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Real Doctors (Life Makers)  |  Clinical  |  Surgery & Surgical Subspecialities.  |  SMALL BOWEL OBSTRUCTION - FULL TEXT « previous next »
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« on: /October/ 19, 2005, 07:47:54 PM »

INTRODUCTION ? Small bowel obstruction (SBO) occurs when the normal flow of intestinal contents is interrupted. The most frequent causes of small bowel obstruction are post-operative adhesions and hernias, which cause extrinsic compression of the intestine. Less frequently, tumors or strictures of the small bowel can cause intrinsic blockage.

Obstruction leads to dilation of the stomach and small intestine proximal to the blockage with decompression of the distal small bowel and colon as luminal contents are passed. Symptoms include obstipation, nausea, vomiting and abdominal pain. As the small bowel dilates, its blood flow can be compromised, leading to necrosis, or strangulation and sepsis. Unfortunately, there is no reliable sign or symptom differentiating patients with strangulation or impending strangulation from those in whom surgery will not be necessary. Herein lies the challenge in treating patients with bowel obstruction.

This topic review will focus on the clinical manifestations and diagnosis of SBO. The treatment of SBO and specific forms of SBO are discussed separately.

EPIDEMIOLOGY ? There are numerous causes of small bowel obstruction . Although hernias were the most common cause during the first third of the century, post-operative adhesions now cause approximately three-fourths of small bowel obstructions because of the increase in survival and the large number of patients undergoing laparotomy. The remainder are caused by various hernias, and, less frequently, from obstruction due to tumors (most commonly metastatic colorectal carcinoma, with a smaller number being caused by primary small bowel tumors or ovarian cancers) account for only a small percentage of cases.

The incidence of SBO was estimated in a study of hospital discharges from a National database, which showed that there were more than 300,000 hospitalizations for adhesiolysis (the majority of which were related to SBO), resulting in over 800,000 days of inpatient care and $1.3 billion in expenditures . The rate of hospitalization for adhesiolysis did not change between 1994 and 1998 despite the increasing use of laparoscopy, but it is hoped that such a decrease may be seen in the future.

Classical surgical teaching was that obstruction secondary to postoperative adhesions occurred in 5 percent of patients who had a laparotomy. However, this teaching has been challenged by several more recent reports [2-6]. In one series, 15 percent of patients who had abdominal surgery required readmission for small bowel obstruction within two years of their original operation, while approximately 3 percent required reoperation for obstruction [3]. In another report that included 309 patients with mechanical small bowel obstruction, the risk of recurrent obstruction over the next 10 years was 42 percent for all patients, 29 percent for those treated operatively and 53 percent for those treated non-operatively [4]. In most surgical series, 50 to 70 percent of patients admitted with SBO required surgery; the overall mortality has been approximately 5 percent.

The risk of SBO depends in part upon the type of surgery being performed and the cause of the SBO. In the above studies, the risk of recurrence was negligible for patients whose obstructions were caused by hernia. In other reports, SBO was more common after lower intestinal surgery, particularly colon and rectal surgery for cancer. 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]. In another report, the incidence of obstruction after negative laparotomy for trauma was 2 to 3 percent [6].

? The hallmark of SBO is dehydration and its sequelae. When normal luminal flow of intestinal contents is interrupted, the small intestine proximal to the obstruction begins to dilate as intestinal secretions are prevented from passing distally. This has a number of consequences that depend in part upon the site and the degree of obstruction. Patients with proximal obstruction (jejunum) experience repeated bouts of nausea and emesis and typically cease taking in food or liquids orally. These features are less prominent in patients with distal obstruction (ileum).

Swallowed air and gas from bacterial fermentation accumulates, adding to the dilatation. Bacterial overgrowth occurs in the proximal small bowel, the contents of which are normally nearly sterile, and therefore the emesis can become feculent due to bacterial overgrowth. As the process continues, the bowel wall becomes edematous and the intestine's normal absorptive function is lost so that even more fluid is sequestered in the bowel lumen. Secretion of fluid into the lumen of the proximal dilated bowel increases [7]. With worsening edema of the intestine, there is transudative loss of fluid into the peritoneal cavity.

