The etiology of pseudo-obstruction is not clearly understood. However, it is known that the autonomic nervous system is the control center for bowel function. The parasympathetic system innervates the smooth muscle to induce peristalsis, thereby inducing normal defecation. Disruption of the parasympathetic system or innervation of the sympathetic system will disrupt normal bowel function. There are many conditions and interventions that have been shown to be associated with bowel dysmotility resulting in ACPO. The differential diagnoses for this condition should also include mechanical bowel obstruction, toxic megacolon, and severe constipation with fecal impaction. In the case described above, the patient's only significant risk factors for developing ACPO were his CP and overall chronic disability.
Assessment
X-rays should be obtained immediately for a patient if one has concern about an obstructive process, especially if the suspicion is high for perforation. An acute abdominal series with an upright chest can provide vital information. Free air under the diaphragm indicating bowel perforation, differential air fluid levels indicating an ileus, and grossly dilated loops of bowel indicating an obstructive process can typically be seen and diagnosed from an x-ray. Additional information can be obtained from a CT regarding the location of the obstruction based on the transition zone.
Measurement of the colonic distention has been suggested as a potential guide to management and is routinely assessed radiographically. Studies have stated that dilation of the transverse colon of as little as 9 cm is potentially dangerous, and patients with cecal diameters >10-12 cm have been shown to be at higher risk of perforation [5–7]. In fact, the study by Vanek and Al-Salti reported no perforations for patients with <12 cm cecal diameter, a 7% perforation and ischemia rate for 12-14 cm, and 23% for patients with >14 cm cecal dilation [1]. However, some studies found no ischemia or perforation in patients with significant dilation beyond these limits [8]. Our own case reveals a 26-cm dilation of the colon without evidence of perforation or ischemia. Despite the massive dilation of the colon, the patient suffered no significant sequelae. Of additional interest, a retrospective study by Johnson et al. actually concluded that the duration of cecal distention may be associated with the perforation rate, but that the diameter was not. There may also be a significant difference in perforation risk in patients with severe colonic dilation with only moderate cecal dilation; however, no such comparison was found during a review of the literature.
Management
The initial treatment for ACPO includes placement of a nasogastric tube, enemas, fluid resuscitation, and correction of electrolyte abnormalities. Antibiotics may be given to provide some coverage for patients who are suspected to have bowel ischemia or perforation [6]. However, in the study by Vanek and Al-Salti, there was almost no significant difference in symptoms at presentation between patients with these complications and those without [1], although they did note that patients with ischemia and/or perforation had a higher rate of fever (78%) than those that did not (31%). Conservative management is thought to be appropriate in patients without significant pain or dilation (<12 cm).
Anticholinergic agents such as neostigmine have been shown to have high success rates with restoration of peristalsis and have been used to treat ACPO successfully [9–11]. Trevisani showed clinical resolution of the acute pseudo-obstruction in 26 of 28 patients with the use of neostigmine [11]. Neostigmine enhances parasympathetic activity by competing with acetylcholine for attachment to acetylcholinesterase at sites of cholinergic transmission and enhancing cholinergic action. Side effects of neostigmine that may cause significant problems during acute management include increased abdominal pain, excess salivation, vomiting, bradycardia, asystole, hypotension, and seizures. In one article, 2 of the 11 patients treated with neostigmine required atropine for bradycardia [9]. Cardiac telemetry monitoring should be utilized during and after administration of this drug. The dose for neostigmine is 2 mg intravenously over 3-5 min with a cost of less than $10/dose. In a double-blinded placebo-controlled trial by Ponec et al., almost all (10 of 11) patients treated with neostigmine responded with the initial therapy, and none of the placebo group improved [9].
The need for colonoscopic decompression is routinely determined based on the severity of the pseudo-obstruction, and therefore early consultation with surgery or gastroenterology is appropriate. Colonic decompression may be indicated when the cecal diameter is >12 cm [12]. Despite this usual recommendation, our patient did well without this invasive procedure, and success rates may only be as high as 61-78% with a reported recurrence rate of 18-33% [6]. Iatrogenic perforation during this procedure has been reported as 3% [13]. Another invasive, non-surgical method for decompression is fluoroscopic-guided decompression [14].
Surgical interventions, such as tube cecostomy, cecostomy, ileostomy/colostomy, resection, exteriorization, intraoperative long colon tube, and exploratory laparotomy are reserved for patients who failed other management modalities. As expected, morbidity and mortality are greater in patients undergoing surgical interventions (30%/6%), when compared to those managed conservatively (14%/3%) or with colonoscopy (13%/2%) [1].