the area being examined. Most authors recommend beginning at the cecum with the patient in Trendelenburg position and tilted 30 degrees to the left, exposing the right lower quadrant [50,51] .

Numerous retrospective reports indicate that laparoscopic treatment of small bowel obstruction is safe and effective. However, great care must be taken in lysing adhesions and manipulation of distended, edematous bowel. At least one trial indicates that this approach may result in earlier return of bowel function and shorter hospital stays than open surgery [52] . A randomized trial is needed to demonstrate that this procedure is cost-effective and beneficial to patients.

Intraoperative assessment of viability A critical part of the surgical approach to SBO is the assessment of bowel viability. Assessment may be particularly challenging when relief of the bowel obstruction is achieved without bowel resection (such as in the presence of a hernia, adhesions, volvulus, and occasionally intussusception) and in the setting of a complete or closed-loop obstruction. The usual approach to assess bowel viability involves wrapping any questionably viable bowel in warm saline-soaked laparotomy pads and waiting 15 minutes prior to final assessment. Return of normal color, motility, and the presence of mesenteric pulses are signs used by most surgeons to indicate viable intestine.

The use of subjective criteria to assess bowel viability may result in unnecessary resection of viable intestine [55,56] . An alternative technique involves the intravenous injection of fluorescein (1000 mg) with subsequent illumination of the intestine using fluorescent light. Patchy fluorescence or areas of nonfluorescence indicate nonviable bowel. This technique has been found to be superior to standard clinical judgment and standard Doppler ultrasound examination in the setting of intestinal ischemia [55] .

Standard Doppler examination may be useful in delineating the limits of resection of ischemic intestine in that pathologic evidence of progressive intestinal necrosis is found between 2 and 3 cm distal to the closest audible Doppler signal in dogs [57] . Laser Doppler flowmetry (LDF) is a refinement of the Doppler technique, which has also been found to be superior to clinical judgment in a prospective trial involving 48 segments of intestine in 13 patients with superior mesenteric arterial occlusion [58] . Unfortunately LDF requires equipment that is not widely available.

A number of other methods have been described, including pH studies, tonometry, surface oximetry, and myoelectric analysis. A practical approach is to evaluate questionably viable segments first clinically, then with fluorescein if necessary. Standard Doppler examination (or LDF if available) can be used as an adjunctive technique in areas in which the fluorescein examination is difficult to interpret. Because marginally viable segments may survive in the short term only to become strictured later, it is probably better to err on the side of removing most questionable areas. However, in situations where removal of the entire length of marginally viable bowel can lead to short gut syndrome (eg. adhesions in a patient with prior resections for Crohn's disease), preserving bowel of borderline appearance is prudent. When bowel of borderline appearance is not resected, a reexploration 24 hours later is mandated to ascertain return of viability.

TREATMENT OF SBO IN PATIENTS WITH MALIGNANCY Some surgeons are reluctant to operate on patients with previous surgery for intraabdominal malignancy because they believe that an obstruction due to metastatic cancer is not likely to be relieved by surgery [10] . However, the success of surgery for relieving obstruction in patients with cancer is reported as high as 71 percent in a series of 14 patients with malignant gastrointestinal obstruction due to recurrent ovarian cancer [59] . It should also be kept in mind that nonoperative therapy for malignant obstruction is also associated with high mortality (35 to 56 percent) and

a high failure rate [60-62] . (See "Epithelial ovarian cancer: Initial surgical management", section on Bowel obstruction).

It is important to differentiate malignant obstruction from obstruction due to other causes in patients with known malignancy. Even in obstructed patients with known recurrence, about one-third of obstructions are due to benign adhesions [61,63] . In patients operated on for treatment of intraabdominal malignancy, obstructions due to recurrent cancer tend to occur earlier after surgery than adhesive obstructions (21 versus 61 months) [60] . Several recommendations for the care of these patients can be made: As with any patient with partial small bowel obstruction, a trial of nonoperative therapy is warranted [62] . Early surgery should be pursued in those without known recurrent cancer and with long intervals from diagnosis of malignancy to development of obstruction [60] . In those with partial obstruction and either recurrent malignancy or short interval to development of obstruction after surgery for malignancy, prolonged medical management may be offered [62] . Computed tomography (CT) or Positron Emission Tomography (PET) scans may be of help in distinguishing the cause of obstruction in those with a history of cancer without a known recurrence. In addition, the scans can provide evidence of overall disease burden, such that the long-term prognosis can be better assessed.

