The content on the UpToDate website is not intended nor recommended as a substitute for medical
advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health
care professional regarding any medical questions or conditions. The use of this website is governed by
the UpToDate Terms of Use ©2017 UpToDate, Inc.
Epidemiology, clinical features, and diagnosis of mechanical small bowel obstruction in adults
View in Chinese
Authors
Liliana Bordeianou, MD, MPH
Daniel Dante Yeh, MD
Section Editors
David I Soybel, MD
Robert S Hockberger, MD, FACEP
Deputy Editor
Wenliang Chen, MD, PhD
Contributor disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2017. | This topic last updated: Jun 21, 2016.
INTRODUCTION — Bowel obstruction occurs when the normal flow of intraluminal contents is
interrupted. Obstruction can be functional (due to abnormal intestinal physiology) or due to a mechanical
obstruction, which can be acute or chronic [1,2]. Advanced small bowel obstruction leads to bowel dilation
and retention of fluid within the lumen proximal to the obstruction, while distal to the obstruction, as
luminal contents pass, the bowel decompresses. If bowel dilation is excessive, or strangulation occurs,
perfusion to the intestine can be compromised leading to necrosis or perforation, complications which
increase the mortality associated with small bowel obstruction.
The most common causes of mechanical small bowel obstruction are postoperative adhesions and
hernias. Other etiologies of small bowel obstruction include disease intrinsic to the wall of the small
intestine (eg, tumors, stricture, intramural hematoma) and processes that cause intraluminal obstruction
(eg, intussusception, gallstones, foreign bodies).
The clinical manifestations, diagnosis, and etiology of small bowel obstruction will be reviewed here.
(See "Palliative care of bowel obstruction in cancer patients".)
The clinical features and diagnosis of colorectal obstruction is reviewed elsewhere. (See "Overview of
mechanical colorectal obstruction".)
PATHOPHYSIOLOGY — Bowel obstruction occurs when the normal flow of intraluminal contents is
interrupted. The cause of the obstruction may be external to the bowel (extrinsic), within the wall of the
bowel (intrinsic), or due to a luminal defect that prevents the passage of gastrointestinal contents.
Obstruction of the small intestine can be partial or complete. A type of complete obstruction, a closedloop obstruction, occurs when the intestine is obstructed at two locations, creating a segment with no
proximal or distal outlet. Closed-loop obstruction can rapidly progress to bowel strangulation.
(See 'Complete obstruction and closed-loop obstruction' below.)
Normal physiology — The main function of the small intestine is to digest and absorb nutrients. Microvilli
and circular folds (ie, valvulae conniventes, plicae circulares or valves of Kerkring) increase the surface
area available for absorption and cause the intestinal contents to twist while flowing through the small
intestine. These circular folds can be seen in radiographic studies. The small bowel is relatively free of
microbes, whereas the large intestine is populated with commensal bacteria that aid digestion, synthesize
a number of vitamins, and break down bilirubin.
Obstructive physiology — Obstruction leads to progressive dilation of the intestine proximal to the
blockage, while distal to the blockage the bowel will decompress as luminal contents pass. Swallowed air
and gas from bacterial fermentation can accumulate, adding to bowel distention. As the process
continues, the bowel wall becomes edematous, normal absorptive function is lost, and fluid is
sequestered into the bowel lumen [3]. There may also be transudative loss of fluid from the intestinal
lumen into the peritoneal cavity. With proximal bowel obstruction, ongoing emesis leads to additional loss
of fluid containing Na, K, H, and Cl, and metabolic alkalosis. These fluid losses can result in hypovolemia.
Bacterial overgrowth can also occur in the proximal small bowel, which is normally nearly sterile, and
emesis can become feculent.
If bowel dilation is excessive, the intramural vessels of the small intestine become compromised and
perfusion to the wall of the intestine is reduced [4]. If perfusion to a segment of intestine is inadequate to
meet the metabolic needs of the tissue, ischemia will occur, which will eventually lead to necrosis and
perforation unless the process is interrupted [5]. Alternatively, ischemic necrosis of the bowel can be
related to twisting of the bowel and/or its mesentery around an adhesive band or to lax intestinal
attachments.
EPIDEMIOLOGY AND RISK FACTORS — Acute, mechanical small bowel obstruction is a common
surgical emergency [1,2,6]. It is estimated that over 300,000 laparotomies per year are performed in the
United States for adhesion-related obstructions [7,8]. Ischemia, which complicates 7 to 42 percent of
bowel obstructions, significantly increases mortality associated with bowel obstruction [5].
The small bowel is involved in about 80 percent of cases of mechanical intestinal obstruction [9,10]. The
incidence is similar for males and females. In one Polish study of adult patients, the average age of
patients with acute obstruction was 64 years, women comprised 60 percent of the group, and the small
bowel was affected in 76 percent [9].
Risk factors — Factors that increase the risk for the most common etiologies of small bowel obstruction
are given in the table (table 1). (See 'Specific etiologies' below.)
The most important risk factors include:
●Prior abdominal or pelvic surgery
●Abdominal wall or groin hernia
●Intestinal inflammation
●History of, or increased risk for neoplasm
●Prior irradiation
●History of foreign body ingestion
The most important risk factor for mechanical small bowel obstruction in the United States is prior
abdominal surgery causing postoperative adhesions. In a systematic review, the incidence of
postoperative bowel obstruction due to any cause was 9.4 percent; the incidence related to adhesive
disease was 2.4 percent [11]. Patients with a history of prior abdominal or pelvic surgery, and particularly
colorectal surgery, appendectomy, gynecologic surgery, prior adhesiolysis, and resection of malignancy
are prone to adhesive small bowel obstruction [4,11-13]. The risk of early postoperative bowel obstruction
due to adhesions, which is defined as bowel obstruction occurring during the same hospitalization as the
index operation, is increased after exploration for trauma. The incidence was reported at 3.9 percent in a
review of 571 patients, a rate that was increased fourfold in the presence of traumatic gastrointestinal
perforation [14]. (See "Traumatic gastrointestinal injury in the adult patient".)
For patients with a history of prior bowel obstruction, whether managed medically or surgically, the
likelihood of recurrent obstruction increases with an increasing number of episodes [2,15]. Postoperative
adhesions may also be responsible for chronic abdominal pain. In a systematic review, five studies
evaluated the incidence of chronic abdominal pain following surgery. Chronic abdominal pain was
attributable to postoperative adhesions in 34 to 67 percent of patients [11]. In women, chronic pelvic pain
and infertility can also result from adhesions [16]. (See "Causes of chronic pelvic pain in
women" and "Causes of female infertility", section on 'Fallopian tube abnormalities/pelvic adhesions'.)
Adhesive small bowel obstruction can occur in the absence of prior abdominal surgery. In one study of 34
patients without prior history of abdominal surgery, who underwent exploratory surgery for small bowel
obstruction, 29 (85 percent) had adhesions as the cause of the obstruction [17]. Adhesions may have
developed in these patients as a result of intraabdominal inflammation (eg, diverticulitis, Crohn disease).
Alternatively, other pathologies, such as hernia or volvulus, can lead to small bowel obstruction by
causing extrinsic compression of the small bowel.
Diseases intrinsic to the wall of the small intestine (eg, tumor, stricture, intramural hematoma) can cause
small bowel obstruction by encroaching upon the lumen of the bowel because of edema, infiltration of the
bowel wall, or from progressive stricture formation.
Processes that block an otherwise normal bowel lumen (eg, intussusception, gallstones, foreign body)
can also cause mechanical bowel obstruction.
CLINICAL PRESENTATIONS — Patients with bowel obstruction can present with an abrupt onset of
abdominal pain, nausea, vomiting, and abdominal distention, or with intermittent, acute symptoms that
resolve only to recur again. Some patients with chronic, partial obstruction may develop superimposed
symptoms and signs of acute bowel obstruction [1,6,16,18-29].
The history should seek to identify risk factors for bowel obstruction, which will provide clues to the
potential etiology of suspected bowel obstruction or suggest an alternative diagnosis [30,31]. In addition,
prescription or nonprescription medications (including recreational drugs) that may impact bowel function
should be noted (table 2). (See 'Risk factors' above and 'Specific etiologies' below and 'Differential
diagnosis' below.)
Acute small bowel obstruction
Symptoms — The symptoms most commonly associated with acute small bowel obstruction are nausea,
vomiting, cramping abdominal pain, and obstipation (ie, inability to pass flatus or stool).
The frequency of these symptoms is variable and depends upon the etiology and location of obstruction
(proximal versus distal), and degree of obstruction (partial versus complete). One review of 300
patients reported abdominal pain in 92 percent of patients, and vomiting in 82 percent [19]. In a
prospective study of 150 patients, the absence of the passage of flatus (90 percent) or stool (81 percent)
was the most common presenting symptom [5]. In a study of patients with adhesive small bowel
obstruction, the presenting symptoms were cramping abdominal pain in 68 percent, vomiting in 77
percent, absence of passage of flatus and/or feces in 52 percent, and constant pain in 12 percent [24].
Abdominal pain associated with small bowel obstruction is frequently described as periumbilical and
cramping with paroxysms of pain occurring every four or five minutes [26]. A progression from cramping
to more focal and constant pain may indicate peritoneal irritation related to complications (ischemia,
bowel necrosis). A sudden onset of severe pain may suggest acute intestinal perforation. (See "Overview
of gastrointestinal tract perforation".)
