eMedicine Specialties > Emergency Medicine > Gastrointestinal

Obstruction, Small Bowel

Author: Brian A Nobie FACEP, MD, Director of Recruitment, Consulting Staff, Florida Emergency Physicians, Florida Hospital, Celebration Health
Contributor Information and Disclosures

Updated: Nov 12, 2009

Introduction

Background

A small-bowel obstruction (SBO) is caused by a variety of pathologic processes. The leading cause of SBO in developed countries is postoperative adhesions (60%) followed by malignancy, Crohn's 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. 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.

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.

Small bowel obstruction.

Small bowel obstruction.

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Small bowel obstruction.

Small bowel obstruction.


Pathophysiology

Obstruction of the small bowel 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 both 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 incidence of bacteremia due to Escherichia coli, but the clinical significance is unclear.

Frequency

United States

SBO accounts for 20% of all acute surgical admissions.

Mortality/Morbidity

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.

Clinical

History

Obstruction can be characterized as either partial or complete versus simple or strangulated.

  • Abdominal pain (characteristic with most patients)
    • Pain, often described as crampy and intermittent, is more prevalent in simple obstruction.
    • Often, the presentation may provide clues to the approximate location and nature of the obstruction. Usually, pain that occurs for a shorter duration of time and is colicky and accompanied by bilious vomiting may be more proximal. Pain lasting as many as several days, which is progressive in nature and with abdominal distention, may be typical of a more distal obstruction.
    • Changes in the character of the pain may indicate the development of a more serious complication (ie, constant pain of strangulated or ischemic bowel).
  • Nausea
  • Vomiting, which is 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 patient's medical history)
  • History of malignancy (particularly ovarian and colonic)

Physical

  • Abdominal distention
    • Duodenal or proximal small bowel has less distention when obstructed than the distal bowel has when obstructed.
    • Hyperactive bowel sounds occur early as GI contents attempt to overcome the obstruction.
    • Hypoactive bowel sounds occur late.
    • Exclude incarcerated hernias of the groin, femoral triangle, and obturator foramina.
    • Proper genitourinary and pelvic examinations are essential.
    • Look for the following during rectal examination:
      • Gross or occult blood, which suggests late strangulation or malignancy
      • Masses, which suggest obturator hernia
    • Check for symptoms commonly believed to be more diagnostic of intestinal ischemia, including the following:
      • Fever (temperature >100°F)
      • Tachycardia (>100 beats/min)
      • Peritoneal signs
    • No reliable way exists to differentiate simple from early strangulated obstruction on physical examination. Serial abdominal examinations are important and may detect changes early.

Causes

  • The most common cause of 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.
    • The second most common identified cause of SBO is an incarcerated groin hernia.
  • Other etiologies of SBO 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.

More on Obstruction, Small Bowel

Overview: Obstruction, Small Bowel
Differential Diagnoses & Workup: Obstruction, Small Bowel
Treatment & Medication: Obstruction, Small Bowel
Follow-up: Obstruction, Small Bowel
Multimedia: Obstruction, Small Bowel
References
Further Reading
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References

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Further Reading

Clinical guidelines

EAST Practice Parameter Workgroup for Management of Small Bowel Obstruction. Practice management guidelines for small bowel obstruction. Chicago (IL): Eastern Association for the Surgery of Trauma (EAST); 2007. 42 p.

Ros PR, Huprich JE, Bree RL, Foley WD, Gay SB, Glick SN, Heiken JP, Levine MS, Rosen MP, Shuman WP, Greene FL, Expert Panel on Gastrointestinal Imaging. Suspected small bowel obstruction. [online publication]. Reston (VA): American College of Radiology (ACR); 2005. 5 p.

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Keywords

SBO, small bowel obstruction, small bowel obstruction symptoms, small bowel obstruction treatment, small bowel obstruction causes, obstruction of the small bowel, Crohn disease, Crohn's disease, hernia, bowel necrosis, bowel ischemia, peritonitis, inflammatory bowel disease, volvulus, congenital atresia, pyloric stenosis, intussusception

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Contributor Information and Disclosures

Author

Brian A Nobie FACEP, MD, Director of Recruitment, Consulting Staff, Florida Emergency Physicians, Florida Hospital, Celebration Health
Brian A Nobie FACEP, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Joseph J Sachter, MD, FACEP, Consulting Staff, Department of Emergency Medicine, Muhlenberg Regional Medical Center
Joseph J Sachter, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Medical Association, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eugene Hardin, MD, FAAEM, FACEP, Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Steven C Dronen, MD, FAAEM, Director of Emergency Services, Director of Chest Pain Center, Department of Emergency Medicine, Ft Sanders Sevier Medical Center
Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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