The end result is increasing dehydration with concomitant electrolyte derangements and decreased urine output. Tachycardia, oliguria, azotemia, and hypotension can result from progressive dehydration. In more proximal obstruction, emesis causes the loss of fluid containing Na, K, H, and Cl, resulting in metabolic alkalosis.

Strangulation complicates approximately 10 percent of bowel obstructions, and occurs when bowel wall edema and increasing intraluminal pressure compromise perfusion to a segment of intestine [8]. Necrosis ensues, with concomitant fever and leukocytosis, which will eventually lead to perforation unless the process is interrupted. Necrosis of the small bowel during obstruction is most commonly caused by twisting of the mesentery (such as in volvulus) from an adhesive band acting as the point of fixation. Mortality increases in the setting of strangulation from approximately 5 percent for all patients with SBO to as much as 37 percent in some studies [8].

Obstruction of the small intestine can be complete or partial. Strangulation of the intestine almost always occurs in the setting of complete obstruction. One exception to that rule is a Richter's hernia, a condition in which only part of the circumference of a segment of intestine passes through a hernia orifice. In such cases strangulation can occur without complete obstruction of the lumen. A closed-loop obstruction occurs when a segment of intestine is obstructed in two locations, creating a segment with no proximal or distal outlet. If undetected, closed-loop obstruction can rapidly progress to strangulation. In this setting, there may only be a short segment of intestine that is distended, making the diagnosis difficult because of minimal abdominal distention. It is therefore of utmost importance to determine whether a bowel obstruction is complete or partial, and whether strangulation of the intestine is impending or has occurred. The location and cause of obstruction are of secondary importance, although in rare circumstances this information may affect subsequent management decisions.

DIAGNOSIS ? The diagnosis of SBO is generally made based upon clinical and radiographic features and must be distinguished from nonmechanical causes of bowel dilatation.

? The most common symptoms of small bowel obstruction are abdominal distention, vomiting, crampy abdominal pain, and inability to pass flatus. In proximal obstruction, nausea and vomiting can be relatively severe compared to distal obstruction, but distention of the abdomen is somewhat less since the proximal intestine acts as a reservoir as it dilates.

Abdominal pain is frequently described as periumbilical and crampy, with paroxysms of pain occurring every four or five minutes. Some clinicians feel that progression from crampy to constant pain is a sign of impending strangulation. Although this has not been borne out in all studies [9], focal abdominal pain in the presence of other symptoms of obstruction may be an ominous sign and should not be ignored.

Patients may or may not complain of obstipation and inability to pass flatus since the colon requires 12 to 24 hours to empty after the onset of bowel obstruction. As a result, flatus and even passage of feces may continue after onset of symptoms.

History ? A history of previous upper or lower abdominal surgery should be sought. Patients who have had large bowel resection or other pelvic surgery, appendectomy [10], or previous surgery for obstruction [4] are especially prone to becoming obstructed. Patients with Crohn's disease frequently present with obstruction. Intra-abdominal malignancy, especially treated surgically, can also predispose to small bowel obstruction.

Physical examination ? A thorough physical examination is required when evaluating the patient with suspected small bowel obstruction. Systemic signs, such as fever and tachycardia, are associated with strangulating obstruction. Hypotension, oliguria, and dry mucous membranes indicate dehydration. Inspection of the abdomen should reveal any surgical scars and the degree of distention. Auscultation may reveal high-pitched or hypoactive bowel sounds, and is therefore not very helpful. Tenderness to light percussion suggests the presence of peritonitis, as does rebound, guarding, and localized tenderness. Tympany is usually present due to air-filled loops of bowel or stomach. The presence of any abdominal mass may indicate an abscess, volvulus, or tumor. A thorough search for inguinal, femoral, and incisional hernias must be undertaken. Rectal examination may reveal an empty rectal vault and occasionally a rectal mass can be the cause of obstruction. Gross or occult blood can be found with intestinal neoplasm, ischemia, and intussusception.

Laboratory diagnosis ? Laboratory studies are generally not helpful in determining the presence of small bowel obstruction, but can help in the assessment of the degree of dehydration. The urea nitrogen and creatinine and the hematocrit can be used to gauge the degree of dehydration. Leukocytosis with leftward shift may indicate the presence of strangulation. As discussed above, metabolic alkalosis can be seen in patients who have frequent emesis. Metabolic (lactic) acidosis can result if the bowel becomes ischemic or if dehydration is severe enough to cause hypoperfusion of the gut and other tissues. Although there is no reliable clinical or laboratory marker for strangulation, serum lactate is found to be elevated in patients with mesenteric ischemia and is a sensitive, though not specific, marker of strangulation in SBO [11,12].