With proximal small bowel obstruction (duodenum, proximal jejunum), nausea and vomiting can be
relatively severe, and patients with proximal small bowel obstruction typically cease taking in food or
liquids orally.
Physical examination — The physical examination should evaluate the patient overall for systemic signs
related to the bowel obstruction. A hallmark of small bowel obstruction is dehydration, which manifests as
tachycardia, orthostatic hypotension, and reduced urine output, and if severe, dry mucus membranes.
Fever may be associated with infection (eg, abscess) or other complications of obstruction (ischemia,
necrosis), and although fever suggests infection, its absence does not rule it out, particularly in older or
immunocompromised patients. Hematochezia may be a sign of tumor, ischemia, or inflammatory mucosal
injury, or intussusception.
Abdominal inspection will identify a variable degree of abdominal distention in most patients with acute
bowel obstruction. Abdominal inspection should also look for any surgical scars and evidence for
abdominal wall hernia (including incisional hernia) or groin hernias. (See "Classification, clinical features,
and diagnosis of inguinal and femoral hernias in adults".)
In multiple retrospective reviews, abdominal distension was the most frequent physical finding on clinical
examination occurring in 56 to 65 percent of patients [5,19,24]. Although nausea and vomiting may be
less severe in patients with distal small bowel obstruction compared with proximal obstruction, abdominal
distention is greater because the more proximal bowel acts as a reservoir. Swallowed air and gas from
bacterial fermentation can also accumulate, adding to the abdominal distention. It is important to
remember, however, in patients with a closed-loop obstruction, abdominal distention can be minimal.
(See 'Pathophysiology' above.)
Acute mechanical bowel obstruction is characterized by high-pitched “tinkling” sounds associated with the
pain. With significant bowel distention, bowel sounds may become muffled, and as the bowel
progressively distends, bowel sounds can become hypoactive.
Distention of the bowel results in hyperresonance or tympany to percussion throughout the abdomen.
However, fluid-filled loops will result in dullness. If percussion over the liver is tympanitic rather than dull, it
may be indicative of free intraabdominal air. Tenderness to light percussion suggests peritonitis.
Abdominal palpation may identify any abdominal wall or groin hernias, or abnormal masses, which, in the
setting of small bowel obstruction, may indicate an abscess, volvulus, or tumor as the source of
obstruction. Digital rectal examination should be performed to identify fecal impaction or rectal mass as
the source of obstruction. Gross or occult blood may be related to intestinal tumor, ischemia, inflammatory
mucosal injury, or intussusception.
Laboratory studies — The typical laboratory evaluation for patients who present with significant
abdominal pain includes a complete blood count with differential and electrolytes including blood urea
nitrogen and creatinine. Although routine laboratory studies are not specific for a diagnosis of small bowel
obstruction, these studies help assess the presence and severity of hypovolemia, leukocytosis, and
metabolic abnormalities (hyponatremia, hypokalemia). Leukocytosis with leftward shift may indicate the
presence of complications. Anemia may point to a specific etiology (eg, Crohn’s disease, tumor, Meckel’s
diverticulum).
In patients who present with systemic signs (eg, fever, tachycardia, hypotension, altered mental status),
additional laboratory investigation should include arterial blood gas (ABG), serum lactate, and blood
cultures. Metabolic alkalosis can result from severe vomiting, but metabolic (lactic) acidosis can also
occur if the bowel becomes ischemic, or if hypovolemia is severe enough to cause hypoperfusion of other
organs [32]. Although there is no reliable clinical or laboratory marker for ischemia, elevated serum
lactate is sensitive, but not specific, for ischemia in patients with small bowel obstruction (sensitivity 90 to
100 percent, specificity 42 to 87 percent) [27,28].
Chronic, partial obstruction — Chronic small bowel obstruction occurs in a fixed segment of bowel and
the obstruction is, by definition, partial. The most common causes of chronic, partial small bowel
obstruction are chronic stricture from Crohn’s disease, adhesions from prior surgery, slowly-growing
tumors, and stricture related to prior bowel resection or irradiation.
Patients usually present with chronic postprandial abdominal discomfort and variable nausea. Abdominal
distention and tympany may be present, but usually without any fluid or electrolyte derangements. When
a patient with chronic, partial small bowel obstruction becomes completely obstructed, the clinical
presentation becomes indistinguishable from acute obstruction as described above.
Recurrent obstruction — The patient who presents with recurrent, intermittent obstruction, typically due
to adhesions, is distinguished from the patient with a chronic, partial small bowel obstruction. Recurrent
obstruction due to adhesions can occur in a fixed segment of bowel or differing segments of bowel. Those
that occur at the same site due to a focal band adhesion are more likely to respond to surgery compared
with those that occur at varying locations within the abdomen due to diffuse adhesions, for which surgery
is likely to increase the risk of future obstructions.
During an episode of obstruction, symptoms are identical to those of patients with acute small bowel
obstruction described above, but symptoms resolve and the patient may report postobstructive diarrhea.
In the period between obstructive episodes, the patient is usually asymptomatic with a normal abdominal
exam.
For patients with a history of prior bowel obstruction, whether managed medically or surgically, the
likelihood of recurrent obstruction increases with an increasing number of episodes, and the
asymptomatic time period between episodes decreases [2]. After three prior episodes, the likelihood of
recurrent obstruction is >80 percent [15].
DIAGNOSIS — Although mechanical small bowel obstruction may be suspected (or obvious) based upon
risk factors, symptoms, and physical exam findings consistent with obstruction, abdominal imaging is
usually needed to confirm the diagnosis, identify the location of obstruction, judge whether the obstruction
is partial or complete, identify complications related to obstruction (ischemia, necrosis, perforation) and
determine the potential etiology, all of which will help determine the urgency and nature of further
treatment (conservative, endoscopy, surgery) [33,34]. (See "Overview of management of mechanical
small bowel obstruction in adults".)
Confirming the diagnosis — Multiple imaging modalities are available to confirm a suspected diagnosis
of small bowel obstruction, but plain radiography and computed tomography of the abdomen are the most
practical and useful. For most patients, we obtain plain radiographs to quickly confirm a diagnosis of
bowel obstruction and, provided the films do not have findings that indicate the need for immediate
intervention, we use computed tomography (CT) of the abdomen to further characterize the nature,
severity, and potential etiologies of the obstruction.
Abdominal CT has largely replaced fluoroscopic studies for this purpose, but these and other studies,
such as ultrasound, endoscopy, and magnetic resonance enterography, may be useful in certain patient
populations. (See 'When to obtain other studies' below.)
Plain radiography — For most patients, we suggest plain radiographs to quickly confirm a diagnosis of
bowel obstruction because it is widely available, inexpensive, and may demonstrate findings that indicate
the immediate need for urgent decompression (eg, sigmoid volvulus) or surgical intervention (eg,
pneumoperitoneum, cecal or midgut volvulus) [35]. Plain radiography also assesses the lungs for
evidence of aspiration in those who have been vomiting, and can easily be repeated to follow the patient’s
progress. (See "Overview of management of mechanical small bowel obstruction in adults", section on
'Serial monitoring'.)
The basic radiologic examination should include an upright chest film and upright and supine abdominal
films (image 1 and image 2). If the patient cannot be placed into an upright position, a lateral decubitus
abdominal film can show free air and/or air-fluid levels.
Findings on plain radiography consistent with small bowel obstruction include the following:
●Dilated loops of bowel with air-fluid levels
•In the supine position, the air-fluid interface is parallel to the x-ray plate, and the entire width
of air and fluid-filled loops of bowel will be visible (image 3). This allows an estimation of the
amount of distention.
•In an upright (or lateral) position, the air-fluid interface is perpendicular to the film and is
evident as an air-fluid level (image 4). Multiple air-fluid levels with distended loops of small
bowel are seen in small bowel obstruction.
●Proximal bowel dilation with distal bowel collapse – Small bowel obstruction can be diagnosed if
the more proximal small bowel is dilated more than 2.5 cm (outer wall to outer wall) and the more
distal small bowel is not dilated [5,36]. The stomach may also be dilated. The presence of air-fluid
levels differing more than 5 mm from each other within the same loop of small bowel on upright films
supports a diagnosis of mechanical small bowel obstruction [37].
●Gasless abdomen – A gasless abdomen may be due to complete filling of loops of bowel with
sequestered fluid. The severity of the bowel obstruction may be underestimated. A string of beads
(or pearls) sign may be seen in predominantly fluid-filled small bowel loops on upright or lateral
films, as small amounts of intraluminal gas collect along the superior bowel wall separated by the
valvulae conniventes [36].
The site or cause of obstruction is usually not apparent on plain films since a transition point between the
dilated proximal and nondilated distal small bowel often cannot be established with certainty. For a
diagnosis of small bowel obstruction using plain radiographs, the sensitivity, specificity, and accuracy are
79 to 83 percent, 67 to 83 percent, and 64 to 82 percent, respectively [37-39].
Although plain abdominal films have a reasonable sensitivity for the detection of high-grade small bowel
obstruction, they are less useful differentiating small from large bowel obstruction, and differentiating
partial obstruction from ileus [38,40].
