Ileus
Published on September 14, 2026
Risk Factors
Recent abdominal or pelvic surgery, opioid use, electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia), prolonged immobilization, critical illness, sepsis
Etiology
Functional inhibition of coordinated intestinal peristalsis without a mechanical cause; driven by autonomic dysregulation, local inflammation, or metabolic derangement
Presentation
Diffuse abdominal distension, nausea, vomiting, inability to pass flatus or stool; onset typically 2 to 5 days after surgery or inciting event
Classic Exam
Distended but non-tender abdomen, absent or markedly hypoactive bowel sounds on auscultation, tympany to percussion; no peritoneal signs
Diagnostics
Abdominal X-ray showing diffuse gaseous dilation of both small and large bowel with no transition point; electrolyte panel revealing hypokalemia or other derangements
Management
NPO status, nasogastric tube decompression, aggressive IV fluid resuscitation, electrolyte repletion, opioid minimization, early ambulation
01Pathophysiology
Normal intestinal motility depends on a complex interplay between the enteric nervous system (the intrinsic neural plexuses of Auerbach and Meissner), the autonomic nervous system (sympathetic inhibition vs. parasympathetic stimulation), and local hormonal and inflammatory mediators. Ileus occurs when this coordinated system is disrupted, resulting in a functional paralysis of the gut wall without any physical blockage.
The most heavily tested cause is postoperative ileus. Surgical manipulation of the bowel triggers a local inflammatory cascade. Handling of intestinal loops activates resident macrophages within the muscularis externa, releasing cytokines (IL-6, TNF-alpha) and prostaglandins that directly suppress smooth muscle contractility. Simultaneously, the surgical stress response drives a sympathetic surge that inhibits parasympathetic tone throughout the gut. The combination of local inflammation and systemic sympathetic overdrive produces a diffuse, non-propulsive state across the entire intestinal tract.
Electrolyte imbalances are the second most common tested trigger. Hypokalemia is the highest-yield association: potassium is essential for smooth muscle depolarization and contraction. When serum drops below 3.0 mEq/L, the resting membrane potential of smooth muscle cells becomes hyperpolarized, making it harder for the cell to reach the threshold for contraction. The same principle applies to hypomagnesemia (magnesium is a cofactor for channels and -ATPase) and hypocalcemia ( is the final common pathway for smooth muscle contraction).
Opioids act on mu-receptors in the myenteric plexus, directly inhibiting acetylcholine release from excitatory motor neurons. This decreases propulsive contractions and increases non-propulsive segmental tone, effectively bringing transit to a halt. This explains why the exam frequently places the patient on a morphine PCA pump and then presents worsening distension on postoperative day 3.
The result of all these mechanisms is the same: intestinal contents (gas, fluid, swallowed air) accumulate within a hypotonic, dilated bowel. Because the process is diffuse, both small and large bowel dilate uniformly. This is the critical imaging distinction from mechanical obstruction, where dilation occurs proximal to a single point and decompressed bowel is seen distally.
02Classification and Clinical Manifestation
Ileus is not formally staged, but it is classified by etiology because the cause dictates management. The table below organizes the categories most frequently tested.
Postoperative
COMMON CAUSES
Abdominal or pelvic surgery (open > laparoscopic), prolonged operative time, extensive bowel manipulation
DISTINGUISHING CLINICAL FEATURES
Onset typically postoperative day 2 to 5; expected to resolve within 3 to 5 days; failure to resolve by day 5 to 7 is considered prolonged
Metabolic / Electrolyte
COMMON CAUSES
Hypokalemia, hypomagnesemia, hypocalcemia, hyponatremia, uremia, diabetic ketoacidosis
DISTINGUISHING CLINICAL FEATURES
May present outside the surgical setting; always check a basic metabolic panel; correction of the electrolyte defect resolves the ileus
Drug-Induced
COMMON CAUSES
Opioids (most common), anticholinergics, calcium channel blockers, clonidine, phenothiazines
DISTINGUISHING CLINICAL FEATURES
Temporal correlation with drug initiation or dose escalation; reversal agents may be indicated
Inflammatory / Infectious
COMMON CAUSES
Peritonitis (any cause), intra-abdominal abscess, pancreatitis, appendicitis, sepsis
DISTINGUISHING CLINICAL FEATURES
Ileus is secondary; treating the primary process is the priority
Neurogenic
COMMON CAUSES
Spinal cord injury, retroperitoneal hemorrhage or surgery, vertebral fracture
DISTINGUISHING CLINICAL FEATURES
Bowel dysfunction accompanies neurological deficits; retroperitoneal pathology is a classic exam scenario
Critical Illness
COMMON CAUSES
ICU patient, mechanical ventilation, vasopressor use, multiorgan dysfunction
DISTINGUISHING CLINICAL FEATURES
Often multifactorial; these patients are sedated, immobile, and receiving opioids simultaneously
CATEGORY | COMMON CAUSES | DISTINGUISHING CLINICAL FEATURES |
|---|---|---|
Postoperative | Abdominal or pelvic surgery (open > laparoscopic), prolonged operative time, extensive bowel manipulation | Onset typically postoperative day 2 to 5; expected to resolve within 3 to 5 days; failure to resolve by day 5 to 7 is considered prolonged |
Metabolic / Electrolyte | Hypokalemia, hypomagnesemia, hypocalcemia, hyponatremia, uremia, diabetic ketoacidosis | May present outside the surgical setting; always check a basic metabolic panel; correction of the electrolyte defect resolves the ileus |
Drug-Induced | Opioids (most common), anticholinergics, calcium channel blockers, clonidine, phenothiazines | Temporal correlation with drug initiation or dose escalation; reversal agents may be indicated |
Inflammatory / Infectious | Peritonitis (any cause), intra-abdominal abscess, pancreatitis, appendicitis, sepsis | Ileus is secondary; treating the primary process is the priority |
Neurogenic | Spinal cord injury, retroperitoneal hemorrhage or surgery, vertebral fracture | Bowel dysfunction accompanies neurological deficits; retroperitoneal pathology is a classic exam scenario |
Critical Illness | ICU patient, mechanical ventilation, vasopressor use, multiorgan dysfunction | Often multifactorial; these patients are sedated, immobile, and receiving opioids simultaneously |
Clinical manifestation across all categories follows a predictable pattern: progressive abdominal distension is the earliest and most consistent sign. Patients then develop nausea and vomiting (initially gastric contents, later bilious if the small bowel is significantly dilated). Absent bowel sounds on auscultation are the hallmark physical exam finding; this contrasts with the high-pitched, tinkling bowel sounds of mechanical obstruction. Patients report inability to pass flatus or stool (obstipation). Importantly, the abdomen is usually non-tender and soft unless an underlying inflammatory process is present. Pain, when present, is mild and diffuse rather than colicky.
