Postoperative Ileus

Updated: Nov 01, 2021
Author: Burt Cagir, MD, FACS; Chief Editor: Vinay K Kapoor, MBBS, MS, FRCSEd, FICS, FAMS 



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.



History and Physical Examination


Patients with ileus typically have vague, mild diffuse abdominal pain, distention, fullness, and bloating. They may report nausea, vomiting, and poor appetite. Abdominal cramping is usually not present. Patients may or may not continue to pass flatus and stool.

A relapse of paralytic ileus is not uncommon in psychiatric patients with a history of ileus; risk factors include being older, having a history of abdominal surgery, or having a longer duration of psychiatric disorders.[22]

In renal transplant candidates with a history of peritoneal dialysis treatment, prior to transplantation, carefully evaluate for symptoms of& intermittent bowel obstruction.[23] Encapsulating peritoneal sclerosis is a rare cause of ileus in patients during or following peritoneal dialysis or renal transplantation.[23]

Physical examination

The abdomen may be distended and tympanic, depending on the degree of abdominal and bowel distention, and may be tender. A distinguishing feature is absent or hypoactive bowel sounds, in contrast to the high-pitched sound of obstruction. The silent abdomen of ileus reveals no discernible peristalsis or succussion splash.



Diagnostic Considerations

The common differentials for ileus are pseudo-obstruction, also referred to as Ogilvie syndrome, and mechanical bowel obstruction.


Pseudo-obstruction is defined as acute, marked distention of the large bowel. As with ileus, it occurs in the absence of a definable mechanical pathology. Several texts and articles tend to use ileus synonymously with pseudo-obstruction or refer to "colonic ileus." However, the two conditions are definitely distinct entities. Pseudo-obstruction is clearly limited to the colon alone, whereas ileus involves both the small bowel and colon. The right colon is involved in classic pseudo-obstruction, which typically occurs in elderly bedridden patients with serious extraintestinal illness or in trauma patients. Pharmacologic agents, aerophagia, sepsis, and electrolyte discrepancies may also contribute to this condition.

The condition termed chronic intestinal pseudo-obstruction is also observed in patients with collagen-vascular diseases, visceral myopathy, or neuropathy. This chronic form of pseudo-obstruction involves dysmotility of both the large and small intestine. This dysmotility is due to loss of the migrating motor complex and bacterial overgrowth. This entity manifests as clinical small bowel obstruction.

Physical examination usually reveals marked abdominal distention without pain or tenderness; however, patients may have symptoms mimicking obstruction. Plain abdominal radiography reveals isolated, proximal large bowel dilatation, as shown in the image below, and contrast imaging distinguishes this from mechanical obstruction.

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.

The colonic distention may lead to perforation of the cecum, especially if the cecal diameter exceeds 12 cm. The mortality rate for pseudo-obstruction is 50% if patients progress to ischemic necrosis and perforation.[17]

Initial treatment includes hydration, rectal and nasogastric tube placement, correction of electrolyte imbalances, and discontinuation of medications that hinder bowel motility. Decompression via colonoscopy is quite effective in relieving pseudo-obstruction. Intravenous neostigmine may also be effective, resulting in resolution of pseudo-obstruction within 10-30 minutes.[24] A 2.5-mg dose of neostigmine is slowly infused over 3 minutes under close cardiac monitoring, particularly in patients with known cardiac conditions, to observe for bradycardia. If bradycardia occurs, atropine should be administered. Laparotomy with ostomy creation and bowel resection for peritonitis and ischemia is the last resort.

Mechanical obstruction

Mechanical bowel obstruction can be caused by postoperative adhesions, volvulus, hernias, intussusception, foreign bodies, or neoplasms. Patients present with severe cramping abdominal pain that is paroxysmal in nature. Physical examination reveals borborygmi coincident with the abdominal cramping. In thin patients, peristaltic waves may be visualized. Auscultation may reveal high-pitched, tinkling sounds associated with gurgles and rushes, which is in marked contrast to the hypoactive or absent bowel sounds of ileus. If obstruction is complete, patients report constipation or obstipation. Vomiting may or may not occur if the ileocecal valve is competent and prevents reflux. Peritoneal signs manifest if patients develop a strangulated obstruction or perforation.