Abdominal CT — Multidetector CT of the abdomen is more useful than plain radiographs for identifying
the specific site (ie, transition point) and severity of obstruction (partial versus complete) [35]; determining
the etiology by identifying hernias, masses [41,42], or inflammatory changes; and for identifying
complications (ischemia, necrosis, perforation) [36]. Plain films can be equivocal in 20 to 30 percent of
patients and are "normal, nonspecific, or misleading" in 10 to 20 percent of patients [5,43]. Thus, some
have argued that because abdominal CT is more effective for identifying patients who will need
intervention, abdominal CT should be performed initially instead of plain films. However, we generally
obtain plain abdominal films (flat and upright/left lateral decubitus) prior to proceeding to abdominal CT
scan, since radiographs are readily available, less expensive, expose the patient to less radiation, and
may obviate the need for abdominal CT in some patients. (See 'Plain radiography' above.)
One study compared the efficacy of plain radiography and CT scan in 32 patients presenting with a
clinical suspicion for bowel obstruction [39]. The sensitivity and specificity of CT scanning was 93 and 100
percent, respectively, compared with 50 and 75 percent for plain radiography. The level of obstruction
was correctly predicted in 93 percent on CT scan compared with only 60 percent for plain films. CT was
also superior for determining the cause of the obstruction (87 versus 7 percent). In another study, the
negative predictive value of abdominal CT for excluding strangulation was 95 percent [44]. For high-grade
small bowel obstruction, the sensitivity, specificity, and accuracy of CT scan are reported to be 90 to 94
percent, 96 percent, and 95 percent, respectively [45-50]. For low-grade obstruction, the accuracy of CT
is reduced [51]. It is important to note that the sensitivity and specificity of CT scan for a diagnosis of
bowel obstruction increases with an increasing number of slices. In a systematic review and
metaanalysis, the sensitivities and specificities for various slice widths were as follows [18]:
●50 mm: sensitivity 79 percent, specificity 87 percent (one study)
●5 to 10 mm: 87 percent sensitivity (pooled estimate), 81 percent specificity (pooled estimate)
●0.75 mm: sensitivity 96 percent, specificity 100 percent (one study)
Similar to the findings on plain abdominal radiography, a diagnosis of bowel obstruction on abdominal CT
can be made by the findings of dilated proximal bowel with distal collapsed bowel, and air-fluid levels
(image 5 and image 6) [5]. (See 'Plain radiography' above.)
CT can usually locate the transition point, and can identify hernias or a mass lesion as the cause of the
obstruction. (See "Classification, clinical features, and diagnosis of inguinal and femoral hernias in
adults", section on 'Diagnosis'.)
Additional findings on abdominal CT scan consistent with a diagnosis of bowel obstruction include [5255]:
●Bowel wall thickening >3 mm (nonspecific)
●Submucosal edema/hemorrhage
●Mesenteric edema
●Ascites
●“Target sign”– alternating hypo/hyperdense layers, indicative of intussusception
●“Whirl sign” – rotation of small bowel mesentery, suggesting a twist or a volvulus
●“Venous Cut-off Sign” – venous flow to a loop of small bowel that is “cut off” suggests thrombosis
Identifying the transition point between dilated and nondilated bowel, although not required to make the
diagnosis of obstruction, may establish the site and cause of small bowel obstruction [36]. Reconstruction
in multiple planes allows the tortuous small bowel to be followed in the search for a transition point, which
may be a sharply defined point, as with band adhesions, or a longer segment, as seen with matted
adhesions or radiation enteritis. However, the location of obstruction as identified on CT only correlates
with the intraoperative locations in about 60 to 70 percent of patients [56,57]. In addition, the presence of
a transition point on abdominal CT does not appear to accurately predict the need for immediate or
delayed operative intervention, and thus should not be used as a major initial criterion influencing a
decision to operate [14,56]. (See "Overview of management of mechanical small bowel obstruction in
adults", section on 'Indications for surgical exploration'.)
The administration of oral and intravenous contrast optimizes the information provided by abdominal CT
scanning (image 7A-B). However, for those who cannot tolerate oral contrast, retained intraluminal fluid
within dilated bowel loops usually provides adequate enhancement when evaluating patients for ischemic
complications. A lack of bowel wall enhancement, an early sign of ischemia, may be easier to identify in
the absence of oral contrast agents. (See 'Bowel ischemia and perforation' below.)
Complete obstruction and closed-loop obstruction — The history should determine whether the
patient is continuing to pass any gas or stool from the rectum. Cessation of passage of stool or flatus
indicates a complete obstruction, which is more likely to be associated with complications (ischemia,
necrosis, perforation). However, it is important to remember that passage of flatus or feces can continue
for 12 to 24 hours after the onset of symptoms as the more distal bowel decompresses. The absence of
air or fluid in the distal small bowel or colon on plain abdominal radiographs or CT scan supports a
diagnosis of complete obstruction.
A special type of complete obstruction, a closed-loop obstruction, may be more difficult to identify on
radiologic studies. A closed-loop obstruction occurs when a segment of intestine, usually small bowel, is
obstructed in two locations, creating a segment with no proximal or distal outlet. Only a short segment of
intestine may be distended because of minimal abdominal distention. Closed-loop obstruction can rapidly
lead to complications (ischemia, necrosis, perforation); thus, early identification and treatment are
important to restore perfusion to the affected segment of bowel. In many cases abdominal exploration will
be needed to make a definitive diagnosis [58].
On imaging studies, a closed-loop obstruction often appears as a distended, fluid-filled, sometimes Cshaped or U-shaped bowel segment (image 8) with prominent mesenteric vessels converging on a point
of torsion (CT whirl sign) or incarceration [52]. Other signs include a triangular loop, the beak sign, and
the presence of two collapsed bowel loops adjacent to the obstruction site [53].
Bowel ischemia and perforation — Patients with complications (ischemia, necrosis, perforation) related
to bowel obstruction are typically very ill in appearance and may have systemic signs of toxicity and
laboratory features that suggest that complications related to bowel obstruction have occurred, such as
lactic acidosis, and leukocytosis.
Bowel ischemia leading to intestinal necrosis and perforation almost always occurs in the setting of
complete obstruction. An exception is a Richter's hernia, a condition in which only a portion of the
intestinal wall protrudes through a hernia defect and which can lead to ischemia and perforation without
complete obstruction of the lumen (figure 1).
A diagnosis of perforation relies on the finding of extraluminal air in diagnostic imaging studies.
●Pneumoperitoneum is a sign of perforation of the intraabdominal gastrointestinal tract (small
bowel, transverse colon, sigmoid colon) and may be detected as:
•Free air under the diaphragm on upright chest or upright abdominal radiograph (image 9)
•Free air over the spleen or liver on lateral abdominal film or abdominal CT
•Free air as a “football sign” on supine abdominal film or abdominal CT
●Air in the retroperitoneum may indicate perforation of the duodenum or retroperitoneal portions of
the colon.
•Psoas sign on supine abdominal film
•Air adjacent to the second portion of the duodenum on plain abdominal film or abdominal CT
Abdominal CT is more sensitive for detecting extraluminal air, particularly air in the retroperitoneum, and
in some patients, free air demonstrated on CT scan is not apparent on plain radiographs.
Abdominal CT is also better than plain radiographs for detecting signs of bowel ischemia. Advanced
bowel ischemia can generally be recognized on CT scan (image 10); however, lesser degrees of
ischemia are more difficult to confidently diagnose [5]. Findings associated with small bowel ischemia on
abdominal CT are listed below [59-63]. However, none of these signs are highly sensitive or specific
[59,60]. The presence of a combination of these findings increases the reliability of diagnosing ischemia
[64,65].
●Poor or absent segmental bowel wall enhancement
●Delayed hyperenhancement
●Bowel wall thickening
●Small bowel feces sign (image 11 and image 12)
●Air in the bowel wall (pneumatosis intestinalis)
●Edematous, thickened mesentery
●Engorgement of mesenteric vessels
●Hemorrhage in the mesentery
●Portal or mesenteric venous gas
●Ascites
When to obtain other studies — Other studies, such as ultrasound, magnetic resonance enterography,
and gastrointestinal contrast studies can also be used to evaluate the patient with suspected bowel
obstruction. These adjunctive studies can be time-consuming and invasive, and following plain
radiographs we recommend abdominal CT over any of these studies for difficult-to-diagnose bowel
obstruction, which is more likely to be a problem in patients who present with chronic symptoms [66].
(See 'Abdominal CT' above.)
Abdominal ultrasonography — Abdominal ultrasonography may be useful for the diagnosis of small
bowel obstruction in selected patients. Ultrasound is limited by poor visualization of gas-filled structures
[39], but is increasingly used in the emergency department to evaluate abdominal pain [18], to assess for
occult hernias, which may be the site of incarcerated small bowel, and in patients with contraindications to
CT scanning, such as those with contrast allergies [35], pregnant patients, and critically ill patients for
whom the study can be performed at the bedside [67].
Ultrasound is more sensitive and specific than plain films for the diagnosis of small bowel obstruction
[18,68,69], but not as helpful for determining the location, cause, and potential complications of bowel
obstruction. In a study that compared the efficacy of plain radiography, ultrasound, and CT scan in 32
patients presenting with clinical suspicion of intestinal obstruction [39], the sensitivity and specificity of
ultrasound were 75 percent each, compared with CT scanning at 93 and 100 percent, respectively. The
level of obstruction was correctly predicted in 70 percent of patients using ultrasound, but in 93 percent of
patients on CT scan. Ultrasound was also inferior to CT for determining the cause of the obstruction (23
versus 87 percent). In another study, the positive predictive value of an akinetic dilated loop on ultrasound
for strangulation was 73 percent [70].
