Small-Bowel Obstruction

Updated: Jan 20, 2015
  • Author: Brian A Nobie, MD; Chief Editor: Steven C Dronen, MD, FAAEM  more...
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Practice Essentials

A small-bowel obstruction (SBO) is caused by a variety of pathologic processes. The leading cause of SBO in industrialized countries is postoperative adhesions (60%), followed by malignancy, Crohn disease, and hernias. See the image below.

Small bowel obstruction. Image courtesy of Ademola Small bowel obstruction. Image courtesy of Ademola Adewale, MD.

See Can't-Miss Gastrointestinal Diagnoses, a Critical Images slideshow, to help diagnose the potentially life-threatening conditions that present with gastrointestinal symptoms.

Signs and symptoms

Obstruction can be characterized as either partial or complete versus simple or strangulated. Abdominal pain, often described as crampy and intermittent, is more prevalent in simple obstruction. Usually, pain that occurs for a shorter duration of time and is colicky and accompanied by bilious vomiting may be more proximal. Pain that lasts as long as several days, is progressive in nature, and is accompanied by abdominal distention may be typical of a more distal obstruction.

Some signs and symptoms associated with SBO include the following:

  • Nausea
  • Vomiting - Associated more with proximal obstructions
  • Diarrhea - An early finding
  • Constipation - A late finding, as evidenced by the absence of flatus or bowel movements
  • Fever and tachycardia - Occur late and may be associated with strangulation
  • Previous abdominal or pelvic surgery, previous radiation therapy, or both - May be part of the patient's medical history
  • History of malignancy - Particularly ovarian and colonic malignancy

See Clinical Presentation for more detail.


Lab tests

The following are adjunctive lab tests used in the evaluation of SBO:

  • Serum chemistries
  • Blood urea nitrogen (BUN) level
  • Creatinine
  • Complete blood count (CBC)
  • Lactate dehydrogenase tests
  • Urinalysis
  • Type and crossmatch

Laboratory tests to exclude biliary or hepatic disease are also needed; they include the following:

  • Phosphate level
  • Creatine kinase level
  • Liver panels

Imaging tests

Obtain plain radiographs first for patients in whom SBO is suspected. At least 2 views, supine or flat and upright, are required. Plain radiographs are diagnostically more accurate in cases of simple obstruction.

Enteroclysis is valuable in detecting the presence of obstruction and in differentiating partial from complete blockages. This study is useful when plain radiographic findings are normal in the presence of clinical signs of SBO or when plain radiographic findings are nonspecific.

Computed tomography (CT) scanning is the study of choice if the patient has fever, tachycardia, localized abdominal pain, and/or leukocytosis.

Ultrasonography is less costly and invasive than CT scanning and may reliably exclude SBO in as many as 89% of patients; specificity is reportedly 100%.

See Workup for more detail.


Nonoperative treatment

Nonoperative treatment for several types of SBO are as follows:

  • Malignant tumor - Obstruction by tumor is usually caused by metastasis; initial treatment should be nonoperative (surgical resection is recommended when feasible)
  • Inflammatory bowel disease - To reduce the inflammatory process, treatment generally is nonoperative in combination with high-dose steroids; consider parenteral treatment for prolonged periods of bowel rest, and undertake surgical treatment, bowel resection, and/or stricturoplasty if nonoperative treatment fails.
  • Intra-abdominal abscess - CT scan ̶ guided drainage is usually sufficient to relieve obstruction
  • Radiation enteritis - If obstruction follows radiation therapy acutely, nonoperative treatment accompanied by steroids is usually sufficient; if the obstruction is a chronic sequela of radiation therapy, surgical treatment is indicated
  • Incarcerated hernia - Initially use manual reduction and observation; advise elective hernia repair as soon as possible after reduction
  • Acute postoperative obstruction - This is difficult to diagnose, because symptoms often are attributed to incisional pain and postoperative ileus; treatment should be nonoperative
  • Adhesions - Decreasing intraoperative trauma to the peritoneal surfaces can prevent adhesion formation

Surgical care

A strangulated obstruction is a surgical emergency. In patients with a complete small-bowel obstruction (SBO), the risk of strangulation is high and early surgical intervention is warranted. Laparoscopy has been shown to be safe and effective in selected cases of SBO. [1, 2]

See Treatment and Medication for more detail.