Radiologic diagnosis ? Basic radiologic examination should include an upright chest film to rule out the presence of free air as well as supine and upright abdominal films. When the patient is supine, the entire width of air and fluid-filled loops of bowel will be visible, since the air-fluid interface is parallel to the x-ray plate. This permits an estimate of the amount of distention. When the patient is in the upright position, the air-fluid interface is perpendicular to the film and shows as an air-fluid level. Multiple air-fluid levels with distended loops of small bowel are seen in small bowel obstruction, although occasionally they can be seen in the setting of a paralytic ileus. The presence of air in the colon or rectum makes the diagnosis of complete obstruction less likely, particularly if symptoms have been present for more than 24 hours. If the patient cannot be placed into an upright position, a left lateral decubitus abdominal film can reveal the presence of free air and/or air-fluid levels.

? Computerized tomography ? The diagnosis of small bowel obstruction can be made by history and physical examination in the majority of patients. Plain abdominal radiography is used to confirm the diagnosis; in most patients, no further radiologic tests are needed. However, plain films can be equivocal in 20 to 30 percent of patients and are "normal, nonspecific, or misleading" in 10 to 20 percent [8,13]. In the past, the diagnosis was often confirmed by a small bowel follow-through. More recently, computerized tomography (CT) has been replacing the small bowel series as the adjunctive study of choice since it can simultaneously provide information about the presence, level, severity, and cause of obstruction. In addition, other abdominal pathology can be detected. In some cases, closed-loop or strangulating obstruction may be demonstrated.

For a CT scan, dilute barium or water-soluble contrast is given either orally or via the nasogastric tube approximately 30 to 120 minutes prior to scanning. Intravenous contrast is also given. The diagnosis of obstruction is made when there is a discrepancy in the caliber of proximal and distal small bowel [8]. Often a point of transition can be identified. Absence of air or fluid in the distal small bowel or colon denotes a complete obstruction. Closed-loop obstruction often appears as a distended, fluid-filled, sometimes C-shaped or U-shaped loop of bowel with prominent mesenteric vessels converging on the point of torsion or incarceration. Proximal loops are dilated and filled with gas and fluid. Intestinal pneumatosis and hemorrhagic mesenteric changes can be seen in advanced strangulation. In most cases of SBO, no obvious source of obstruction is seen, since adhesions cannot be detected by CT scan [8].

? Small bowel series ? The diagnosis and degree of small bowel obstruction can also be confirmed by a small bowel follow-through series or by enteroclysis, in which the duodenum is intubated and air and contrast are instilled directly into the small intestine. These studies are highly sensitive and are the gold standard for determining whether an obstruction is partial or complete. The presence of water soluble contrast in the cecum within 24 hours predicts resolution of adhesive small bowel obstruction (sensitivity and specificity of 96 percent) [14]. Although it has been suggested that water soluble contrast may have a therapeutic role in resolving an episode of small bowel obstruction, the available evidence indicates that the need for surgical intervention is not decreased by the use of such agents [14].

However, small bowel studies are inferior to CT in the detection of closed-loop obstruction or ischemia, and rarely offer any indication of the etiology of the obstruction. As a result, most radiologists currently recommend CT as the first study after plain films in difficult-to-diagnose bowel obstructions, to be followed by a small bowel series if the scan is not diagnostic [15].

? Ultrasonography ? Abdominal ultrasonography can also be useful. It is more sensitive and specific than plain films for the diagnosis of small bowel obstruction but not as accurate as CT. One study, for example, compared the efficacy of plain radiography, ultrasound, and CT scan in 32 patients presenting with clinical suspicion of intestinal obstruction [16]. The gold-standard for diagnosis was either surgery, small bowel follow-through, or clinical follow-up. The sensitivity and specificity of CT scanning was 93 and 100 percent, respectively, compared to 83 and 100 percent for ultrasound, and 50 and 75 percent for plain radiography. The level of obstruction was correctly predicted in 93 percent on CT scan compared to only 70 and 60 percent for ultrasound and plain films, respectively. CT was superior to ultrasound and plain radiography for determining the cause of the obstruction (87 versus 23 and 7 percent, respectively). In another report, the positive predictive value of an akinetic dilated loop on ultrasound for strangulation was 73 percent [17].

