Etiology

The etiology is multifactorial and is related to a disruption in the normal motility of the intestine. Predisposing factors include:

  • Electrolyte imbalances

  • Release of inflammatory agents

  • Deregulation of the sympathetic and parasympathetic input to the gastrointestinal (GI) tract

  • Exogenous compounds, such as analgesics and anesthetics.

Predisposing factors are most likely to occur after GI surgery, but may also occur with:

  • Nonabdominal surgery (thoracic, cardiac, or extremity)[18][19]

  • Other retroperitoneal pathology such as aortic or urinary disorders[3]​​

  • Acute or systemic illness (e.g., myocardial infarction, acute cholecystitis, pancreatitis, peritonitis, sepsis)

  • Pharmacologic agents (e.g., opioids, anticholinergics)

  • Multi-organ trauma​

  • Cardiopulmonary bypass.[10][19]​​

Pathophysiology

Gastrointestinal motility is controlled by neurogenic, hormonal, and inflammatory factors.[20] During the postoperative period, catecholamine levels are higher than usual, which is believed to contribute to decreased GI motility. This also occurs in other nonsurgical conditions, including systemic illnesses, sepsis, and trauma. GI motility is inhibited by nitric oxide, vasoactive intestinal peptide, calcitonin gene-related peptide, and substance P.[3][21] Studies in animals have shown that antagonists to these substances may improve postoperative ileus, although this has not been substantiated in humans.

In addition, corticotropin-releasing factor levels rise as part of the stress response, causing a delay in gastric emptying. The macrophages in the wall of the intestine are activated by bowel manipulation and secrete various substances (nitric oxide, prostaglandins, COX-2, interleukin-6, tissue necrosis factor alpha) that contribute to the decreased motility of the GI tract.[21][22]

Classification

Classification according to type of ileus

Postoperative ileus

  • The normal slowing of bowel motility in response to the trauma of surgery. This usually follows GI surgery but is also associated with nonabdominal surgery.

  • Gastric motility recovers first, followed by small bowel motility (in 24 to 48 hours) then colon motility (in about 48 to 72 hours).[2]

  • Prolonged postoperative ileus is defined as two or more of the following occurring on or after day 4 postsurgery without prior resolution of postoperative ileus: vomiting, abdominal distension, inability to tolerate oral feeding, absence of flatus.[3][4] Definitions across literature for return of bowel function after GI surgery are very varied, with the most commonly reported outcome measure being "time to passage of flatus".[5]

Ileus with systemic illness

  • Paralysis of bowel motility accompanying certain acute illnesses, such as myocardial infarction, acute pancreatitis, sepsis, and GI disorders.

Narcotic ileus

  • Slowing of bowel motility associated with opioid use, thought to be caused by opioid action on mu receptors.[3]

Use of this content is subject to our disclaimer