Chapter 26

This chapter will discuss general features of BO and various ICU specific issues. BO occurs when the normal passage of enteric material through the gastro-intestinal (GI) tract is impaired by the mechanical blockage of the bowel lumen. In contrast, functional BO (“paralytic ileus”) occurs when normal GI peristalsis ceases due to some physiologic disruption. Patients with BO present with varying degrees of abdominal pain, nausea, vomiting and obstipation depending on the cause, location, severity and duration of the BO. Physiologically, BO can result in hypovolemia, electrolyte deficiencies and acid– base imbalances which require urgent correction. BO classically describes blockage of the small or large intestine. The most common cause of small bowel obstruction (SBO) in adults is postoperative intra-abdominal adhesions, whereas the most common cause of large bowel obstruction (LBO) is malignancy (i.e., colorectal cancer). The diagnosis of BO is clinical; however, the use of radiographic imaging, especially computed tomography (CT), is very helpful in determining the underlying etiology of BO, as well as initial management (operative or nonoperative). Considerations for urgent surgery include hemodynamic instability, peritonitis, closed loop BO, concerns of bowel ischemia or perforation and low likelihood of nonoperative resolution.

BO is a clinical state in which the normal anterograde passage of digestive materials along the GI tract is partially or completely interrupted by mechanical obstruction of the bowel lumen by a mechanical and/or anatomical phenomenon.1,2 This is distinguished from ileus, in which effective GI transit is hampered by diminished intestinal peristalsis, typically due to more systemic or physiological factors (i.e., sepsis, electrolyte abnormalities).²

The management principles of BO depend to some degree on the underlying obstructive etiology. All cases mandate traditional management principles of: identifying and treating the underlying cause; prevention and correction, as necessary, of volume, electrolyte and acid–base disturbances; proximal decompression of the GI tract; and symptom relief of resultant pain, nausea and vomiting with analgesic and anti-emetic medications.^3,4 In some cases, parenteral nutritional support may be needed if there is a prolonged cessation of GI function. The role and timing of emergency surgery for BO depends on the overall patient status, etiology and severity of the obstruction, as well as the degree of concern for intestinal ischemia, perforation or peritonitis.

As such, critical care providers should be comfortable with the medical and surgical management principles for BO. Delay in diagnosing and appropriately managing BO will result in greater overall physiologic disruption, increased likelihood of requiring bowel resection, and overall increased morbidity and mortality.⁷

Epidemiology/Risk Factors

BO accounts for approximately 15% of all in-patient general surgery admissions and adhesive SBO (ASBO), which occur in up to 25% of patients following GI surgery, results in more than $1.3 billion (USD) in annual associated healthcare costs in the United States, alone.^5,6

Globally, SBO is much more common than LBO, with their relative incidences occurring in a 4:1 ratio.⁸ The most common causes of SBO in North American and Europe are post-surgical adhesions (65–75%), abdominal wall hernias (10–15%) and intraperitoneal malignancy (5–10%) (Table 1).^1,7 This contrasts with African and Asian populations, in which hernias are by far the most common cause of SBO.^7,8

Table 1. Common causes of bowel obstruction.

The risk of ASBO varies depending on the type of surgery. For instance, larger pelvic surgeries such as hysterectomy, abdominal-perineal resection and ileo-anal pouch formation are associated with lifetime rates of 25–38% for at least one ASBO episode. Prior laparotomy for acute perforation with notable peritoneal contamination and inflammation are also associated with more extensive adhesions.10,11 These rates contrast with the lifetime BO incidence of 0.1–2% in individuals without prior intra-abdominal surgery.⁸ Additionally, patients undergoing minimally-invasive surgery are much less likely to develop ASBO.¹¹

The most common causes of LBO in Western nations are colorectal cancer (60–80%), diverticular strictures (15–20%) and colonic (cecal and sigmoid) volvulus (5–10%) (Table 1). Conversely, in Asia and Africa, volvulus is the most common cause of LBO (upwards of 40%) and colorectal cancer is much less common. Anatomically, the sigmoid colon is the most common site for LBO, and overall, malignant LBO episodes are more likely to be distal or left-sided.²

Diverticular disease tends to cause LBO via structuring and narrowing of the colonic lumen at sites of recurrent inflammation and subsequent scarring. Risk factors for colonic volvulus include congenital colonic abnormalities (i.e., non-fixation) and factors associated with underlying chronic constipation (which include narcotic use, institutionalization, increasing age and diet imbalances) leading to colonic redundancy.⁸

Pathophysiology

The common underlying pathophysiology of BO is a physical (or “mechanical”) occlusion of the GI tract lumen that cannot be overcome by peristalsis, resulting in partial or complete blockage of anterograde flow of digestive contents beyond the point of obstruction. As a result, numerous pathophysiologic processes occur. These include changes in fluid volume distribution, electrolyte and acid–base disturbances, changes in the distribution of GI flora, malnutrition and in severe cases, decreased blood supply of the affected segment of intestine which may subsequently result in intestinal ischemia, infarction and finally perforation with resultant peritonitis and sepsis.8

The etiology of BO is classically organized by the location of the obstructing mechanism relative to the intestinal wall (Table 2). ‘Extrinsic’ processes compress or twist the lumen of the intestine and may cause pressure necrosis or restrict blood supply to the affected bowel, which can result in ischemia and subsequent perforation. ‘Mural’ phenomena that arise from the intestinal wall itself cause obstruction by narrowing or obliterating the lumen at the involved location. Finally, ‘intraluminal’ causes physically occlude the lumen.^2,7

Table 2. Etiology of mechanical bowel obstruction.

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