A small-bowel obstruction (SBO) is caused by a variety of pathologic processes. The leading cause of SBO in industrialized countries is postoperative adhesions (60%), followed by malignancy, Crohn disease, and hernias, although some studies have reported Crohn disease as a greater etiologic factor than neoplasia. Surgeries most closely associated with SBO are appendectomy, colorectal surgery, and gynecologic and upper gastrointestinal (GI) procedures (see the image below). (See Etiology.)

Small bowel obstruction. Image courtesy of Ademola Small bowel obstruction. Image courtesy of Ademola Adewale, MD.

One study from Canada reported a higher frequency of SBO after colorectal surgery, followed by gynecologic surgery, hernia repair, and appendectomy. Lower abdominal and pelvic surgeries lead to obstruction more often than upper GI surgeries. (See Etiology.)

SBOs can be partial or complete, simple (ie, nonstrangulated) or strangulated. Strangulated obstructions are surgical emergencies. If not diagnosed and properly treated, vascular compromise leads to bowel ischemia and further morbidity and mortality. Because as many as 40% of patients have strangulated obstructions, differentiating the characteristics and etiologies of obstruction is critical to proper patient treatment. SBO accounts for 20% of all acute surgical admissions. (See Clinical, Workup, and Treatment.)



Small-bowel obstruction (SBO) leads to proximal dilatation of the intestine due to accumulation of GI secretions and swallowed air. This bowel dilatation stimulates cell secretory activity, resulting in more fluid accumulation. This leads to increased peristalsis above and below the obstruction, with frequent loose stools and flatus early in its course.

Vomiting occurs if the level of obstruction is proximal. Increasing small-bowel distention leads to increased intraluminal pressures. This can cause compression of mucosal lymphatics, leading to bowel wall lymphedema. With even higher intraluminal hydrostatic pressures, increased hydrostatic pressure in the capillary beds results in massive third spacing of fluid, electrolytes, and proteins into the intestinal lumen. The fluid loss and dehydration that ensue may be severe and contribute to increased morbidity and mortality.

Strangulated SBOs are most commonly associated with adhesions and occur when a loop of distended bowel twists on its mesenteric pedicle. The arterial occlusion leads to bowel ischemia and necrosis. If left untreated, this progresses to perforation, peritonitis, and death.

Bacteria in the gut proliferate proximal to the obstruction. Microvascular changes in the bowel wall allow translocation to the mesenteric lymph nodes. This is associated with an increase in the incidence of bacteremia due to Escherichia coli, but the clinical significance is unclear.



The most common cause of small-bowel obstruction (SBO) is postsurgical adhesions. Postoperative adhesions can be the cause of acute obstruction within 4 weeks of surgery or of chronic obstruction decades later. The incidence of SBO parallels the increasing number of laparotomies performed in developing countries.

Prevention of SBO may be essentially limited to decreasing the risk of adhesion formation by decreasing the number of intra-abdominal procedures (ie, laparotomies) and resultant scar formation. In a study by Van Der Wal et al, the incidence of chronic abdominal symptoms was significantly reduced after the use of a hyaluronic acid ̶ carboxymethylcellulose membrane (Seprafilm). However, Seprafilm placement did not provide protection against SBO. [3]

Another commonly identified cause of SBO is an incarcerated groin hernia. Other etiologies include malignant tumor (20%), hernia (10%), inflammatory bowel disease (5%), volvulus (3%), and miscellaneous causes (2%). The causes of SBO in pediatric patients include congenital atresia, pyloric stenosis, and intussusception.



With proper diagnosis and treatment of the obstruction, prognosis in small-bowel obstruction (SBO) is good. Complete obstructions treated successfully nonoperatively have a higher incidence of recurrence than do those treated surgically.

Complications of SBO include the following:

  • Sepsis
  • Intra-abdominal abscess
  • Wound dehiscence
  • Aspiration
  • Short-bowel syndrome (as a result of multiple surgeries)
  • Death (secondary to delayed treatment)

Mortality and morbidity are dependent on the early recognition and correct diagnosis of obstruction. If untreated, strangulated obstructions cause death in 100% of patients. If surgery is performed within 36 hours, the mortality rate decreases to 8%. The mortality rate is 25% if the surgery is postponed beyond 36 hours in these patients.

Some factors associated with death and postoperative complications include age, comorbidity, and treatment delay. According to one Norwegian group, morbidity and mortality decreased from 1961 to 1995.