Endoscopy and contrast imaging aid in the diagnosis of mechanical bowel obstruction. In mechanical obstruction, imaging reveals enlarged bow-shaped loops of small intestine with steplike air-fluid levels; the colon may have a paucity of gas distal to the lesion on plain radiographs, as demonstrated in the images below.

Mechanical bowel obstruction due to a left colon c Mechanical bowel obstruction due to a left colon carcinoma. Note the paucity of bowel gas throughout the colon.
Contrast study, in the same patient as in the prev Contrast study, in the same patient as in the previous image with mechanical bowel obstruction due to a left colon carcinoma. This image shows the classic "apple-core" lesion of colon carcinoma.

The following table summarizes the differences between ileus, pseudo-obstruction, and mechanical obstruction.

Table. Characteristics of Ileus, Pseudo-obstruction, and Mechanical Obstruction (Open Table in a new window)




Mechanical Obstruction (Simple)


Mild abdominal pain, bloating, nausea, vomiting, obstipation, constipation

Crampy abdominal pain, constipation, obstipation, nausea, vomiting, anorexia

Crampy abdominal pain, constipation, obstipation, nausea, vomiting, anorexia

Physical Examination Findings

Silent abdomen, distention, tympanic

Borborygmi, tympanic, peristaltic waves, hypoactive or hyperactive bowel sounds, distention, localized tenderness

Borborygmi, peristaltic waves, high-pitched bowel sounds, rushes, distention, localized tenderness

Plain Radiographs

Large and small bowel dilatation, diaphragm elevated

Isolated large bowel dilatation, diaphragm elevated

Bow-shaped loops in ladder pattern, paucity of colonic gas distal to lesion, diaphragm mildly elevated, air-fluid levels



Laboratory Studies

Laboratory studies and blood work should focus on evaluations for infectious, electrolytic, and metabolic derangements. Inflammatory markers such as interleukins 1 and 6 (IL-1, IL-6) and tumor necrosis factor alpha (TNF-a) could help identify early the presence of protracted postoperative ileus.[25]

Preoperative low serum albumin[26] , postoperative deep venous thrombosis, and electrolyte levels are associated with postoperative ileus. Age, previous abdominal surgery, and chronic preoperative use of narcotics were independently correlated with postoperative ileus.[27]

Imaging Studies

Computed tomography (CT) scanning

Findings from a systematic review indicate that CT scanning with Gastrografin may have the best specificity and sensitivity for differentiating between postoperative ileus and other conditions, whereas clinical findings and x-ray studies were of limited value in the differential diagnosis.[25]

The German Society of Gastroenterology, Digestive and Metabolic Diseases (DGVS) recommends obtaining CT scanning before considering endoscopic intervention to differentiate between mechanical obstruction and paralytic ileus/intestinal pseudo-obstruction.[28] It is also crucial to identify the presence of tumors and their site; localization guides selection of the decompression procedure.[28]

Multidetector CT (MDCT) scanning has the potential to be an effective and reliable tool in the early identification of chronic gallstone perforation and ileus. In one study, this imaging modality was able to differentiate and locate 88.5% of ectopic biliary stones compared with 50% with abdominal radiography, as well as reveal the presence of cholecystitis, edema, discontinuous walls of the gallbladder and intestine, and bilioenteral fistula.[29] In the same study, MDCT scanning and magnetic resonance imaging (MRI) provided precise visualization of the bilioenteral fistula and the ruptured bile duct.


On plain abdominal radiographs, ileus appears as copious gas dilatation of the small intestine and colon with air fluid levels; however there is no transition point as is seen in mechanical obstruction. With enteroclysis, the contrast medium in patients with paralytic ileus should reach the cecum within 4 hours; if the contrast medium remains stationary for longer than 4 hours, mechanical obstruction is suggested.[30]  The oral contrast is hyperosmolar; it draws water from the bowel wall in to the lumen – this reduces the bowel wall edema and may help in resolution of the ileus.




Medical Care

The management of ileus may vary greatly depending on the nature of the disease and the surgical procedure. Management of ileus starts with correction of underlying medical conditions, electrolyte abnormalities, and acid base abnormalities.