Although not as helpful as CT for diagnosis of location, cause, and possible strangulation, ultrasound may be appropriate for pregnant patients or as a bedside test for the critically ill.

Differential diagnosis ? Small bowel obstruction must be differentiated from non-obstructive intestinal motility disorders such as paralytic ileus and intestinal pseudo-obstruction. Paralytic ileus occurs to some degree after almost all open abdominal operations and can also be caused by peritonitis, trauma, and intestinal ischemia. It is exacerbated by electrolyte disorders, particularly hypokalemia. As the intestine becomes distended, the patient experiences many of the symptoms of obstruction described above, despite the absence of a mechanical obstruction.

On radiologic examination there is air in the colon and rectum, and by CT or small bowel series there is no demonstrable obstruction. Similarly, intestinal pseudo-obstruction is a chronic condition characterized by symptoms of recurrent abdominal distention. The colon is generally affected more than the small intestine. No mechanical cause can be demonstrated in these patients, and they frequently have a history of several previous operations for bowel obstruction during which no cause for obstruction could be found. Laparotomy should be avoided in these patients; once diagnosed, the preferred treatment is nasogastric suction, correction of any metabolic abnormalities, and in some cases parenteral nutrition [18].

RECOMMENDATIONS ? The most frequent causes of small bowel obstruction are post-operative adhesions and hernias, which cause extrinsic compression of the intestine. Less frequently, tumors or strictures of the small bowel can cause intrinsic blockage.

The most common symptoms are abdominal distention, vomiting, crampy abdominal pain, and inability to pass flatus. In proximal obstruction, nausea and vomiting can be relatively severe compared to distal obstruction, but distention of the abdomen is somewhat less since the proximal intestine acts as a reservoir as it dilates.

The diagnosis can be made by history and physical examination in the majority of patients. Plain abdominal radiography is used to confirm the diagnosis; in most patients, no further radiologic tests are needed. Small bowel obstruction must be differentiated from non-obstructive intestinal motility disorders such as paralytic ileus and intestinal pseudo-obstruction
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« Reply #1 on: /October/ 19, 2005, 07:51:33 PM »


INITIAL EVALUATION ? The primary goals in the initial evaluation of patients with SBO are to determine:

 ? The degree of dehydration and metabolic derangement present

 ? Need for and timing of operative intervention

Suspected impending or ongoing strangulation warrants operative intervention as soon as the patient is stable, whereas other situations may permit a period of safe observation prior to surgery. Even if strangulation is suspected, it may be necessary to resuscitate the patient in an intensive care unit, which can also help to prevent hypotension upon the induction of anesthesia.

Adequate intravenous access should be obtained. A nasogastric tube can prevent aspiration subsequent to emesis by emptying the stomach of fluid and suctioning away swallowed air and upper gastrointestinal secretions. Although nasogastric suction may prevent further bowel distension, it is not an effective means to decompress the bowel.

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.

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.

However, several settings may lend themselves to relatively safe nonoperative management. Nonoperative management is more likely to be successful in patients with partial compared to complete SBO. This was illustrated in a study that included 311 patients in whom successful nonoperative management was observed far more often in those with partial SBO (84 versus 19 percent) [1]. The authors recommended that patients with complete obstruction should be brought expeditiously to the operating room, whereas those with partial obstruction should be managed initially with nasogastric suction and intravenous fluids.

Patients with obstruction due to metastatic intraabdominal malignancy, recurrent adhesive obstruction, obstructing radiation enteritis, or during the early postoperative period can also be safely managed with an initial trial of nasogastric suction. As with any group of patients, operative therapy should be undertaken if signs or symptoms of strangulation occur. Radiologic demonstration of mesenteric ischemia or closed-loop obstruction in any patient should also warrant prompt surgical intervention.

NONOPERATIVE MANAGEMENT ? 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) [2].

