Introduction

Acute colonic pseudo-obstruction, also known as Ogilvie syndrome, is a nonmechanical, functional obstruction of the large intestine. It has become a well-known clinical entity, but in many regards it is poorly understand and difficult to manage. In 1948 a British surgeon, Sir Heneage Ogilvie, first described acute colonic pseudo-obstruction in two patients who had colonic dilatation without an obvious mechanical cause. Both patients had extensive invasion and destruction of the celiac plexus associated with retroperitoneal malignancy. Ogilvie hypothesized that this neural involvement produced a functional obstruction. Today, acute colonic pseudo-obstruction is a differential diagnosis for hospitalized patients who have abdominal distention. Diagnosis without undue delay is crucial because of the need to exclude a mechanical obstruction and the risk of colonic perforation. Conservative measures often lead to resolution. When medical therapy fails or is contraindicated, endoscopy can be effective in achieving decompression, and surgery is the last resort. New advanced techniques in endoscopy, such as the use of decompression tubes and percutaneous endoscopic cecostomy, have decreased the need for resection.

Epidemiology

The incidence of Ogilvie syndrome is unknown, but most studies indicate that elderly patients are at greatest risk. In a review by Vanek et al of 400 cases, a list of associated conditions was compiled, which included obstetric, gynecologic, or pelvic surgery (19%); trauma/orthopedic procedures (18%); infection (10%); cardiac events (10%); and neurologic events (9%). Other conditions connected with acute pseudo-obstruction of the colon included electrolyte imbalances, certain medications, organ transplant, connective tissue disorders, and debilitated states ( Box 53-1 ).

Etiology

Several hypotheses have been proposed regarding the cause of pseudo-obstruction, but it is unlikely that any single theory can explain all cases. It is a functional disturbance in colonic motility in that there is no mechanical obstruction.

The enteric nervous system is the primary determinant of motility function in both the small and large intestines, whereas the central nervous system modulates motility patterns established by the enteric system. Enteric nerves contain a variety of neurotransmitters responsible for smooth muscle contraction or relaxation; acetylcholine, neurokinin A, and substance P are stimulatory neurotransmitters, and vasoactive intestinal polypeptide and nitric oxide are inhibitory. The extrinsic influences of the sympathetic nerves from the thoracic and lumbar segments of the spinal cord tend to decrease motility, whereas parasympathetic nerves from the brainstem via the vagus nerve, as well as sacral spinal segments, increase motility.

To explain an acute colonic pseudo-obstruction, Ogilvie theorized that there was an imbalance in the activity of the autonomic nervous system, with parasympathetic overactivity leading to dilatation of the colon. However, current evidence favors a relatively increased sympathetic tone and/or a decreased parasympathetic tone leading to a functionally obstructed distal colon and a relaxed proximal colon (adynamic colon). The evidence that favors this theory is the association of acute pseudo-obstruction with diseases that cause disturbances in the autonomic input to the gut and the remarkable response to pharmacologic therapy.

In other instances, the anticholinergic activity of certain drugs decreases parasympathetic activity, thereby creating an atonic segment of bowel. Other theories point to factors that produce excess sympathetic activity, such as myocardial infarction, surgery, or trauma, as the precipitating cause.