Postoperative Ileus

Updated: Nov 01, 2021
  • Author: Burt Cagir, MD, FACS; Chief Editor: Vinay K Kapoor, MBBS, MS, FRCSEd, FICS, FAMS  more...
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Ileus occurs from hypomotility of the gastrointestinal tract in the absence of mechanical bowel obstruction. When a similar condition occurs in the stomach (eg, in diabetes or after pancreatoduodenectomy), it is called gastroparesis or delayed gastric emptying (DGE). Although the exact pathogenesis of ileus remains multifactorial and complex, the clinical picture appears to be transiently impaired propulsion of intestinal contents. The complex interaction between autonomic and central nervous system function, as well as local and regional substances, may alter the intestinal equilibrium, resulting in disorganized electrical activity and paralysis of intestinal segments. This lack of coordinated propulsive action leads to the accumulation of gas and fluids within the bowel.

Note the images below.

Postoperative ileus after an open cholecystectomy. Postoperative ileus after an open cholecystectomy.
Ogilvie pseudo-obstruction in a septic elderly pat Ogilvie pseudo-obstruction in a septic elderly patient. Note the massive dilatation of the colon, especially the right colon and cecum.

Although ileus has numerous causes, the postoperative state is the most common setting for the development of ileus. Indeed, ileus is an expected consequence of abdominal surgery, with the most common being elective colorectal resection. [1] Physiologic ileus spontaneously resolves within 2-3 days, after sigmoid motility returns to normal. Ileus that persists for more than 3 days following surgery is termed postoperative adynamic ileus, paralytic ileus, or functional ileus. [2] Frequently, ileus occurs after major abdominal operations, but it may also occur after retroperitoneal and extra-abdominal surgery, as well as general anesthesia alone. The longest duration of ileus is noted to occur after colon and rectal surgery. [3, 4] Laparoscopic colon resection has been associated with shorter periods of ileus than open colon and rectal resection. [5]

The clinical consequences of postoperative ileus can be profound. Patients with ileus are immobilized, have discomfort and pain, and are at increased risk for pulmonary complications. Ileus also enhances catabolism because of poor nutrition. Overall, ileus increases the cost of medical care because it prolongs hospital stays. [6] In 1990, Livingston and Passaro estimated that ileus costs $750 million annually ($1500 per patient) in the United States. [2]

Iyer et al assessed healthcare utilization and costs in colectomy surgery patients who developed postoperative ileus versus those who did not. [7] A retrospective cohort study design was used in which 17,876 patients with primary procedure code for colectomy were identified. Mean hospital stay was significantly longer in patients with postoperative ileus (13.8 [13.3] days) compared with patients without postoperative ileus (8.9 [9.5] days; P< .001), and the presence of postoperative ileus was a significant predictor of hospital stay (P< .001). [7] Additional significant predictors of hospital length of stay included female sex (P = 0.002), greater severity level (P< .001), and hospital bed size >500 (P = .013).

The investigators found the presence of postoperative ileus was found to be a significant predictor of hospitalization costs (P< .001), controlling for covariates. [7] The authors concluded that postoperative ileus in colectomy patients is a significant predictor of hospital resource utilization.

The main focus of this article is postoperative ileus.



The exact pathogenesis of ileus remains unclear. Postoperative ileus may be mediated via activation of inhibitory spinal reflex arcs. Anatomically, 3 distinct reflexes are involved: ultrashort reflexes confined to the bowel wall, short reflexes involving prevertebral ganglia, and long reflexes involving the spinal cord. [4] The long reflexes are the most significant. Spinal anesthesia, abdominal sympathectomy, and nerve-cutting techniques have been demonstrated to either prevent or attenuate the development of ileus. [8, 9]

The surgical stress response leads to systemic generation of endocrine and inflammatory mediators that also promote the development of ileus. Rat models have shown that laparotomy, eventration, and bowel compression lead to increased numbers of macrophages, monocytes, dendritic cells, T cells, natural killer cells, and mast cells, as demonstrated by immunohistochemistry. [10] Macrophages residing in the muscularis externa and mast cells are probably the key players in this inflammatory cascade. [11] Calcitonin gene–related peptide, nitric oxide, vasoactive intestinal peptide, and substance P function as inhibitory neurotransmitters in the bowel nervous system. Nitric oxide and vasoactive intestinal peptide inhibitors and substance P receptor antagonists have been demonstrated to improve gastrointestinal function. [12, 13]

Pohl et al suggest that Irf4-dependent CD103+CD11b+ dendritic cells and the intestinal microbiome regulate monocyte and macrophage activation and intestinal peristalsis in postoperative ileus. [14] They report that CD103+CD11b+ dendritic cells and the intestinal microbiome appear to be a prerequisite for the activation of intestinal monocytes and macrophages and for dysregulating intestinal motility in this setting.

Farro et al indicate that C-C motif chemokine receptor 2 (CCR2) monocyte-derived macrophages are crucial for resolution of inflammation and restoration of gut motility in postoperative ileus. [15]



Most cases of ileus occur after intra-abdominal operations. Risk factors that increase the likelihood of ileus include open surgery, lower gastrointestinal (GI) surgery, retroperitoneal spinal surgery, and opioid use. The incidence increases with the duration of surgery and with higher intra-abdominal pressure during minimally invasive surgery. [16]

Normal resumption of bowel activity after abdominal surgery follows a predictable pattern: the small bowel typically regains function within hours; the stomach regains activity in 1-2 days; and the colon regains activity in 3-5 days. [17]

Serial abdominal radiographs mapping the distribution of radiopaque markers have shown that the colonic gradient for resolution of postoperative ileus is proximal to distal. The return of propulsive activity to the right colon occurs earlier than to the transverse or left colon. [18]

Other causes of adynamic ileus are as follows:

  • Sepsis

  • Drugs (eg, anesthesia, opioids, psychotropics, anticholinergics, antacids, antiemetics, warfarin, amitriptyline, chlorpromazine)

  • Endocrine disorders (eg, diabetes, adrenal insufficiency, hypothyroidism)

  • Metabolic (eg, low potassium, magnesium, or sodium levels; anemia; uremia; hyposmolality)

  • Cardiopulmonary failure (eg, myocardial infarction)

  • Pneumonia

  • Trauma (eg, fractured ribs, fractured spine)

  • Biliary and renal colic

  • Neurosurgical procedures, spinal cord and head injuries

  • Intra-abdominal inflammation and peritonitis

  • Peritoneal carcinomatosis

  • Retroperitoneal and mediastinal pathology (eg, hematomas, infections)



United States data

Postoperative ileus occurs in approximately 50% of patients who undergo major abdominal surgery. [19] Kuruba et al studied the incidence and risk factors for prolonged ileus in patients undergoing elective colon surgery retrospectively. The incidence of prolonged ileus was similar in patients with epidural versus nonepidural versus laparoscopic surgery. The incidence of prolonged ileus was similar in all 3 groups studied. [20]

A pooled, post-hoc, phase III study analyzed placebo groups and partial bowel resection and total abdominal hysterectomy multicenter trials. [21] Postoperative ileus was still observed in 15% of patients in the partial bowel resection group and in 3% of the total abdominal hysterectomy patients, regardless of the standardized accelerated postoperative care pathway used. This study also provides significant differences in gastrointestinal recovery patterns between bowel resection and total abdominal hysterectomy.