The presence of constant abdominal pain or change of pain from colicky to constant has been proposed as a marker of strangulation. However, several studies indicate the difficulty in accurately predicting strangulation preoperatively. One retrospective study of 480 patients with SBO not caused by external hernias or mesenteric vascular occlusion found that the presence of constant abdominal pain could not be used to predict the presence of strangulation [3]. Another study found that no parameter was sensitive, specific, and predictive for strangulation in the setting of small bowel obstruction [4]. Furthermore, 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.

Long decompression tubes ? A variety of long decompression tubes (such as the Miller-Abbot tube) were used in the past in an attempt to decompress the bowel and avoid the need for surgery. The tubes were usually 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 the standard and long tubes found no significant difference in the percentage of patients ultimately requiring surgical intervention [5,6]. Furthermore, the long tubes often do not pass into the small intestine, and when they did, they sometimes formed knots, rendering them difficult to remove. Thus, long tubes are now used rarely.

OPERATIVE MANAGEMENT ? The timing of surgical intervention requires careful consideration. Approximately one-half to three-fourths of patients admitted for small bowel obstruction require operation. Patients suspected of having complete or closed-loop obstruction should be brought to the operating room as quickly as possible. 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, dehydration, 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. Abdominal wall hernias and inguinal hernias can sometimes be reduced and the patient observed until surgery can be scheduled. Operative treatment of most other types of small bowel obstruction requires exploratory laparotomy, usually via a midline incision. The etiology of the obstruction cannot always be determined preoperatively. "De novo" obstruction, or obstruction occurring in a patient without previous laparotomy, is rarely caused by adhesions, and usually requires operation. Specific treatment of different conditions will be discussed subsequently.

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 such subjective criteria is reliable but may result in unnecessary resection of viable intestine [7,8]. 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 [7].

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 of the closest audible Doppler signal in dogs [9]. 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 [10]. 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.

SPECIFIC CAUSES ? Special clinical issues may arise with particular forms of SBO.

Intraluminal small bowel obstruction ? Gastrointestinal bezoars can be caused by high fiber dietary habits, poor dentition with resultant inability to properly chew food, and medications [11]. 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 [11]. (See "Gastric bezoars").

Gallstones cause 1 to 2 percent of small bowel obstructions, usually affecting 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 [12]. (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 [13], and controversy exists regarding whether to perform cholecystectomy at the time of operative treatment of bowel obstruction by enterotomy and stone removal. Severely impacted stones may require removal by bowel resection. Proper surgical therapy also includes palpation of the rest of the intestinal tract and removal of all large stones. In a case series and review, the authors recommend that cholecystectomy be performed as part of the original surgery to avoid late biliary complications [13].

Strictures and small intestinal tumors ? 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 non irradiated bowel [18].

 ? 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").

 ? Intraluminal neoplasms such as carcinoid, small bowel carcinoma, and lymphoma can cause obstruction as well. Symptoms usually develop gradually and progressively. The treatment of choice is resection when possible [20,21].

Trauma ? Traumatic small bowel obstruction is found most commonly in children. Complete or incomplete obstruction caused by intramural hematoma results in nausea, vomiting, and upper abdominal tenderness. The duodenum is the most frequently involved 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.

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 [22]. If obstruction persists longer than 14 days, some authors recommend surgery since irreversible intestinal fibrosis may have occurred [23]. 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 [22].

Intussusception ? The peak incidence of intussusception occurs between five and nine months of age. Diagnosis is usually made clinically. Primary idiopathic intussusception accounts for 90 percent of pediatric cases. In such cases, the lead point causing the intussusceptum (bowel that becomes intussuscepted) to enter the intussuscipiens (bowel into which intussusceptum is drawn) is felt to be hypertrophied lymphatic tissue in the terminal ileum. Eighty percent of pediatric intussusceptions are ileocolic (show picture 1). Clinical signs include episodic abdominal distress, currant jelly stools, and bilious emesis in a previously healthy infant. The treatment of choice is radiographic reduction with either air or barium, with surgery reserved for unreduceability or perforation [24]. (See "Intussusception in children").

Adult intussusception more commonly involves a distinct pathologic lead point, which can be malignant in up to one-half of cases [25]. A "target sign" by computed tomography may be seen. 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. Adults with intussusception usually require surgical reduction and/or resection.

Uncommon hernias ? Congenital and acquired internal hernias cause 0.6 to 5.8 percent of cases of SBO [26]. 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 [27].

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 [27].