Most cases of postoperative ileus resolve with watchful waiting and supportive treatment. Patients should receive intravenous hydration. For patients with vomiting and distention, use of a nasogastric tube provides symptomatic relief; however, no studies in the literature support the use of nasogastric tubes to facilitate resolution of ileus. Long intestinal tubes have no benefit over nasogastric tubes. For postoperative patients receiving vasopressor support, limited data suggest that these patients can be safely initiated and advanced on enteral nutrition; clinicians must take into account the specific vasopressor agent, its dose and changes in regimen, as well as the patient's clinical condition and characteristics.[31]

For patients with protracted ileus, mechanical obstruction must be excluded with contrast studies. Underlying sepsis and electrolyte abnormalities, particularly hypokalemia, hyponatremia, and hypomagnesemia, may worsen ileus. These contributing conditions are easily diagnosed and corrected.

Discontinue medications that produce ileus (eg, opiates). In one study, the amount of morphine administered directly correlated with the time elapsed before the return of bowel sounds and the passage of flatus and stool.[32]

The use of postoperative narcotics can be diminished by supplementation with nonsteroidal anti-inflammatory drugs (NSAIDs). In addition to permitting lower narcotic doses by providing pain relief, NSAIDS may improve ileus by reducing local inflammation. An international multicenter prospective study is in progress to evaluate gastrointestinal recovery following colorectal surgery as well as to assess the role of NSAIDs in accelerating the return of gastrointestinal function.[1]  Myoelectric activities recorded from electrodes placed on the colon have revealed faster resolution from ileus in patients given ketorolac versus those given morphine[33] ; however, the drawbacks of NSAID use include platelet dysfunction and gastric mucosal ulceration. Consider the use of a cyclooxygenase-2 selective agent (ie, celecoxib), which negates these adverse effects.

No single objective variable accurately predicts the resolution of ileus. The clinician must assess the overall status of the patient and evaluate for adequate oral intake and good bowel function. A patient's report of flatus, bowel sounds, or stool passage may prove misleading; therefore, clinicians must not rely solely on self-reporting. Indeed, findings from a systematic review indicate that the best clinical endpoint of postoperative ileus is postoperative defecation in conjunction with solid food tolerance, whereas other clinical signs such as the presence of bowel sounds and the passage of flatus don't appear to correlate with complete recovery of bowel motility.[25]

Surgical Care

Yang and Morgan suggest that postoperative restoration of bowel function following a Hartmann procedure using a laparoscopic approach is not only safe and effective but also may result in significantly faster recovery time and fewer postprocedure complications compared to the open approach; therefore, it may be a viable alternative to open Hartmann reversal.[34] Their retrospective study of reversal of Hartmann procedure (2001-2012) comprised 43 patients who underwent laparoscopic reversal and 64 patients who underwent the open reversal procedure.

Although the operative time was longer for the laparoscopic group compared to the open procedure group (276.4 mins vs 242.0 mins; P = 0.02), the time to passage of flatus (2.8 vs 4.0 days; P< 0.001) and feces (4.2 vs 5.6 days; P = 0.02) and the hospital stay (6.7 vs 10.8 days; P< 0.001) were shorter and there were fewer postprocedure complications (14% vs 31%; P = 0.04) in the laparoscopic group.[34] Postoperative ileus occurred in 2% of patients in this group compared to 17% in the group who underwent the open reversal procedure (P = 0.02). However 3 of 43 patients (7%) required conversion to laparotomy.[34]

Encapsulating peritoneal sclerosis is a rare cause of ileus in renal transplant patients during or following peritoneal dialysis.[23] In a case report of 3 patients with this unusual complication, 1 patient improved with conservative therapy and the remaining 2 patients eventually underwent surgical intervention after a long trial of medical management. The authors of the report advised that, before renal transplantation, obtain a detailed history to evaluate for the presence of intermittent bowel obstruction (ie, symptoms) from patients who have previously received peritoneal dialysis.[23]


It is generally advisable to delay oral feeding until ileus resolves clinically. However, the presence of ileus does not preclude enteral feeding. Postpyloric feeding into the small bowel can be cautiously performed. Start feeds at one-quarter or one-half strength at a slow rate and gradually advance.

