Small bowel obstruction: Clinical manifestations and diagnosis

Authors
Richard A Hodin, MD
Liliana Bordeianou, MD
Section Editors
David Soybel, MD
Lawrence S Friedman, MD
Deputy Editor
Rosemary B Duda, MD, MPH, FACS
Last literature review version 18.2: Maio 2010 | This topic last updated: Setembro 14, 2009 (More)
INTRODUCTION Small bowel obstruction (SBO) occurs when the normal flow of intestinal contents is interrupted.
The most frequent causes 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.
Obstruction leads to dilation of the stomach and small intestine proximal to the blockage, while distal to the blockage
the bowel will decompress 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 causes and treatment of SBO are
discussed separately. (See "Small bowel obstruction: Causes and management".)
PATHOGENESIS 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 [1]. 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. (See "Causes
of metabolic alkalosis".)
Strangulation complicates from 7 to 42 percent of bowel obstructions, and occurs when bowel wall edema and
increasing intraluminal pressure compromise perfusion to a segment of intestine [2]. 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 is significantly increased in the setting of strangulation [2].
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 nonobstructing causes of bowel dilatation.
SYMPTOMS The most common symptoms of SBO 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 [3], focal abdominal pain in the presence of other symptoms of
obstruction may be an ominous sign and should not be ignored. (See "History and physical examination in adults with
abdominal pain".)
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 AND PHYSICAL EXAMINATION A history of previous upper or lower abdominal surgery should be
sought. Patients who have had large bowel resection or other pelvic surgery, appendectomy [4], or previous surgery for
obstruction [5] are especially prone to becoming obstructed. Intra-abdominal malignancy, especially after surgical
treatment, can also predispose to SBO.
Patients with Crohn's disease frequently present with obstruction due to stricture. (See "Clinical manifestations,
diagnosis and prognosis of Crohn's disease in adults".)
Patients who present with SBO but have not had prior abdominal surgery represent a special category of SBO that
requires careful thought. One must assume the presence of a small bowel tumor until proven otherwise in a patient with
a de novo SBO. (See "Treatment of small bowel neoplasms".)
A thorough physical examination is required. 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 highpitched 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, but 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. (See "Approach to the adult with metabolic acidosis".)
Although there is no reliable clinical or laboratory marker for strangulation, serum lactate is elevated in patients with
mesenteric ischemia and is a sensitive, though not specific, marker of strangulation in SBO (sensitivity 90 to 100
percent, specificity 42 to 87 percent) [6,7].
IMAGING The diagnosis of SBO can be made by history and physical examination in the majority of patients.
While imaging is potentially helpful in establishing the diagnosis, in most cases a laparotomy will be needed to make a
definitive diagnosis and for treatment if a patient does not respond to nonoperative management [8].
Plain abdominal radiography Plain abdominal radiography is used to confirm the diagnosis of SBO; 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 [2,9].
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 (picture 1A-B). 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.
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 97 and 96 percent, respectively) [10].
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 [10].
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 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 [11].
Computerized tomography 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 (picture 2). In some cases, closed-loop or
strangulating obstruction may be demonstrated (picture 3).
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 (picture 4A-B). 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 [2]. 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.
Advanced small bowel ischemia can be recognized by intestinal pneumatosis and hemorrhagic mesenteric changes.
Milder ischemia, without actual necrosis, is more difficult to discern on CT [2]. Decreased segmental bowel wall
enhancement, presence of a small bowel feces sign and detection of peritoneal fluid have all been associated with an
increased risk of ischemia at the time of surgery, but none of these findings is very sensitive or specific and should not
be relied upon in isolation [12,13].
Ultrasonography Abdominal ultrasonography can also be useful for the diagnosis of SBO in selected patients. It is
more sensitive and specific than plain films for the diagnosis of small bowel obstruction but not as accurate as CT.
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.
Capsule endoscopy Wireless video endoscopy or video capsule endoscopy (VCE) is a novel noninvasive technology
designed primarily to provide diagnostic imaging of the small intestine, an anatomic site that has proved peculiarly
difficult to visualize. While this technology is useful for making a diagnosis in some situations, it would be
contraindicated in a patient with a SBO. (See "Wireless video capsule endoscopy".)
Comparative studies One study compared the efficacy of plain radiography, ultrasound, and CT scan in 32 patients
presenting with clinical suspicion of intestinal obstruction [14]. 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 [15].
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. (See "Postoperative ileus".)
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 [16].
(See "Acute colonic pseudoobstruction (Ogilvie's syndrome)".)
SUMMARY AND RECOMMENDATIONS

The most frequent causes of small bowel obstruction (SBO) 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. (See 'Introduction' above.)
The most common symptoms of SBO are abdominal distention, vomiting, cramping abdominal pain, and

inability to pass flatus (see 'Symptoms' above).

The diagnosis of SBO can be made by history and physical examination in the majority of patients. (See
'History and physical examination' above.)
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. (See 'Laboratory diagnosis' above.)
Plain abdominal radiography is used to confirm the diagnosis (picture 1A-B); in most patients, no further
radiologic tests are needed. (See 'Imaging' above.)
Small bowel obstruction must be differentiated from non-obstructive intestinal motility disorders such as
paralytic ileus and intestinal pseudo-obstruction. (See 'Differential diagnosis' above.)

