Expert answer:Bowel obstruction in adults
Solved by verified expert:Respond to the topics below for your posting. Support your responses with a rationale.Obtain a current peer-reviewed, evidence-based research article surrounding the physical assessment of a gastrointestinal condition.Briefly discuss the article, associated health condition, and assessment recommendations contained in the article. How do the physical assessment recommendations in the article relate to the anatomy, physiology, and pathological changes associated with this health condition? Are there any lifespan associated changes in the assessment that should be applied when assessing patients with this condition? Please explain. All references should be in APA format.
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Epidemiology, clinical features, and diagnosis of mechanical small bowel obstruction in adults
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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
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