Patients in whom malignant obstruction cannot be relieved medically or surgically may require prolonged hospitalization and nasogastric tube drainage as well as administration of fluids or total parenteral nutrition (TPN). Alternatives include home TPN or gastrostomy tube placement with home electrolyte solution [64-66] . (See "Overview of parenteral and enteral nutrition").

Several small studies have suggested that octreotide, a somatostatin analog, can alleviate vomiting and even permit nasogastric tube removal in patients with terminal cancer and malignant bowel obstruction when traditional anti-nausea agents failed [67-69] . Patients with end-stage malignancy may be best treated with comfort measures only. (See "Overview of symptom control in the terminally ill cancer patient").

PREVENTION Attempts at prevention of small bowel obstruction have been focused largely on the prevention or control of adhesion formation. The earliest methods were mechanical, and involved suturing or plicating the bowel during surgery for adhesive obstruction into patterns or conformations that would prevent

subsequent obstruction. These methods have been found to be ineffective and fraught with complications, and are not currently used.

Another mechanical means of preventing reobstruction involves placement of a long intestinal tube, or Baker tube, via a jejunostomy. The Baker tube traverses the entire small bowel and the end of the tube is left in the distal ascending colon. This technique, known as "stitchless plication," is intended to prevent postoperative kinking of the bowel during the 14 days it is left in place. The Baker tube is not frequently used and has not been definitively shown to decrease the incidence of recurrent adhesive bowel obstruction [70,71] .

Many different agents have been tried as chemical means of preventing postoperative adhesions. Application of high-molecular-weight dextran solution to peritoneal or denuded surfaces decreases adhesion formation [72] . However, along with this decrease comes an inhibition of the host's ability to wall off infection, as evidenced by an increased rate of peritonitis in experimental animals [72] .

One technology for adhesion prevention involves bioresorbable barrier membranes. Currently, there are two commercially available membranes. Both the "Intercede" membrane (oxygenated regenerated cellulose, Ethicon Inc, Somerville, New Jersey) and "Seprafilm" (sodium hyaluronate-based carboxymethylcellulose, Genzyme Corp, Cambridge, Massachusetts), appear to be safe and effective in preventing adhesions to surfaces on which they are placed intraoperatively [73-77] . These products are somewhat difficult to handle surgically and do not affect adhesion formation in other places in the abdomen. (See "Preventing postoperative peritoneal adhesions").

In a prospective multicenter trial, Seprafilm did not decrease the incidence of postoperative small bowel obstruction, although SBO specifically due to adhesions were slightly decreased [78] . In a later controlled trial of 150 patients undergoing surgery for gastric cancer, there was no significant difference in the incidence of small bowel obstruction after three years of follow-up [79] .

Based upon some work in experimental animals, there has been concern that these agents will lead to an increase in the incidence of septic complications [80,81] , but this was not seen in the two trials cited above [78,79] . These barriers should not be

used to wrap intestinal anastomoses, since they can result in a higher leak rate [76] .

Lastly, laparoscopic surgery, when possible, appears to lead to a decrease in the frequency of postoperative adhesions. (See "Adhesions" above).

SUMMARY AND RECOMMENDATIONS Small bowel obstruction (SBO) occurs when the normal flow of intestinal contents is interrupted. (See "Introduction" above). The most frequent causes of small bowel obstruction are postoperative adhesions, malignancies and hernias, which cause extrinsic compression of the intestine. Less frequently, strictures of the small bowel can cause intrinsic blockage. (See "Causes of obstruction" above). The initial management of patients with SBO includes volume resuscitation, correction of metabolic abnormalities and an assessment of the need for operative intervention. (See "Initial management" above). Nonoperative management with nasogastric suction and intravenous fluids can sometimes be successful in patients with partial SBO. This approach requires frequent reassessments of the patient to ensure that there are no developing signs of strangulation. (See "Nonoperative management" above). We suggest giving a hypertonic water soluble contrast agent (eg, Gastrografin) as part of nonoperative treatment of partial small bowel obstruction (Grade 2B). Patients who receive gastrografin have more rapid resolution of symptoms, a shorter length of hospital stay, and possibly less need for surgical intervention. (See "Nonoperative management" above). We suggest a period of observation prior to surgery for patients with partial small bowel obstruction, provided that small bowel strangulation has been ruled out to the extent possible (Grade 2C). (See "Nonoperative management" above). Patients with suspected, impending, or ongoing strangulation require prompt operative intervention. (See "Operative management" above).