ACKNOWLEDGMENT The editors would like to recognize Dr. Robert Quickel, who contributed to previous
versions of this review.

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
Rosemary B Duda, MD, MPH, FACS
Last literature review version 18.2: Maio 2010 | This topic last updated: Junho 3, 2010 (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 (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 "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 an internal hernia
("Petersen Hernia") through the defect created in the mesocolon through which the Roux limb passes (picture 1).
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) (picture 2) [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 (IV) 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 IV 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 IV hydration. Nasogastric losses can be replaced
with IV 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 mercuryfilled 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, watersoluble 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. 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 [45]. 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 [45-49].
In a meta-analysis of 14 prospective studies examining the diagnostic (seven studies) and therapeutic (eight trials) role
of water soluble contrast agents (WCSA), the appearance of WSCA in the colon 4 to 24 hours after administration
predicted resolution of the adhesive SBO with a sensitivity and specificity of 96 and 98 percent, respectively [50].
In the eight trials that examined the therapeutic role of WSCA, there was a significant reduction in the need for an
operative intervention in patients randomly assigned to WSCA versus conventional therapy with bowel rest, nasogastric
aspiration, and intravenous fluid rehydration (20.8 versus 29.6 percent, odds ratio 0.62, 95% CI 0.44-0.88). The WSCA
group also had a significantly shorter hospital stay by almost two days.
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 closed-loop obstruction with fever, leukocytosis, tachycardia, metabolic acidosis, continuous pain or
peritonitis warrant prompt exploration [44].
Every patient considered for exploration due to a suspected small bowel obstruction, whether open or laparoscopically,
should be appropriately resuscitated prior to surgery with IV fluids and have their electrolytes repleted, as indicated.
This is especially important for patients with copious emesis resulting from more proximal obstruction, obstruction
lasting several days, or obstruction causing large-volume intraluminal fluid sequestration. These patient may have

severe metabolic acidosis, volume depletion, and electrolyte abnormalities, and need 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.
Exploratory laparotomy Incision planning is critically important when performing exploratory laparotomy for small
bowel obstruction. A new incision or extension of the previous incision in a cephalad direction will allow entry into a
"virgin" area, avoiding adhesions and bowel loops adherent to the abdominal wall at the site of prior incisions [51,52].
The goals of the operation are to diagnose and resolve the source of the obstruction, resect any nonviable bowel and
minimize the occurrence of an incidental enterotomy. An enterotomy or perforation will lead to peritoneal
contamination with stagnant bowel contents with bacterial overgrowth [51].
Upon entering the peritoneal cavity, it is important to handle dilated bowel proximal to the point of obstruction gently
because the bowel wall can be thin and is easily injured. Cultures of any cloudy fluid should be obtained. Ideally, the
distal, decompressed bowel loops are identified first and followed to the point of obstruction. Dissection should start
from the areas that are relatively free of scar to facilitate proper identification of anatomical structures along the way,
thereby minimizing the chances of injury.
Adhesiolysis is best done with appropriate and gentle traction to maximally expose the adhesion and then cutting the
adhesion with sharp scissors or cautery. The adhesions can be gently stretched over the surgeon's index finger, allowing
clear visibility and traction for division of adhesions [51]. In rare cases, the density of the adhesions and close
adherence of bowel loops may require a scalpel for effective adhesiolysis to be accomplished.
The precise mechanism for the obstruction should be noted [52]. If there is one single adhesive band causing the
obstruction, severing this band may be all that is necessary. If multiple broad based adhesions are present and multiple
bowel loops are involved, an extensive lysis of adhesions may be required. Any internal hernias will require reduction
of the herniated intestine and obliteration of the opening that allowed herniation.
After the site of obstruction is relieved, the need for lysis of all remaining adhesions is debatable. It is probably best to
lyse all adhesions, except in cases where the dissection is difficult and there is added concern about the possibility of an
enterotomy.
Intraoperative assessment of viability With the obstruction relieved, a critical part of the surgical approach to SBO is
to assess bowel viability and decide whether any bowel needs to be resected. 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 [53,54].
An alternative technique involves the IV 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 [53].
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 [55]. 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 [56]. 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.
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 [57-60]. 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 [61].
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 [57,58].
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 [59]. A randomized trial is needed to demonstrate that this procedure is cost-effective and beneficial to patients.
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 [62]. 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 [63-65]. (See "Epithelial ovarian cancer: Initial
surgical management", section on 'Bowel resection'.)
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 [64,66]. 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) [63]. 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 [65].
Early surgery should be pursued in those without known recurrent cancer and with long intervals from
diagnosis of malignancy to development of obstruction [63].
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 [65]. 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 [67-69]. (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 [70-72]. 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 [73,74].
Many different agents have been tried as chemical means of preventing postoperative adhesions. Application of highmolecular-weight dextran solution to peritoneal or denuded surfaces decreases adhesion formation [75]. 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 [75].

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 [76-80]. 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 [81]. 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 [82].
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 [83,84], but this was not seen in the two trials cited above [81,82]. These barriers
should not be used to wrap intestinal anastomoses, since they can result in a higher leak rate [79].
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.)