Bowel Obstruction

Mechanical bowel obstruction can be caused by lesions outside or within the bowel wall, or within the lumen itself. It may be partial or complete, strangulating or non-strangulating. Paralytic ileus may mimic obstruction but there is no mechanical cause; rather, it is associated with abnormal propulsive motility. Pseudo-obstruction is also associated with abnormal neuromuscular activity but is more chronic.

Either the small bowel or large bowel may be affected. Signs and symptoms include abdominal pain, vomiting, bloating and not passing gas.

Aetiology and Pathophysiology

Common causes of small bowel obstruction (SBO) include adhesions, hernias Opens in new window, and neoplasms. Less common causes include inflammatory bowel disease, gallstones, foreign bodies, strictures, radiation, diverticulitis, endometriosis and abscesses.

Common causes of large bowel obstruction (LBO) include neoplasm, diverticulitis, and volvulus. Faecal impaction, inflammatory bowel disease, strictures and extraintestinal tumors are less common causes.

Paralytic ileus can be caused by a wide range of conditions. Metabolic causes include hypokalaemia (most common), hyponatraemia, hypomagnesaemia, and hypoalbuminaemia. Drugs such as tricylic antidepressants, opiates, antihistamines, β-adrenergic agonists and quinidine have also been implicated.

The pathophysiology of mechanical bowel obstruction relates to rising intraluminal pressure, mucosal injury, bacterial overgrowth and inflammatory response. Bowel proximal to the obstruction distends with gas, fluid and electrolytes, then hypersecretion escalates, bowel absorptive ability decreases, and progressive systemic volume losses occur.

As obstruction persists and intraluminal pressure rises, local vascular compromise can occur, especially venous stasis. Vomiting may ensue, worsening dehydration and electrolyte disturbances. As pressures rise and/or blood flow diminishes, strangulation, haemorrhagic necrosis and/or gangrene may follow, with consequent perforation and sepsis.

A closed-loop obstruction implies both proximal and distal obstruction (e.g. strangulating hernia or volvulus), leading to vascular compromise more quickly, hence a higher risk of strangulation, necrosis and perforation.

Clinical Features

1. History

In early bowel obstruction abdominal pain is poorly localized and colicky, but later may become more constant and, if severe, suggests ischaemia or peritonitis. Pain from SBO tends to be more severe earlier, and cramps tend to be more frequent, compared to LBO where dull, lower abdominal cramps are more common.

Vomiting is more common in SBO and is a late symptom in LBO. Faeculent vomiting or distension suggests a more distal SBO. Obstipation was thought typical, but the passage of flatus and stool may continue.

The gastrointestinal and surgical history helps differentiate causes of mechanical obstruction, and drug history and systems enquiry may identify potential causes of non-mechanical obstruction.

2. Disposition

Patients with bowel obstruction associated with haemodynamic compromise, shock or sepsis require combined ongoing management by surgical and intensive-care teams. Patients with suspected strangulating bowel obstruction or perforation should have urgent surgery. Stable patients and those with partial bowel obstruction can be started on conservative therapy and monitored closely as surgical inpatients for signs of deterioration.