Having patients chew gum has been advocated as a means of promoting recovery from postoperative ileus. Chewing gum may constitute a form of sham feeding that stimulates gastrointestinal motility. Meta-analyses have shown that gum chewing can reduce the time to first flatus and passage of feces, and marginally decrease the length of hospital stay after intestinal surgery.[5, 35, 36, 37]


Conventional wisdom and wide practice foster the notion that ambulation stimulates bowel function and improves postoperative ileus, although this has not been shown in the literature.

In a nonrandomized study evaluating 34 patients, seromuscular bipolar electrodes were placed in segments of the gastrointestinal tract after laparotomy. Ten patients were assigned to ambulate on postoperative day 1, and the other 24 were assigned to ambulate on postoperative day 4. No significant difference between the two groups was displayed in myoelectric recovery in the stomach, jejunum, or colon.[38] Hence, postoperative ambulation remains beneficial in preventing the formation of atelectasis, deep vein thrombosis, and pneumonia but has no role in treating ileus.


Enhanced recovery after surgery (ERAS) protocols are being used more and more frequently to decrease the incidence and reduce the duration of postoperative paralytic ileus. These protocols include shorter duration of fasting (2-3 hours for clear fluids), high carbohydrate fluid, no nasogastric tube (NGT), early mobilization, restricted intravenous fluids, early oral feeding, no opiates, analgesia using paracetomal and nonsteroidal anti-inflammatory drugs (NSAIDs), and epidural catheter for postoperative analgesia.



Medication Summary

Thoracic epidural administration has been shown to be beneficial, both with open and with endoscopic colorectal surgery.[39] Epidural blockade with local anesthetics improves postoperative ileus by blockage of inhibitory reflexes and efferent sympathetics. Studies have shown that combinations of thoracic epidurals containing bupivacaine alone or in combination with opioids improve postoperative ileus.[40, 41] Continuous intravenous administration of lidocaine during and after abdominal surgery may decrease the duration of postoperative ileus.[42]

In a randomized study, systemic infusion of lidocaine is compared with placebo infusions in postoperative patients. Patients in the lidocaine group appear to have earlier return of flatus, bowel function, and discharge to home. Although only 11 patients were used in the each arm, systemic lidocaine lessened the postoperative pain sensation. Therefore, it is recommended that further studies are warranted to evaluate systemic lidocaine infusion in postoperative patients.[43]

Peripherally selective opioid antagonists are an option for the treatment of postoperative ileus.[44] Methylnaltrexone (Relistor) and alvimopan (Entereg) are approved by the Food and Drug Administration. These agents inhibit peripheral mu-opioid receptors, which abolishes the adverse gastrointestinal effects of opioids; however, because these agents do not cross the blood-brain barrier, they do not impair the analgesic effects of opioids.[45]

Methylnaltrexone is indicated for opioid-induced constipation in patients with advanced illness receiving palliative care, when response to laxatives has not been sufficient. In a study of 14 healthy volunteers evaluating the use of morphine plus oral methylnaltrexone in increasing doses, methylnaltrexone significantly reduced morphine-induced delay in oral-cecal transit.[46] Another study reported subcutaneous methylnaltrexone is effective in inducing laxation in patients receiving palliative care who have opioid-induced constipation and in whom conventional laxatives have failed.[47] However, because methylnaltrexone received relatively recent approval by the US Food and Drug Administration (FDA), more rigorous trials are needed.

Another phase III multicenter, double-blind, placebo-controlled study revealed that methylnaltrexone at 12-mg and 24-mg doses did not reduce the duration of postoperative ileus.[48] Although the utility of intravenous methylnaltrexone was not demonstrated, it was well tolerated by postcolectomy patients.[48]

Alvimopan is indicated to help prevent postoperative ileus following bowel resection. It has a longer duration of action than methylnaltrexone. Using data from four phase 3 bowel trials and one phase 4 radical cystemectomy trial, investigators evaluating the economic impact of postoperative administration of alvimopan (accounting for varying definitions of postoperative ileus) found that the addition of this agent to existing treatment strategies for those undergoing abdominal procedures resulted in overall hospital savings.[49]