Magnetic resonance enterography — Magnetic resonance (MR) enterography is an increasingly
attractive option for the assessment of small bowel obstruction [36]. Multiplanar MR enterography can be
used in the same way as multidetector computed tomography to look for evidence of a transition point
and features indicative of complications. However, the increased time for image acquisition and the need
for repeated breath-holds to obtain high-quality images limit the general applicability of MR enterography
in patients with acute small bowel obstruction.
MR enterography is most useful in the setting of low-grade bowel obstruction, provided the patient can
tolerate the procedure. MR enterography may therefore be most suitable for diagnosing bowel obstruction
associated with chronic small bowel conditions such as Crohn’s disease, a population of younger patients
for whom reducing the accumulated dose of ionizing radiation is highly desirable [36,71]. In a study of 28
patients, MR (HASTE MR, Siemens) had a higher sensitivity and specificity than helical CT for the cause
of obstruction [72].
Small bowel contrast studies — Although small bowel follow-through series and enteroclysis can
confirm the diagnosis of bowel obstruction and can determine if an obstruction is partial or complete, they
are inferior to abdominal CT for detecting closed-loop obstruction or ischemia, and only rarely point to the
etiology of the obstruction. Thus, these studies have a limited role in the initial diagnosis of small bowel
obstruction [36,73]. Small bowel follow-through is contraindicated if there are any signs of
strangulation.
Fluoroscopic findings consistent with small bowel obstruction are dilated loops of proximal small bowel
opacified with contrast material, and a change in the diameter of the small bowel at the transition zone.
Minimal or no contrast material opacifying the small bowel loops distal to the transition zone indicates
high-grade obstruction.
The transition zone at the site of small bowel obstruction can be missed using small bowel follow-through
(or abdominal CT) because water-soluble contrast agents become diluted as they pass through dilated
fluid-filled bowel loops. Consequently, the degree of opacification may not be sufficient to identify the
transition point at the site of obstruction. The transition zone is, however, readily identified with
enteroclysis.
Enteroclysis is a procedure in which the duodenum is intubated with a nasojejunal tube, and a large
volume of air and contrast (barium and methylcellulose) are instilled directly into the small intestine while
repeatedly imaging over time using fluoroscopy. The volume challenge caused by methylcellulose
administration accentuates the effect of low-grade obstruction. For patients with chronic or recurrent small
bowel obstruction, enteroclysis distends the small bowel sufficiently to identify areas of stenosis [36,74].
However, enteroclysis is not appropriate for patients with acute obstruction. The prolonged transit time of
contrast material through obstructed bowel means that follow-through radiographs require several hours
to obtain, which can delay the diagnosis. In addition, patients with acute small bowel obstruction tolerate
oral contrast material poorly, and it is preferable not to have large quantities of barium in the small bowel
lumen if surgery is a possibility.
Contrast enema — Contrast enema can be helpful to diagnose small bowel obstruction in patients who
have undergone proctocolectomy with an ileoanal J pouch reconstruction (eg, ulcerative colitis) or
patients with a subtotal colectomy and ileorectal anastomosis (eg, Crohn’s disease, ulcerative colitis,
cancer). Water soluble contrast is preferred over barium if bowel perforation is a concern.
DIFFERENTIAL DIAGNOSIS — Nausea and vomiting may be a manifestation of a myriad of disorders
(table 3). Although bowel obstruction is uncommon relative to all the possible causes of nausea and
vomiting and abdominal pain, it is important to make the diagnosis expediently because of the potential
for complications. For many medical conditions, vomiting is more likely to precede the onset of significant
abdominal pain, whereas pain often precedes vomiting when associated with an acute surgical etiology.
(See "Evaluation of the adult with abdominal pain" and "Causes of abdominal pain in adults".)
Bowel dilation due to mechanical obstruction must be differentiated from nonobstructive intestinal motility
disorders such as adynamic (paralytic) ileus and intestinal pseudo-obstruction (table 4). Either disorder
can be related to electrolyte derangement, major surgery, trauma, intestinal ischemia, or peritonitis from
other causes. Patients can develop the same symptoms as obstruction, but these disorders can be
distinguished from mechanical bowel obstruction by history and abdominal imaging.
Adynamic (paralytic) ileus — Paralytic ileus occurs to some degree after almost all open abdominal
operations and can also be caused by peritonitis, trauma, intestinal ischemia, and medications (eg,
opiates, anticholinergics). It is exacerbated by electrolyte disorders, particularly hypokalemia. As the
intestine becomes distended, the patient experiences many of the same symptoms as mechanical
obstruction. However, on radiologic examination there is air in the colon and rectum, and on abdominal
computed tomography (CT) or small bowel series there is no demonstrable mechanical obstruction
[75,76].
In differentiating early postoperative ileus from postoperative adhesive disease, it is useful to note that
nearly all patients with early postoperative bowel obstruction have an initial of return of bowel function and
oral intake, which is then followed by nausea, vomiting, abdominal pain, and distention, whereas patients
with adynamic ileus do not experience return of bowel function [77]. (See "Postoperative ileus".)
Pseudoobstruction — Intestinal pseudoobstruction is a chronic condition characterized by symptoms of
recurrent abdominal distention that may be associated with nausea, vomiting, and diarrhea. The colon is
generally affected more than the small intestine. No mechanical cause can be demonstrated, and the
patient frequently has a history of several previous operations for bowel obstruction during which no
cause for obstruction could be found. (See "Chronic intestinal pseudo-obstruction".)
Large bowel obstruction — The clinical presentation of large bowel obstruction depends upon the
location and etiology of the obstruction. Tumor is the most common cause of large bowel obstruction,
followed by adhesive disease and volvulus.
Diseases affecting the proximal colon, such as cecal volvulus or adhesions, are more likely to be
confused with acute small bowel obstruction compared with distal disease. In a study of patients with
colonic volvulus, the most frequent symptoms were abdominal pain (58 percent) and obstipation (55
percent) [25]. Most patients with cecal volvulus presented with abdominal pain, which occurred in 89
percent of patients. The interval at which cramping pain occurs is typically longer with colonic obstruction
compared with small bowel obstruction, and occurs lower in the abdomen between the umbilicus and
pubic tubercle.
Typical findings on plain abdominal films or abdominal CT scan of a grossly dilated cecum (image 13A-B)
or sigmoid colon (image 14) quickly distinguish volvulus from small bowel obstruction and indicate the
need for treatment, which is surgical (right colectomy) for cecal volvulus, and, for sigmoid volvulus,
involves endoscopic decompression and derotation, followed by surgery in selected patients. (See "Cecal
volvulus" and "Sigmoid volvulus".)
In the large bowel, adenocarcinoma of the colon and rectum is the predominant malignancy causing
obstruction. Colonic obstruction complicates 10 to 20 percent of colon cancers. Because tumors are slow
growing and often located more distally in the colon, symptoms are chronic and progressive, and rarely
confused with acute small bowel obstruction. Tumors that cause colon obstruction commonly cause
“apple-core” lesions, which are readily demonstrated on CT scan. In addition to identifying a mass as a
cause of large bowel obstruction, the abdominal CT scan may demonstrate a synchronous lesion,
enlarged lymph nodes, or metastases. (See "Clinical presentation, diagnosis, and staging of colorectal
cancer".)
SPECIFIC ETIOLOGIES — Once a diagnosis of small bowel obstruction has been established, it is
important to try to determine the specific etiology (table 1) responsible for the obstruction. The patient’s
age or medical history often suggests the possible etiology. (See 'Epidemiology and risk factors' above
and 'Clinical presentations' above.)
In the United States and Western Europe, the most common cause of mechanical small bowel
obstruction is intraperitoneal adhesions followed by tumors and complicated hernias [5,9]. Less frequent
causes of obstruction include Crohn’s disease (3 to 7 percent) [6,23], gallstones (2 percent), volvulus (4
to 15 percent) [20,78,79], and intussusception (4 to 8 percent) [78,80].
Patients who present with clinical manifestations consistent with a small bowel obstruction but who do not
have a history of prior abdominal surgery, and have none of the other common risk factors for bowel
obstruction, should be presumed to have small bowel tumor until proven otherwise. (See "Epidemiology,
clinical features, and types of small bowel neoplasms".)
Unique clinical and diagnostic features associated with the more common etiologies of small bowel
obstruction are briefly reviewed below and discussed more fully in linked topic reviews. The general
clinical presentation and diagnosis of bowel obstruction are discussed above. (See 'Clinical
presentations' above and 'Diagnosis' above.)
Adhesive bowel disease — Adhesions are the most common etiology for small bowel obstruction, with
up to 70 percent of cases of bowel obstruction in developed countries attributable to adhesions within the
abdomen or pelvis [36]. Approximately 80 percent of patients with adhesive small bowel obstruction have
a history of prior intraabdominal surgery; the remainder have prior peritonitis or no precipitating cause for
their adhesions [36].
Peritoneal adhesive bands are the most frequent etiology of bowel obstruction following abdominal or
pelvic surgery. Although intraabdominal adhesions form in more than 90 percent of patients after open
abdominal surgery [81], few patients require surgery to manage adhesive bowel obstruction. In large
reviews, between 7 and 17 percent of patients will require admission for small bowel obstruction related
to adhesions, but of these, only 2 to 5 percent will need adhesiolysis [13,82,83].
