In the Rapid Review series, I briefly review the key points of a clinical review paper (or two). The topic this time: Acute colonic pseudo-obstruction (Ogilvie’s syndrome)
Pereira P, Djeudji F, Leduc P, Fanget F, Barth X. Ogilvie’s syndrome-acute colonic pseudo-obstruction. Journal of visceral surgery. 2015; 152(2):99-105. PMID: 25770746
What is acute colonic pseudo-obstruction?
Acute colonic pseudo-obstruction (or “Ogilvie’s syndrome”) is a potentially deadly disorder characterized by acute and extensive dilatation of all or part of the colon in the absence of anatomic obstruction or extrinsic inflammation.
What causes it?
Honestly, we don’t know. There are many theories as to the underlying pathophysiology. The predominant theory focuses on underactive parasympathetic tone, potentially combined with increased sympathetic tone. However, ischemia, hormonal changes, metabolic causes, drugs, and even herpes zoster (which is blamed for everything at some point) have all been implicated.
Who gets it?
The typical patient is an elderly with multiple chronic illnesses.
How does it present?
The presentation is much like an anatomic large bowel obstruction, with significant abdominal distension, as well as abdominal pain, nausea, and vomiting. There may be constipation and decreased flatus, but there can also be a secretory diarrhea. It is generally well tolerated, so significant abdominal tenderness, fever, hypotension, or tachycardia should signal possible complications such as perforation.
How is the diagnosis made?
Acute colonic pseudo-obstruction is a diagnosis of exclusion. Labs rarely help, but electrolyte imbalances may contribute and so should be corrected. The key to diagnosis is imaging, focusing on ruling out mechanical obstruction, alternate causes of obstruction, and complications. CT scan has a sensitivity of 96% and a specificity of 93%.
What is the differential diagnosis?
Other considerations are ileus, mechanical large bowel obstruction, toxic megacolon secondary to Clostridium difficile colitis, ischaemic colitis, and sigmoid or caecal volvulus.
What are the complications?
The distention can become large enough to cause ischemia and perforation. The incidence of perforation 15-20% and when it occurs there is a morality of up to 50%.
How is it treated?
As long as the patient is stable, does not have peritoneal signs on exam, and the cecal size is less than 12 cm, the management is conservative. This includes correcting electrolytes, correcting fluid imbalances, and stopping oral intake. Any medications that can slow colonic motility, such as opioids and anticholinergics, should be discontinued. Nasogastric tubes are generally recommended, but given the lack of evidence in mechanical obstruction and the fact that they are rated as among the most painful things we do to patients, I would probably skip it initially. Keeping patients out of bed and walking is also essential (so don’t tether them with an unnecessary foley or IV line).
That will cover the emergency department management for most patients. If it fails, you may see surgeons prescribe neostigmine, decompress the colon endoscopically, place a rectal tube, or potentially even take the patient for surgery.
Once resolved, it is recommended that patients take long term polyethylene glycol.
Who was Ogilvie?
Ogilvie’s syndrome is named for the British surgeon Sir William Heneage Ogilvie (1887- 1971), who first described it in 1948.
“A misleading symptom is misleading only to one able to be misled.” – Sir William Heneage Ogilvie