Taguchi et al examined 78 postoperative patients randomized to receive either placebo or alvimopan.[50] Fifteen patients underwent partial colectomy, 36 were status post simple hysterectomy, and the remaining 27 underwent radical hysterectomy. All of the patients were on patient-controlled analgesia pumps using either meperidine or morphine. Compared with patients on placebo, patients on alvimopan had their first bowel movement 2 days earlier, resumed a solid diet 1.3 days earlier, and returned home 1.4 days earlier. Other completed trials include a meta-analysis comparing alvimopan with placebo[51] and a study that found alvimopan to accelerate gastrointestinal tract recovery after bowel resection, regardless of age, sex, race, or concomitant medication.[52]

Use of prokinetic agents has shown mixed results. Randomized trials have shown some benefit of the colon-stimulating laxative bisacodyl for the treatment of ileus.[53, 54] Erythromycin, a motilin receptor agonist, has been used for postoperative gastric paresis but has not been shown to be beneficial for ileus.[55] Metoclopramide (Reglan), a dopaminergic antagonist, has antiemetic and prokinetic activities, but data have shown that the drug may actually worsen ileus. In a randomized controlled study on 210 patients undergoing major abdominal surgery, Wattchow et al reported that perioperative low dose celecoxib markedly reduced the development of paralytic ileus compared to diclofenac.[56] The effect was independent of narcotic use and was not associated with any increase in postoperative complications.

A review of meta-analyses and randomized controlled trials on drugs used for post-operative ileus was reported by Yeh et al.[57] The investigators identified three meta-analyses (2 on gum-chewing and 1 on alvimopan) and 18 clinical trials. Only gum chewing and alvimopan were effective in preventing ileus but due to safety concerns and costs with alvimopan, gum chewing may be preferred as first-line therapy. Gum chewing has also been used in women recovering from caesarian section with good effect when compared to standard of care in a randomized study conducted.[58]

In summary, ileus remains a significant health problem in North America. Successful therapy involves multimodality treatment such as minimally invasive/less traumatic surgery, opiate-sparing pain management, and fast tract recovery protocols.

Opioid Antagonist, Selective

Class Summary

Selective opioid antagonists are indicated to prevent postoperative ileus.

Alvimopan (Entereg)

Peripherally acting mu-opioid receptor antagonist. Binds mu-opioid receptors in gut, thereby selectively inhibiting negative opioid effects on GI function and motility. Indicated for postoperative ileus following bowel resection with primary anastomosis. Five clinical studies with enrollment >2500 patients demonstrated accelerated recovery time of upper and lower tract GI function with alvimopan compared with placebo. Decrease of hospital days also observed in the alvimopan group compared with placebo.

Only available to hospitals after they complete a registration process designed to maintain the benefits associated with short-term use and prevent long-term, outpatient use (Entereg Access Support and Education [EASE] program).


Questions & Answers


What is postoperative ileus?

What causes postoperative ileus and what is the typical duration?

What are the clinical consequences of postoperative ileus?

How does postoperative ileus affect healthcare costs?

What is the pathogenesis of postoperative ileus?

What is the role of endocrine and inflammatory mediators in the pathophysiology of postoperative ileus?

What is the most common etiology of postoperative ileus?

What causes adynamic postoperative ileus?

What is the prevalence of postoperative ileus?


What are symptoms of postoperative ileus?

Which physical findings are characteristic of postoperative ileus?


What are the most common differentials for postoperative ileus?

How is pseudo-obstruction differentiated from postoperative ileus?

How is pseudo-obstruction treated?

How is mechanical obstruction differentiated from postoperative ileus?

How do the signs and symptoms of pseudo-obstruction, mechanical obstructions and postoperative ileus compare?


What is the role of lab testing in the workup of postoperative ileus?

What is the role of imaging studies in the evaluation of postoperative ileus?


What are the treatment options for postoperative ileus?

What is the role of medication in the treatment of postoperative ileus?

What is the clinical endpoint for postoperative ileus?

What are surgical options for the treatment of postoperative ileus?

What are the benefits of using a laparoscopic approach for surgical treatment of postoperative ileus?

What are the risk factors for encapsulating peritoneal sclerosis in postoperative ileus?

Which dietary restrictions are required during treatment of postoperative ileus?

What is the role of ambulation in the treatment of postoperative ileus?

How is postoperative ileus prevented?


Which medications are used in the treatment and prevention of postoperative ileus?

Which medications in the drug class Opioid Antagonist, Selective are used in the treatment of Postoperative Ileus?