A specific preoperative diagnosis of adhesions as a cause of bowel obstruction is difficult to confirm [53].
However, because adhesions commonly involve the omentum or mesenteric fat, signs that indicate
abnormalities of the normal architecture may indicate that adhesions are responsible for bowel
obstruction. Signs include a “fat-bridging sign,” which is a cord-like structure containing mesenteric fat
that can bridge across the peritoneum; twisting of the mesentery (whirl signs); and tethering of the
omentum. Adhesions are a frequent cause of closed-loop obstruction [84], which, in addition to the
identification of abnormal bands on imaging, may appear as a sac-like clustering of intestine indicating
that the intestine has herniated into an enclosed space [84].
Tumor — Tumors, predominantly metastatic malignant tumors, are the second most common cause of
small bowel obstruction, accounting for about 20 percent of cases [85].
Primary tumor — Primary tumors of the small or large bowel may be responsible for symptoms and
signs of small bowel obstruction.
Intraluminal small bowel neoplasms such as carcinoid, small bowel carcinoma, and lymphoma can cause
small bowel obstruction due to luminal narrowing or intussusception. In one review of 17 patients, the
most frequent primary small bowel tumors as an etiology for small bowel obstruction were gastrointestinal
stromal tumors (GIST) (36 percent), lymphomas (24 percent), and adenocarcinomas (18 percent). Most
tumors (65 percent) were located in the ileum [86]. In patients with symptoms and imaging consistent with
small bowel obstruction but who did not have a history of prior abdominal surgery, and have none of the
other common risk factors for bowel obstruction, additional studies may be needed to rule out small bowel
tumor if the lesion is not apparent on initial imaging. (See "Epidemiology, clinical features, and types of
small bowel neoplasms" and "Diagnosis and staging of small bowel neoplasms".)
Metastatic disease — Metastatic disease is the most frequent neoplastic cause of small bowel
obstruction. In general, small bowel obstruction caused by metastases are frequently preceded by a
period of partial small bowel obstruction, although acute obstruction can sometimes be due to twisting of
the bowel around a metastatic tumor deposit leading to small bowel volvulus. In a patient with a prior
history of surgery, a small bowel obstruction due to metastases cannot be differentiated from a small
bowel obstruction due to adhesive disease.
Tumors with a propensity to cause widespread peritoneal metastases include colonic, ovarian,
pancreatic, and gastric neoplasms [36]. Small bowel obstruction has been described in as many as 28
percent of patients with colorectal carcinoma and 42 percent of women with ovarian carcinoma [87].
Multiple serosal small bowel metastases can form confluent soft-tissue masses that surround the bowel.
Obstruction occurs by extrinsic compression of the small bowel lumen or tethering of bowel loops by
these serosal deposits.
Tumors that spread hematogenously to involve the wall of the small bowel include melanoma, lung,
breast, cervix, sarcoma, and colon cancer. These metastases can cause endoluminal obstruction.
(See "Epidemiology, clinical features, and types of small bowel neoplasms", section on 'Metastatic
lesions'.)
Complicated hernia — Hernias are the third leading cause of intestinal obstruction, accounting for about
10 percent of all cases, and incarcerated hernias are the leading cause of complications (ischemia,
necrosis, perforation) related to bowel obstruction [1,5,79,88].
External hernias occur at sites of muscular or ligamentous weakness in the abdominal wall. Abdominal
wall and inguinal hernias are most commonly represented; femoral, obturator, and parastomal hernias
can also be complicated by small bowel obstruction.
Internal hernias cause 0.6 to 6.0 percent of small bowel obstructions and occur through acquired or
congenital defects in the mesentery (table 5) [89,90]. Acquired internal hernias can be due to adhesions,
or from artificial mesenteric openings created during the course of an operation, such as during small
bowel Roux-en-y (eg, Roux-en-y gastric bypass, pancreaticoduodenectomy) or ileal conduit procedures
[84,91,92].
Some patients with abdominal wall or groin hernia may present with intermittent obstructive symptoms if
their hernia remains reducible; however, incarcerated hernias that cause bowel obstruction typically
present acutely. Abdominal wall, inguinal, and femoral hernias can usually be detected on clinical
examination. Small incisional hernias and hernias in obese individuals may not be clinically evident, but
can usually be identified on CT scan. Typical findings of hernias on abdominal CT are discussed
elsewhere. (See "Classification, clinical features, and diagnosis of inguinal and femoral hernias in adults",
section on 'Diagnosis'.)
Appendicitis/diverticulitis/intraabdominal abscess — Inflammation of the intestine related to luminal
obstruction of the appendages of the intestine (eg, appendix, colonic diverticula, Meckel’s diverticulum) as
well as an abscess due to an inflammatory condition or perforation (eg, Crohn’s disease, appendicitis,
diverticulitis) can lead to an acute mechanical small bowel obstruction as the healthy
small bowel/omentum tries to contain the infectious process. However, in this setting, the symptoms of
small bowel obstruction are typically overshadowed by other clinical features such as fever and
abdominal pain. (See "Acute appendicitis in adults: Clinical manifestations and differential
diagnosis" and "Clinical manifestations and diagnosis of acute diverticulitis in adults" and "Meckel's
diverticulum".)
Traumatic intramural hematoma — A history of blunt abdominal trauma (recent or remote), in the
absence of other risk factors for bowel obstruction, should suggest a diagnosis of traumatic intramural
hematoma as the etiology of acute mechanical bowel obstruction. Late fibrosis of a segment of bowel
previously affected can lead to chronic symptoms of obstruction due to gradual narrowing of the intestinal
lumen [93,94].
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 seatbelt. Other intestinal sites of hematoma causing acute mechanical
obstruction have also been described [95-97].
The presence of an acute intramural hematoma can be established with abdominal CT showing findings
of bowel wall thickening with or without adjacent mesenteric changes (stranding, hematoma) [96,97].
However, other studies, such as upper gastrointestinal contrast studies, may be needed to establish the
diagnosis. (See "Traumatic gastrointestinal injury in the adult patient" and "Hollow viscus blunt abdominal
trauma in children".)
Intestinal stricture — Intestinal stricture as an etiology of bowel obstruction can be due to a number of
disorders, including Crohn's disease, certain drugs such as enteric-coated potassium chloride solutions
and NSAIDs, radiation therapy, and mesenteric ischemia [98]. Strictures can also occur at the site of prior
gastrointestinal anastomoses.
Patients with inflammatory bowel disease (eg, Crohn’s disease) can present with small bowel obstruction
due to adhesions or small bowel stricture. These patients usually present with chronic, intermittent
symptoms from partial rather than complete bowel obstruction. Small bowel obstruction as the source for
symptoms may be overlooked because of the long-standing nature of disease symptoms, and it may be
difficult to distinguish a Crohn’s exacerbation from small bowel obstruction. Additional imaging studies
may be needed. (See "Clinical manifestations, diagnosis and prognosis of Crohn disease in adults",
section on 'Diagnosis' and 'When to obtain other studies' above.)
Small bowel 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 [99]. (See "Overview of intestinal ischemia in adults".)
Radiation therapy for abdominal malignancy can lead to small bowel stricture, particularly in patients who
have undergone prior surgery where adhesions may fix loops of small intestine within the field of radiation
[100]. (See "Overview of gastrointestinal toxicity of radiation therapy", section on 'Enteritis'.)
Volvulus — Volvulus refers to twisting of a segment of the intestinal tract around a fixed point, often
leading to acute mechanical bowel obstruction. The most common sites of volvulus are the cecum and
sigmoid colon [101,102]. Small bowel volvulus is less common in adults, and it is usually due to
congenital intestinal anomalies (primary small bowel volvulus), but may be related to a prior abdominal
procedure, for which intestinal anatomy has been altered, or tumors (secondary small bowel volvulus)
[103,104]. (See "Intestinal malrotation in adults", section on 'Acute clinical presentation'.)
Gallstones or foreign body — Rarely, acute mechanical small bowel obstruction can be caused by
intraluminal material. The site of obstruction is usually at the ileocecal valve, where the lumen of the
bowel is smallest.
●Gallstone ileus occurs when a large gallstone erodes into the small bowel via a biliary-enteric
fistula. In addition to typical symptoms of small bowel obstruction and imaging findings consistent
with small bowel obstruction, other imaging findings of gallstone ileus include biliary air
(pneumobilia) and the finding of an aberrantly located large gallstone, which is often impacted at the
ileocecal valve (image 15 and image 16). (See "Gallstone ileus".)
●Gastrointestinal bezoars, which are composed of ingested material that is not digested within the
gastrointestinal tract, can obstruct the bowel lumen and may be related to a high-fiber diet,
improperly chewed food, hair ingestion, and medications (table 6) [105]. Abdominal radiographs,
abdominal ultrasound, or CT scan may show the bezoar as an intraluminal mass or a filling defect.
(See "Gastric bezoars".)
●Heavy intestinal parasitic infestation with Ascaris lumbricoides can lead to acute mechanical
intestinal obstruction, and in endemic areas, ascariasis causes up to one-third of all bowel
obstructions, typically in children, but adults can also be affected [106-109]. Patients will have typical
symptoms of acute mechanical small bowel obstruction, and emesis may contain worms. An
abdominal mass may be appreciated on physical examination. (See "Ascariasis".)