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 [28]. Other internal hernia defects should be closed after reduction of herniated small bowel has been achieved.

Bowel obstruction in patients with cancer ? Small bowel obstruction in patients with cancer is a common and difficult problem. It has been described in as many as 42 percent of women with ovarian carcinoma and 28 percent of patients with colorectal carcinoma [29]. Some surgeons are reluctant to operate on patients with previous surgery for intraabdominal malignancy because they believe that an obstruction due to cancer is not likely to be relieved by surgery [30]. Furthermore, surgery for malignant obstruction has a high in-hospital mortality (28 to 45 percent). However, the success of surgery for relieving obstruction in patients with cancer has been in the range of 64 to 76 percent in most surgical series, and it should 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 [31-33]. (See "Surgical management and prognosis of epithelial ovarian cancer", section on Bowel obstruction).

It is important to differentiate malignant obstruction from bowel 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 [32,34]. 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) [31]. Although the literature is somewhat confusing, several recommendations can be made:

 ? As with any patient with small bowel obstruction, a trial of nonoperative therapy is warranted for patients without complete obstruction or suspected gangrenous bowel [33].

 ? Early surgery should be pursued in those without known recurrent cancer and with long intervals from diagnosis of malignancy to development of obstruction [31].

 ? 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 [33]. Computed tomography may be of help in distinguishing the cause of obstruction in those with a history of cancer but without a known recurrence.

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. Alternatives include gastrostomy tube placement with home electrolyte solution or TPN [35,36]. In addition, 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 [37,38]. Patients with end-stage malignancy may be best treated with comfort measures only. (See "Symptom control in the terminally ill cancer patient").

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 below).

Early postoperative obstruction and adynamic ileus can be distinguished clinically in that 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 [39]. Patients with adymanic ileus do not experience this postoperative period of return of bowel function. The two entities can also 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 [40].

Management has traditionally been conservative, ie, nonoperative, for the first 7 to 14 days after diagnosis, since about 90 percent will resolve spontaneously [41]. 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 post-laparoscopic 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 [42]. 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 trochar site problem requiring surgical intervention. On the other hand, in more complicated laparoscopic procedures, other causes of obstruction may be seen and not all of these will require surgery.

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« Reply #2 on: /October/ 19, 2005, 07:51:58 PM »

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 [43-45]. Authors typically point out that patients without intraabdominal malignancy, inflammatory bowel disease, or more than one previous laparotomy for bowel obstruction are candidates.

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 [43,44].

Numerous retrospective reports indicate that laparoscopic treatment of small bowel obstruction is safe and effective. However, great care must be taken in lysing adhesions that are associated with distended bowel. At least one trial indicates that this approach may result in earlier return of bowel function and shorter hospital stays [45]. A randomized prospective trial is needed to demonstrate that this procedure is cost-effective and beneficial to patients.

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 [46,47].

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 [48]. 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 [48].

The most promising technologies for adhesion prevention involve 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 [49-53]. These products are somewhat difficult to handle surgically and do not affect adhesion formation in other places in the abdomen. Neither "Intercede" nor "Seprafilm" has thus far been shown to decrease the incidence of post-operative adhesive small bowel obstruction. Furthermore, based upon some work in experimental animals, it is possible that these agents will lead to an increase in the incidence of septic complications [54,55], but this important issue will need to be resolved with further studies.

SUMMARY AND RECOMMENDATIONS ? Small bowel obstruction occurs when the normal flow of intestinal contents is interrupted. The most frequent causes of small bowel obstruction are postoperative adhesions and hernias, which cause extrinsic compression of the intestine. Less frequently, tumors or strictures of the small bowel can cause intrinsic blockage.

The primary goals in the initial evaluation of patients with SBO are to determine:

? ?The degree of dehydration and metabolic derangement present

? ?Need for and timing of operative intervention

Suspected impending or ongoing strangulation warrants operative intervention as soon as the patient is stable, whereas other situations may permit a period of safe observation prior to surgery. Even if strangulation is suspected, it may be necessary to resuscitate the patient in an intensive care unit, which can also help to prevent hypotension upon the induction of anesthesia.

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.

The timing of surgical intervention requires careful consideration. Approximately one-half to three-fourths of patients admitted for small bowel obstruction require operation. The nature of the obstruction determines the type and extent of surgery.

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