Ogilvie's syndrome

Abstract

Ogilvie's syndrome, also known as acute colonic pseudo-obstruction, refers to pathologic dilation of the colon without underlying mechanical obstruction, occurring primarily in patients with serious comorbidities. Diagnosis of Ogilvie's syndrome is based on clinical and radiologic grounds, and can be treated conservatively or with interventions such as acetylcholinesterase inhibitors (such as neostigmine), decompressive procedures including colonoscopy, and even surgery. Based on our clinical experience we hypothesized that conservative management yields similar, if not superior, results to interventional management. Therefore, we retrospectively examined all patients over the age of 18 with Ogilvie's syndrome who presented to the Medical University of South Carolina (MUSC). The diagnosis of Ogilvie's syndrome was confirmed by clinical criteria, including imaging evidence of colonic dilation ≥9 cm. Patients were divided and analyzed in 2 groups based on management: conservative (observation, rectal tube, nasogastric tube, fluid resuscitation, and correction of electrolytes) and interventional (neostigmine, colonoscopy, and surgery). Use of narcotics in relation to maximal bowel size was also analyzed. Over the 11-year study period (2005–2015), 37 patients with Ogilvie's syndrome were identified. The average age was 67 years and the average maximal bowel diameter was 12.5 cm. Overall, 19 patients (51%) were managed conservatively and 18 (49%) underwent interventional management. There was no significant difference in bowel dilation (12.0 cm vs 13.0 cm; P = .21), comorbidities (based on the Charlson Comorbidity Index (CCI), 3.2 vs 3.4; P = .74), or narcotic use (P = .79) between the conservative and interventional management groups, respectively. Of the 18 patients undergoing interventional management, 11 (61%) had Ogilvie's-syndrome-related complications compared to 4 (21%) of the 19 patients in the conservative management group (P < .01). There was no difference in overall length of stay in the 2 groups. Two patients, one in each group, died from complications unrelated to their Ogilvie's syndrome. We conclude that Ogilvie's syndrome, although uncommon, and typically associated with severe underlying disease, is currently associated with a low inpatient mortality. While interventional management is often alluded to in the literature, we found no evidence that aggressive measures lead to improved outcomes.

An “Expressionistic” Look at Serrated Precancerous Colorectal Lesions

“…The third gene that was highly expressed in SSA/Ps and HPs, ACHE (acetylcholinesterase), is instead typically expressed in conducting tissues, such as those of the central and peripheral (including the enteric) nervous systems, and at neuromuscular junctions [55]. It terminates signal transmission by hydrolyzing the neurotransmitter acetylcholine at cholinergic synapses in the brain and at neuromuscular junctions, and pharmacologic inhibition of this enzymatic activity is used to treat colonic pseudoobstruction [56]. We found high levels of ACHE mRNA in epithelial cells at the surface of the normal colorectal mucosa, but even higher levels were found in serrated glands, extending about half-way down toward the base of the crypts (Fig.…”

Ogilvie Syndrome Following an Inflatable Penile Implant

“…The management of Ogilvie syndrome is a stepwise approach that consists of conservative management, medical interventions, or surgery, depending on the severity and extent of colonic dilation [14,15]. Conservative measures include giving the patient intravenous fluids, not allowing the patient to given anything by mouth, decompression of the gastrointestinal tract by nasogastric tube, and encouraging the patient to ambulate if possible.…”

An “expressionistic” look at serrated precancerous colorectal lesions

“…The third gene that was highly expressed in SSLs and HPs, ACHE (acetylcholinesterase), is instead typically expressed in conducting tissues, including those of the enteric nervous system, and at neuromuscular junctions [48]. It terminates signal transmission by hydrolyzing the neurotransmitter acetylcholine at cholinergic synapses in the brain and at neuromuscular junctions, and pharmacologic inhibition of this enzymatic activity is used to treat colonic pseudo-obstruction [49]. We found high levels of ACHE mRNA in epithelial cells at the surface of the normal colorectal mucosa, but even higher levels were found in serrated glands, extending about half-way down toward the base of the crypts (Figure 2, Supplementary Figure 6).…”