Intussusception — Intestinal intussusception is rare in adults, accounting for 1 to 5 percent of
mechanical bowel obstructions [110,111]. In adults, intussusception is typically due to pathologic lead
point within the bowel, which is malignant in over half of cases [89,110]. The lead point is pulled forward
by normal peristalsis, telescoping or prolapsing the affected segment of bowel (intussusceptum) into
another segment of bowel (intussuscipiens) (picture 1) [110,112]. An increased incidence of
intussusception has been reported in patients with acquired immune deficiency syndrome (AIDS)
[90,112]. 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 "Epidemiology, clinical features, and types of small bowel neoplasms".)
Intussusception can be classified by etiology (benign lesion [eg, polyps, Meckel’s diverticulum], malignant
lesion, or idiopathic) or by location as entero-enteric, which is limited to the small bowel; ileo-colic with
prolapse of the terminal ileum into the ascending colon; and colo-colic, which is limited to the large bowel.
In adults, intermittent abdominal pain is the most common presentation; however, patients can also
present with symptoms consistent with intermittent partial bowel obstruction with nausea, vomiting,
melena, weight loss, fever, and constipation [112]. Plain abdominal films may show the typical features of
distal small bowel obstruction. The diagnosis is often made on abdominal CT [112,113]. The distended
loop of bowel appears thickened because it represents two layers of bowel [36]. A “target sign” may be
seen on the sagittal view of the abdominal CT (image 17), while on axial or coronal view, the
intussusception will appear as a sausage-shaped mass.
Other unusual etiologies
●Splenosis, which is autotransplanted splenic tissue usually as a result of traumatic splenic rupture,
can cause bowel obstruction due to extrinsic compression (image 18), but intussusception has also
been reported [114-116].
●Superior mesenteric artery syndrome is an unusual cause of proximal small bowel obstruction. The
syndrome is characterized by compression of the third portion of the duodenum due to narrowing of
the space between the superior mesenteric artery and aorta, and is primarily attributed to loss of the
intervening mesenteric fat pad. (See "Superior mesenteric artery syndrome".)
●Congenital anomalies of the gastrointestinal tract can cause obstructive symptoms. Although rare
in adults, malrotation and annular pancreas can cause proximal small bowel obstruction.
(See 'Volvulus' above and "Intestinal malrotation in adults".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The
Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at
the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have
about a given condition. These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated,
and more detailed. These articles are written at the 10th to 12th grade reading level and are best for
patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail
these topics to your patients. (You can also locate patient education articles on a variety of subjects by
searching on “patient info” and the keyword(s) of interest.)
●Basics topics (see "Patient education: Small bowel obstruction (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Bowel obstruction occurs when the normal flow of intraluminal contents is interrupted, which leads
to bowel dilation and sequestration of fluid within the lumen of the intestine proximal to the blockage,
while distal to the blockage, as luminal contents pass, the bowel decompresses.
(See 'Introduction' above and 'Pathophysiology' above.)
●Compromised blood flow to the intestinal tissue due to excessive bowel dilation or strangulation
can lead to complications (ischemia, necrosis, perforation), which significantly increase mortality
associated with bowel obstruction. (See 'Introduction' above and 'Pathophysiology' above.)
●The most common cause of mechanical small bowel obstruction is postoperative adhesions from
prior abdominal or pelvic surgery. Adhesions cause extrinsic compression of the bowel. Patients
who have undergone appendectomy, gynecologic surgery, prior adhesiolysis, exploration for
abdominal trauma, and prior resection for malignancy are particularly prone to adhesive small bowel
obstruction. Adhesive small bowel obstruction can occur in the absence of prior surgery due to
intestinal inflammation (Crohn’s disease, diverticular disease). Other etiologies that cause extrinsic
compression of the intestine are hernia and volvulus. (See 'Epidemiology and risk factors' above
and 'Adhesive bowel disease' above and 'Complicated hernia' above and 'Volvulus' above.)
●Bowel obstruction can also be due to disease intrinsic to the wall of the intestine (eg, tumor,
stricture, intramural hematoma) or processes that cause intraluminal obstruction (eg,
intussusception, gallstones, foreign body). Patients who present with symptoms consistent with a
small bowel obstruction but who do not have a history of prior abdominal surgery, and have no other
obvious risk factors (eg, hernia, inflammatory bowel disease) for bowel obstruction, should be
presumed to have small bowel tumor until proven otherwise. (See 'Epidemiology and risk
factors' above and 'Tumor' above and 'Intestinal stricture' above and 'Traumatic intramural
hematoma' above and 'Gallstones or foreign body' above and 'Intussusception' above.)
●The clinical presentation of mechanical small bowel obstruction depends upon the site and etiology
of obstruction. Patients can present with acute symptoms of nausea, vomiting and abdominal pain,
intermittent obstructive symptoms (asymptomatic periods between episodes), or with chronic
postprandial discomfort and abdominal distention. Vomiting can be severe in patients with proximal
small bowel obstruction, while in patients with distal small bowel obstruction, abdominal distension
may be more prominent. (See 'Clinical presentations' above.)
●In patients with acute small bowel obstruction, routine laboratory studies help assess the presence
and severity of hypovolemia and electrolyte abnormalities, and may indicate the possibility of
complications (eg, leukocytosis, metabolic acidosis). Although there are no reliable laboratory
markers for bowel ischemia, elevated serum lactate is sensitive, but not specific. Laboratory studies
in patients with chronic bowel obstruction are usually normal. (See 'Laboratory studies' above.)
●A presumptive diagnosis of acute mechanical small bowel obstruction can be made by history and
physical examination in many patients, particularly those with a history of prior abdominal surgery,
or an obviously strangulated hernia. However, abdominal imaging is generally needed to confirm a
diagnosis of mechanical bowel obstruction, identify the location of obstruction, judge whether the
obstruction is partial or complete, identify complications related to obstruction (ischemia, necrosis,
perforation) and determine the potential etiology, all of which will help determine the urgency and
nature of further treatment (conservative, endoscopy, surgery). (See 'Diagnosis' above
and 'Differential diagnosis' above.)
●For most patients, we suggest obtaining plain abdominal films to confirm a suspected diagnosis of
mechanical small bowel obstruction. Findings on plain film that indicate that small bowel obstruction
is present include dilated loops of bowel with air-fluid levels, proximal bowel dilation with distal bowel
collapse, or a gasless abdomen. For many patients, no further radiologic tests will be needed
because the films may demonstrate findings that indicate the immediate need for urgent
decompression (eg, sigmoid volvulus) or surgical intervention (eg, pneumoperitoneum, cecal or
midgut volvulus). (See 'Plain radiography' above.)
●Abdominal computed tomography (CT) is the imaging modality of choice for identifying the specific
site (ie, transition point, small versus large bowel) and severity of obstruction (partial versus
complete, or closed-loop obstruction); determining the etiology by identifying hernias, masses, or
inflammatory changes; and for identifying complications (ischemia, necrosis, perforation).
(See 'Abdominal CT' above and 'Complete obstruction and closed-loop obstruction' above
and 'Bowel ischemia and perforation' above.)
●Some patients may require additional studies to diagnose obstruction if abdominal CT is equivocal
(eg, chronic symptoms, partial obstruction) or abdominal CT cannot be performed (eg, contrast
allergy, inability to transport patient). These might include ultrasound, magnetic resonance
enterography, or contrast studies. (See 'When to obtain other studies' above.)
ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Dr. Richard Hodin,
who contributed to earlier versions of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Mucha P Jr. Small intestinal obstruction. Surg Clin North Am 1987; 67:597.
2. Miller G, Boman J, Shrier I, Gordon PH. Natural history of patients with adhesive small bowel obstruction.
Br J Surg 2000; 87:1240.
3. Wright HK, O'Brien JJ, Tilson MD. Water absorption in experimental closed segment obstruction of the
ileum in man. Am J Surg 1971; 121:96.
4. Noer RJ, Derr JW, Johnston CG. The Circulation of the Small Intestine: An Evaluation of its
Revascularizing Potential. Ann Surg 1949; 130:608.
5. Markogiannakis H, Messaris E, Dardamanis D, et al. Acute mechanical bowel obstruction: clinical
presentation, etiology, management and outcome. World J Gastroenterol 2007; 13:432.
6. Miller G, Boman J, Shrier I, Gordon PH. Etiology of small bowel obstruction. Am J Surg 2000; 180:33.
7. Ray NF, Denton WG, Thamer M, et al. Abdominal adhesiolysis: inpatient care and expenditures in the
United States in 1994. J Am Coll Surg 1998; 186:1.
8. Scott FI, Osterman MT, Mahmoud NN, Lewis JD. Secular trends in small-bowel obstruction and
adhesiolysis in the United States: 1988-2007. Am J Surg 2012; 204:315.
9. Drożdż W, Budzyński P. Change in mechanical bowel obstruction demographic and etiological patterns
during the past century: observations from one health care institution. Arch Surg 2012; 147:175.
10. Kozol R. Mechanical bowel obstruction: a tale of 2 eras. Arch Surg 2012; 147:180.
11. ten Broek RP, Issa Y, van Santbrink EJ, et al. Burden of adhesions in abdominal and pelvic surgery:
systematic review and met-analysis. BMJ 2013; 347:f5588.
12. Matter I, Khalemsky L, Abrahamson J, et al. Does the index operation influence the course and outcome
of adhesive intestinal obstruction? Eur J Surg 1997; 163:767.
