Small-Bowel Obstruction

Updated: Apr 28, 2017
  • Author: Mityanand Ramnarine, MD, FACEP; Chief Editor: Steven C Dronen, MD, FAAEM  more...
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Overview

Practice Essentials

Small-bowel obstruction (SBO) is caused by a variety of pathologic processes. The most common cause of SBO in developed countries is intra-abdominal adhesions, accounting for approximately 65% to 75% of cases, followed by hernias, Crohn disease, malignancy, and volvulus. [1]  In contrast, SBO in developing countries is primary caused by hernias (30-40%), adhesions (about 30%), and tuberculosis (about 10%), along with malignancy, Crohn disease, volvulus, and parasitic infections. [2] The general trend in developing countries is an increased incidence of SBO from adhesions, with a higher incidence of laparotomies. 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

Symptoms of SBO can be characterized as either partial or complete versus simple or strangulated. The classic symptoms of nausea, vomiting, abdominal pain, and constipation are rarely present in all cases of SBO. Abdominal pain associated with SBO is often described as crampy and intermittent. Without treatment, the abdominal pain can increase as a result of bowel perforation and ischemia. Therefore, having a clinical suspicion for the condition is paramount to early identification and intervention. Furthermore, the clinical presentation of the patients varies and no one clinical symptom on its own identifies the majority of patients with SBO. Some studies have suggested that the absence of passage of flatus and/or feces and vomiting are the most common presenting symptoms, with abdominal discomfort/distention the most frequent physical examination findings. [3] Other studies have shown that abdominal pain is present in the majority of patients found to have SBO. 

Some signs and symptoms associated with SBO include the following:

  • Nausea/vomiting (60-80%): The vomitus can often be bilious in nature 
  • Constipation/absence of flatus (80-90%): Typically a later finding of SBO
  • Abdominal distention (60%)
  • Fever and tachycardia: Late findings and may be associated with strangulation

Some risk factors associated with SBO include the following:

  • 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
  • Inflammatory bowel disease 

See Presentation for more detail.

Workup

Laboratory tests

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

  • Serum chemistries: Rarely abnormal early in the disease unless due to vomiting or dehydration 
  • BUN/creatinine levels: May be elevated in dehydration due to vomiting 
  • CBC count: Elevation can be associated with complications 
  • Serum lactate levels: Elevation is suggestive of dehydration or tissue hypoperfusion
  • Urinalysis
  • Type and crossmatch
  • PT, PTT, and INR measurements

Laboratory tests to exclude biliary or hepatic disease are also needed. They include the following:

  • Phosphate level
  • Creatine kinase level
  • Liver panel: AST, ALT, ALP, and bilirubin levels

Imaging tests

Obtain plain radiographs first for patients in whom SBO is suspected. Although not sensitive, upright abdominal films may help substantiate the diagnosis if the presence of air-fluid levels or a paucity of gas is observed. Note that supine films may obscure the detection of air-fluid levels. [4]

Multislice CT has been show to be a particularly effective imaging tool for evaluating patients suspected of having SBO, with a sensitivity of over 95%. [5] CT imaging is also capable of detecting complications of SBO not visualized on plain films, including ischemia, perforation, mesenteric edema, and pneumatosis.

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%. It may be a useful alternative imaging modality in children and pregnant women.

Enteroclysis is another valuable diagnostic test 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. However, CT imaging has superseded enteroclysis due to the increased availability of CT scanners as well as owing to the procedure's increased risk of perforation and aspiration.

See Workup for more detail.

Management

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 are often 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. [6, 7]

See Treatment and Medication for more detail.

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Background

In the United States, 15 of every 100 admissions for abominal pain are due to small-bowel obstruction (SBO), with 300,000 admissions annually. [8]  An SBO is caused by a variety of pathologic processes. The leading cause of SBO in industrialized countries is postoperative adhesions (65-75%), 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. Differentiating the characteristics and etiologies of obstruction is critical to proper patient treatment because as many as 40% of patients have strangulated obstructions. SBO accounts for 20% of all acute surgical admissions. (See Presentation, Workup, and Treatment.)

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Pathophysiology

Small-bowel obstruction (SBO) leads to proximal dilatation of the intestine due to accumulation of gastrointestinal (GI) secretions and swallowed air. Bowel dilatation stimulates cell secretory activity, resulting in more fluid accumulation. This, in turn, 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.

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Etiology

The most common cause of small-bowel obstruction (SBO) in developed countries is intra-abdominal adhesions, accounting for approximately 65% to 75% of cases. [1] 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. [9]

Following adhesions, the most common causes of SBO in developed regions are hernias (incarcerated groin hernias) (10-20%), malignancy (10-20%), inflammatory bowel disease (5%), volvulus (3%), and miscellaneous causes (2%). [1]  The causes of SBO in pediatric patients include congenital atresia, pyloric stenosis, and intussusception.

In contrast, SBO in developing countries is primarily caused by hernias (30-40%), adhesions (about 30%), and tuberculosis (about 10%), along with malignancy, Crohn disease, volvulus, and parasitic infections. [2]

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Prognosis

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.

Morbidity/mortality

Morbidity and mortality 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 from SBO decreased from 1961 to 1995; the mortality was reported to be about 5%. [10]  

Complications

Complications of SBO also depend on the severity of the condition, the patient's age, the presence of comorbities and, often, the duration of symptoms/signs, and include the following:

  • Sepsis: Due to translocation of intestinal bacteria from tissue breakdown
  • Intra-abdominal abscess
  • Wound dehiscence
  • Aspiration
  • Short-bowel syndrome (as a result of multiple surgeries)
  • Disability and death (secondary to delayed treatment)

Cardiac and pulmonary complications may result from procedures and hospitalization, neurologic complications, thrombosis/embolism, major hemorrhage, incision infection or rupture, and abdominal abscess or fistula formation. They include the following [3, 10] :

  • Pneumonia: Including aspiration, ventilator associated, and/or hospital acquired
  • Bowel ischemia/perforation
  • Peritonitis
  • Acute kidney injury/acute renal failure
  • Surgical complications
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