Ogilvie syndrome pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

Pathogenesis

The precise mechanism by which colonic dilation occurs in patients with acute colonic pseudo-obstruction is unknown. The association with trauma, spinal anesthesia, and pharmacologic agents suggests an impairment of the autonomic nervous system. Interruption of the parasympathetic fibers from S2 to S4 leaves an atonic distal colon and a functional proximal obstruction . However, there is no proposed mechanism to explain colonic dilation in those patients without obvious involvement of the parasympathetic nerves.

In patients with acute colonic pseudo-obstruction, increasing colonic diameter accelerates the rise in tension on the colonic wall, increasing the risk of colonic ischemia and perforation. The risk of colonic perforation increases when cecal diameter exceeds 10 to 12 cm and when the distention has been present for greater than six days [12]. The duration of dilation is probably more important than the absolute diameter of the colon.

Rare cases have been reported in association with atrophic visceral myopathy with an extremely thin colonic wall, atrophic circular, and longitudinal muscularis propria without inflammation or fibrosis, and unaffected ganglion cells and myenteric plexus. The cause of the smooth muscle atrophy was unclear and the only potential association was with prior hypothyroidism.

Ogilvie's syndrome

• The association of spinal anaesthesias, drugs and nervous trauma has lead to the understanding that Ogilvie syndrome (colonic dilatation without pseudo-obstruction) may be caused by impairment of the autonomic nervous system.
• Damage to the parasympathetic fibers of S2 - S4 causes the distal colon to become atonic and become obstructed proximally.
• However, the exact mechanism is unknown, especially in patients who present with this syndrome without an obvious injury to the parasympathetic nerves.
• Acute colonic pseudo-obstruction occurs when the colon's diameter rises quickly, which increases the tension in the colonic wall, leading to colonic ischemia and possibly, perforation with a diameter exceeding 10 - 12cm.
• A rare case of Ogilvie syndrome showed atrophic myopathy with a thinned out colonic wall, despite a perfectly intact myenteric plexus and unaffected ganglion cells, with no evidence of fibrosis or inflammation.

Paralytic ileus

• The majority of paralytic (adynamic) ileus cases occur after major abdominal surgery, such as hysterectomy.
• Paralytic ileus is thought to occur with manipulation and trauma of the intestinal tract.
• Post operative dysmotility is associated with inflammation, impaired neural reflexes and the release of neural hormone peptides.
  • Inflammation:
    • Intestinal manipulation leads to intestinal ischemia, and shifting of endogenous cellular danger molecules and cytokines away from the site of trauma.
    • Leukocytic infiltration, macrophage and mast cell stimulation commences and causes muscular dysfunction, and therefore inflammation in the manipulated segment.
  • Neural reflexes:
    • Inhibitory sympathetic neural reflexes increase due to noxious spinal afferent signals, therefore, the use of epidural local anesthetics or topical capsaicin is encouraged to prevent paralytic ileus.
  • Neurohormonal peptides:
    • Inhibitory neurotransmitters are released and cause the gut motility to slow down.
    • Inhibitory neurotransmitters include, nitric oxide, vasoactive intestinal polypeptide, and substance P.