13. Parker MC, Ellis H, Moran BJ, et al. Postoperative adhesions: ten-year follow-up of 12,584 patients
undergoing lower abdominal surgery. Dis Colon Rectum 2001; 44:822.
14. Barmparas G, Branco BC, Schnüriger B, et al. In-hospital small bowel obstruction after exploratory
laparotomy for trauma. J Trauma 2011; 71:486.
15. Barkan H, Webster S, Ozeran S. Factors predicting the recurrence of adhesive small-bowel obstruction.
Am J Surg 1995; 170:361.
16. Vrijland WW, Jeekel J, van Geldorp HJ, et al. Abdominal adhesions: intestinal obstruction, pain, and
infertility. Surg Endosc 2003; 17:1017.
17. Butt MU, Velmahos GC, Zacharias N, et al. Adhesional small bowel obstruction in the absence of
previous operations: management and outcomes. World J Surg 2009; 33:2368.
18. Taylor MR, Lalani N. Adult small bowel obstruction. Acad Emerg Med 2013; 20:528.
19. Cheadle WG, Garr EE, Richardson JD. The importance of early diagnosis of small bowel obstruction. Am
Surg 1988; 54:565.
20. Gürleyik E, Gürleyik G. Small bowel volvulus: a common cause of mechanical intestinal obstruction in our
region. Eur J Surg 1998; 164:51.
21. Tamijmarane A, Chandra S, Smile SR. Clinical aspects of adhesive intestinal obstruction. Trop
Gastroenterol 2000; 21:141.
22. Sarr MG, Bulkley GB, Zuidema GD. Preoperative recognition of intestinal strangulation obstruction.
Prospective evaluation of diagnostic capability. Am J Surg 1983; 145:176.
23. Bizer LS, Liebling RW, Delany HM, Gliedman ML. Small bowel obstruction: the role of nonoperative
treatment in simple intestinal obstruction and predictive criteria for strangulation obstruction. Surgery
1981; 89:407.
24. Perea García J, Turégano Fuentes T, Quijada García B, et al. Adhesive small bowel obstruction:
predictive value of oral contrast administration on the need for surgery. Rev Esp Enferm Dig 2004;
96:191.
25. Lau KC, Miller BJ, Schache DJ, Cohen JR. A study of large-bowel volvulus in urban Australia. Can J Surg
2006; 49:203.
26. Flasar MH, Goldberg E. Acute abdominal pain. Med Clin North Am 2006; 90:481.
27. Murray MJ, Gonze MD, Nowak LR, Cobb CF. Serum D(-)-lactate levels as an aid to diagnosing acute
intestinal ischemia. Am J Surg 1994; 167:575.
28. Lange H, Jäckel R. Usefulness of plasma lactate concentration in the diagnosis of acute abdominal
disease. Eur J Surg 1994; 160:381.
29. Jackson PG, Raiji MT. Evaluation and management of intestinal obstruction. Am Fam Physician 2011;
83:159.
30. Böhner H, Yang Q, Franke C, et al. Simple data from history and physical examination help to exclude
bowel obstruction and to avoid radiographic studies in patients with acute abdominal pain. Eur J Surg
1998; 164:777.
31. Eskelinen M, Ikonen J, Lipponen P. Contributions of history-taking, physical examination, and computer
assistance to diagnosis of acute small-bowel obstruction. A prospective study of 1333 patients with acute
abdominal pain. Scand J Gastroenterol 1994; 29:715.
32. Takeuchi K, Tsuzuki Y, Ando T, et al. Clinical studies of strangulating small bowel obstruction. Am Surg
2004; 70:40.
33. Gerhardt RT, Nelson BK, Keenan S, et al. Derivation of a clinical guideline for the assessment of
nonspecific abdominal pain: the Guideline for Abdominal Pain in the ED Setting (GAPEDS) Phase 1
Study. Am J Emerg Med 2005; 23:709.
34. Cartwright SL, Knudson MP. Evaluation of acute abdominal pain in adults. Am Fam Physician 2008;
77:971.
35. Catena F, Di Saverio S, Kelly MD, et al. Bologna Guidelines for Diagnosis and Management of Adhesive
Small Bowel Obstruction (ASBO): 2010 Evidence-Based Guidelines of the World Society of Emergency
Surgery. World J Emerg Surg 2011; 6:5.
36. Mullan CP, Siewert B, Eisenberg RL. Small bowel obstruction. AJR Am J Roentgenol 2012; 198:W105.
37. Thompson WM, Kilani RK, Smith BB, et al. Accuracy of abdominal radiography in acute small-bowel
obstruction: does reviewer experience matter? AJR Am J Roentgenol 2007; 188:W233.
38. Maglinte DD, Reyes BL, Harmon BH, et al. Reliability and role of plain film radiography and CT in the
diagnosis of small-bowel obstruction. AJR Am J Roentgenol 1996; 167:1451.
39. Suri S, Gupta S, Sudhakar PJ, et al. Comparative evaluation of plain films, ultrasound and CT in the
diagnosis of intestinal obstruction. Acta Radiol 1999; 40:422.
40. Maglinte DD, Heitkamp DE, Howard TJ, et al. Current concepts in imaging of small bowel obstruction.
Radiol Clin North Am 2003; 41:263.
41. Soyer P, Dohan A, Eveno C, et al. Carcinoid tumors of the small-bowel: evaluation with 64-section CTenteroclysis. Eur J Radiol 2013; 82:943.
42. Gong JS, Kang WY, Liu T, et al. CT findings of a gastrointestinal stromal tumor arising from small bowel.
Quant Imaging Med Surg 2012; 2:57.
43. Balthazar EJ. George W. Holmes Lecture. CT of small-bowel obstruction. AJR Am J Roentgenol 1994;
162:255.
44. Balthazar EJ, Liebeskind ME, Macari M. Intestinal ischemia in patients in whom small bowel obstruction is
suspected: evaluation of accuracy, limitations, and clinical implications of CT in diagnosis. Radiology
1997; 205:519.
45. Mallo RD, Salem L, Lalani T, Flum DR. Computed tomography diagnosis of ischemia and complete
obstruction in small bowel obstruction: a systematic review. J Gastrointest Surg 2005; 9:690.
46. Shakil O, Zafar SN, Zia-ur-Rehman, et al. The role of computed tomography for identifying mechanical
bowel obstruction in a Pakistani population. J Pak Med Assoc 2011; 61:871.
47. Megibow AJ, Balthazar EJ, Cho KC, et al. Bowel obstruction: evaluation with CT. Radiology 1991;
180:313.
48. Fukuya T, Hawes DR, Lu CC, et al. CT diagnosis of small-bowel obstruction: efficacy in 60 patients. AJR
Am J Roentgenol 1992; 158:765.
49. Jaffe TA, Nelson RC, Johnson GA, et al. Optimization of multiplanar reformations from isotropic data sets
acquired with 16-detector row helical CT scanner. Radiology 2006; 238:292.
50. Jaffe TA, Martin LC, Thomas J, et al. Small-bowel obstruction: coronal reformations from isotropic voxels
at 16-section multi-detector row CT. Radiology 2006; 238:135.
51. Maglinte DD, Gage SN, Harmon BH, et al. Obstruction of the small intestine: accuracy and role of CT in
diagnosis. Radiology 1993; 188:61.
52. Ho YC. "Venous cut-off sign" as an adjunct to the "whirl sign" in recognizing acute small bowel volvulus
via CT scan. J Gastrointest Surg 2012; 16:2005.
53. Balthazar EJ, Birnbaum BA, Megibow AJ, et al. Closed-loop and strangulating intestinal obstruction: CT
signs. Radiology 1992; 185:769.
54. Duda JB, Bhatt S, Dogra VS. Utility of CT whirl sign in guiding management of small-bowel obstruction.
AJR Am J Roentgenol 2008; 191:743.
55. Zalcman M, Sy M, Donckier V, et al. Helical CT signs in the diagnosis of intestinal ischemia in smallbowel obstruction. AJR Am J Roentgenol 2000; 175:1601.
56. Colon MJ, Telem DA, Wong D, Divino CM. The relevance of transition zones on computed tomography in
the management of small bowel obstruction. Surgery 2010; 147:373.
57. Petrovic B, Nikolaidis P, Hammond NA, et al. Identification of adhesions on CT in small-bowel obstruction.
Emerg Radiol 2006; 12:88.
58. Yang XY, Chen CX, Zhang BL, et al. Diagnostic effect of capsule endoscopy in 31 cases of subacute
small bowel obstruction. World J Gastroenterol 2009; 15:2401.
59. O'Daly BJ, Ridgway PF, Keenan N, et al. Detected peritoneal fluid in small bowel obstruction is
associated with the need for surgical intervention. Can J Surg 2009; 52:201.
60. Sheedy SP, Earnest F 4th, Fletcher JG, et al. CT of small-bowel ischemia associated with obstruction in
emergency department patients: diagnostic performance evaluation. Radiology 2006; 241:729.
61. Jones K, Mangram AJ, Lebron RA, et al. Can a computed tomography scoring system predict the need
for surgery in small-bowel obstruction? Am J Surg 2007; 194:780.
62. Biondo S, Parés D, Frago R, et al. Large bowel obstruction: predictive factors for postoperative mortality.
Dis Colon Rectum 2004; 47:1889.
63. Taourel PG, Fabre JM, Pradel JA, et al. Value of CT in the diagnosis and management of patients with
suspected acute small-bowel obstruction. AJR Am J Roentgenol 1995; 165:1187.
64. Lazarus DE, Slywotsky C, Bennett GL, et al. Frequency and relevance of the "small-bowel feces" sign on
CT in patients with small-bowel obstruction. AJR Am J Roentgenol 2004; 183:1361.
65. Ha HK, Kim JS, Lee MS, et al. Differentiation of simple and strangulated small-bowel obstructions:
usefulness of known CT criteria. Radiology 1997; 204:507.
66. Peck JJ, Milleson T, Phelan J. The role of computed tomography with contrast and small bowel followthrough in management of small bowel obstruction. Am J Surg 1999; 177:375.
67. Schmutz GR, Benko A, Fournier L, et al. Small bowel obstruction: role and contribution of sonography.
Eur Radiol 1997; 7:1054.
68. Musoke F, Kawooya MG, Kiguli-Malwadde E. Comparison between sonographic and plain radiography in
the diagnosis of small bowel obstruction at Mulago Hospital, Uganda. East Afr Med J 2003; 80:540.
69. Jang TB, Schindler D, Kaji AH. Bedside ultrasonography for the detection of small bowel obstruction in
the emergency department. Emerg Med J 2011; 28:676.
70. Ogata M, Imai S, Hosotani R, et al. Abdominal ultrasonography for the diagnosis of strangulation in small
bowel obstruction. Br J Surg 1994; 81:421.
71. Fidler JL, Guimaraes L, Einstein DM. MR imaging of the small bowel. Radiographics 2009; 29:1811.
72. Beall DP, Fortman BJ, Lawler BC, Regan F. Imaging bowel obstruction: a comparison between fast
magnetic resonance imaging and helical computed tomography. Clin Radiol 2002; 57:719.
73. Makanjuola D. Computed tomography compared with small bowel enema in clinically equivocal intestinal
obstruction. Clin Radiol 1998; 53:203.
74. Shrake PD, Rex DK, Lappas JC, Maglinte DD. Radiographic evaluation of suspected small bowel
obstruction. Am J Gastroenterol 1991; 86:175.
75. Frager D, Medwid SW, Baer JW, et al. CT of small-bowel obstruction: value in establishing the diagnosis
and determining the degree and cause. AJR Am J Roentgenol 1994; 162:37.
76. Frager DH, Baer JW, Rothpearl A, Bossart PA. Distinction between postoperative ileus and mechanical
small-bowel obstruction: value of CT compared with clinical and other radiographic findings. AJR Am J
Roentgenol 1995; 164:891.
77. Stewart RM, Page CP, Brender J, et al. The incidence and risk of early postoperative small bowel
obstruction. A cohort study. Am J Surg 1987; 154:643.
78. Lawal OO, Olayinka OS, Bankole JO. Spectrum of causes of intestinal obstruction in adult Nigerian
patients. S Afr J Surg 2005; 43:34, 36.
79. McEntee G, Pender D, Mulvin D, et al. Current spectrum of intestinal obstruction. Br J Surg 1987; 74:976.
80. Kirshtein B, Roy-Shapira A, Lantsberg L, et al. Laparoscopic management of acute small bowel
obstruction. Surg Endosc 2005; 19:464.
81. Menzies D, Ellis H. Intestinal obstruction from adhesions--how big is the problem? Ann R Coll Surg Engl
1990; 72:60.
82. Beck DE, Opelka FG, Bailey HR, et al. Incidence of small-bowel obstruction and adhesiolysis after open
colorectal and general surgery. Dis Colon Rectum 1999; 42:241.
83. Nieuwenhuijzen M, Reijnen MM, Kuijpers JH, van Goor H. Small bowel obstruction after total or subtotal
colectomy: a 10-year retrospective review. Br J Surg 1998; 85:1242.
84. Hongo N, Mori H, Matsumoto S, et al. Internal hernias after abdominal surgeries: MDCT features. Abdom
Imaging 2011; 36:349.
85. Kendrick ML. Partial small bowel obstruction: clinical issues and recent technical advances. Abdom
Imaging 2009; 34:329.
86. Beltran MA, Cruces KS. Primary tumors of jejunum and ileum as a cause of intestinal obstruction: a case
control study. Int J Surg 2007; 5:183.
87. Ripamonti C, De Conno F, Ventafridda V, et al. Management of bowel obstruction in advanced and
terminal cancer patients. Ann Oncol 1993; 4:15.
88. Ihedioha U, Alani A, Modak P, et al. Hernias are the most common cause of strangulation in patients
presenting with small bowel obstruction. Hernia 2006; 10:338.
89. Newsom BD, Kukora JS. Congenital and acquired internal hernias: unusual causes of small bowel
obstruction. Am J Surg 1986; 152:279.
90. Bergstein JM, Condon RE. Obturator hernia: current diagnosis and treatment. Surgery 1996; 119:133.
91. Lall CG, Sandrasegaran K, Maglinte DT, Fridell JA. Bowel complications seen on CT after pancreas
transplantation with enteric drainage. AJR Am J Roentgenol 2006; 187:1288.
92. Lockhart ME, Tessler FN, Canon CL, et al. Internal hernia after gastric bypass: sensitivity and specificity
of seven CT signs with surgical correlation and controls. AJR Am J Roentgenol 2007; 188:745.
93. Touloukian RJ. Protocol for the nonoperative treatment of obstructing intramural duodenal hematoma
during childhood. Am J Surg 1983; 145:330.
94. Northcutt A, Hamidian Jahromi A, Johnson L, Youssef AM. Unusual late occurrence of bowel obstruction
following blunt abdominal trauma. J La State Med Soc 2011; 163:305.
95. Vollmer CM Jr, Schmieg RE, Freeman BD, Balfe DM. Traumatic colonic hematoma. J Trauma 2000;
49:1155.
96. LeBedis CA, Anderson SW, Soto JA. CT imaging of blunt traumatic bowel and mesenteric injuries. Radiol
Clin North Am 2012; 50:123.
97. Ekeh AP, Saxe J, Walusimbi M, et al. Diagnosis of blunt intestinal and mesenteric injury in the era of
multidetector CT technology--are results better? J Trauma 2008; 65:354.
98. Speed CA, Bramble MG, Corbett WA, Haslock I. Non-steroidal anti-inflammatory induced diaphragm
disease of the small intestine: complexities of diagnosis and management. Br J Rheumatol 1994; 33:778.
99. Thaker P, Weingarten L, Friedman IH. Stenosis of the small intestine due to nonocclusive ischemic
disease. Arch Surg 1977; 112:1216.
100.
Jackson BT. Bowel damage from radiation. Proc R Soc Med 1976; 69:683.
101.
Ballantyne GH, Brandner MD, Beart RW Jr, Ilstrup DM. Volvulus of the colon. Incidence and
mortality. Ann Surg 1985; 202:83.
102.
Northeast AD, Dennison AR, Lee EG. Sigmoid volvulus: new thoughts on the epidemiology. Dis
Colon Rectum 1984; 27:260.
103.
Ruiz-Tovar J, Morales V, Sanjuanbenito A, et al. Volvulus of the small bowel in adults. Am Surg
2009; 75:1179.
104.
Coe TM, Chang DC, Sicklick JK. Small bowel volvulus in the adult populace of the United States:
results from a population-based study. Am J Surg 2015; 210:201.
105.
Robles R, Parrilla P, Escamilla C, et al. Gastrointestinal bezoars. Br J Surg 1994; 81:1000.
106.
Hesse AA, Nouri A, Hassan HS, Hashish AA. Parasitic infestations requiring surgical
interventions. Semin Pediatr Surg 2012; 21:142.
107.
Teneza-Mora NC, Lavery EA, Chun HM. Partial small bowel obstruction in a traveler. Clin Infect
Dis 2006; 43:214, 256.
108.
Khuroo MS. Ascariasis. Gastroenterol Clin North Am 1996; 25:553.
109.
Reeder MM. The radiological and ultrasound evaluation of ascariasis of the gastrointestinal,
biliary, and respiratory tracts. Semin Roentgenol 1998; 33:57.
110.
Marinis A, Yiallourou A, Samanides L, et al. Intussusception of the bowel in adults: a review.
World J Gastroenterol 2009; 15:407.
111.
Zubaidi A, Al-Saif F, Silverman R. Adult intussusception: a retrospective review. Dis Colon
Rectum 2006; 49:1546.
112.
Gayer G, Zissin R, Apter S, et al. Pictorial review: adult intussusception--a CT diagnosis. Br J
Radiol 2002; 75:185.
113.
Lvoff N, Breiman RS, Coakley FV, et al. Distinguishing features of self-limiting adult small-bowel
intussusception identified at CT. Radiology 2003; 227:68.
114.
Gincu V, Kornprat P, Thimary F, et al. Intestinal obstruction caused by splenosis at the
rectosigmoid junction, mimicking malignant pelvic tumor. Endoscopy 2011; 43 Suppl 2 UCTN:E260.
115.
Abeles DB, Bego DG. Occult gastrointestinal bleeding and abdominal pain due to entero-enteric
intussusception caused by splenosis. Surg Endosc 2003; 17:1494.
116.
Sirinek KR, Livingston CD, Bova JG, Levine BA. Bowel obstruction due to infarcted splenosis.
South Med J 1984; 77:764.
Topic 8037 Version 25.0
Purchase answer to see full
attachment