03Diagnostic Workup
Abdominal X-ray (supine and upright)
ROLE
Best initial test
KEY FINDINGS
Diffuse dilation of both small and large bowel; scattered air-fluid levels; no transition point; no free air
Basic metabolic panel
ROLE
Concurrent with initial imaging
KEY FINDINGS
Hypokalemia ( mEq/L), hypomagnesemia, hypocalcemia; elevated BUN/creatinine if dehydrated
CT abdomen and pelvis with IV contrast
ROLE
Most accurate test (used when diagnosis is uncertain or mechanical obstruction cannot be excluded)
KEY FINDINGS
Diffuse bowel dilation without a discrete point of obstruction; no bowel wall thickening or ischemia; may reveal an underlying cause (abscess, retroperitoneal hematoma)
Complete blood count
ROLE
Supportive
KEY FINDINGS
Leukocytosis suggests an infectious or inflammatory trigger
Serum lactate
ROLE
If ischemia is suspected
KEY FINDINGS
Elevated lactate raises concern for mesenteric ischemia, not simple ileus
TEST | ROLE | KEY FINDINGS |
|---|---|---|
Abdominal X-ray (supine and upright) | Best initial test | Diffuse dilation of both small and large bowel; scattered air-fluid levels; no transition point; no free air |
Basic metabolic panel | Concurrent with initial imaging | Hypokalemia ( mEq/L), hypomagnesemia, hypocalcemia; elevated BUN/creatinine if dehydrated |
CT abdomen and pelvis with IV contrast | Most accurate test (used when diagnosis is uncertain or mechanical obstruction cannot be excluded) | Diffuse bowel dilation without a discrete point of obstruction; no bowel wall thickening or ischemia; may reveal an underlying cause (abscess, retroperitoneal hematoma) |
Complete blood count | Supportive | Leukocytosis suggests an infectious or inflammatory trigger |
Serum lactate | If ischemia is suspected | Elevated lactate raises concern for mesenteric ischemia, not simple ileus |
The diagnostic approach begins with a plain abdominal X-ray, which is the best initial test. The hallmark finding is gaseous distension involving both the small intestine and the colon, distributed diffusely throughout the abdomen. You will see air-fluid levels on the upright film, but unlike mechanical obstruction, these are scattered and do not form a step-ladder pattern confined to one region. The critical negative finding is the absence of a transition point: there is no abrupt cutoff between dilated and decompressed bowel.
If the clinical picture is straightforward (a postoperative patient on opioids with classic findings on X-ray), no further imaging is necessary. However, when the presentation is ambiguous or when you cannot confidently exclude a mechanical obstruction, the next step is a CT abdomen and pelvis with IV contrast. CT is the most accurate test because it can identify a transition point (confirming mechanical obstruction), detect closed-loop obstruction or strangulation, and reveal underlying causes of ileus such as an abscess, pancreatitis, or retroperitoneal pathology.
Simultaneously, you must order a complete metabolic panel. This is not optional. Correctable electrolyte abnormalities (particularly , , and ) are both a cause and a perpetuating factor of ileus. Finding and correcting these is considered a core management step and frequently appears as the "next best step" answer choice.
One important distinction for the exam: if the vignette describes a patient with only colonic dilation (cecum markedly dilated, small bowel normal or minimally dilated), consider Ogilvie syndrome (acute colonic pseudo-obstruction) rather than generalized ileus. This distinction matters because the management pathways diverge.
04Management and Treatment
NPO status
DETAILS
Strict nil per os until bowel function returns
NOTES
Resume oral intake gradually once flatus or bowel movements return
Nasogastric (NG) tube decompression
DETAILS
Low intermittent suction
NOTES
Relieves gastric distension and reduces vomiting risk; not always necessary in mild cases
IV fluid resuscitation
DETAILS
Normal saline or lactated Ringer's; volume based on clinical assessment of dehydration
NOTES
Third-spacing from distended bowel can cause significant intravascular volume depletion
Electrolyte repletion
DETAILS
Potassium: target mEq/L (IV KCl 10 to 20 mEq/hr via central line or 40 mEq/L via peripheral line); Magnesium: 1 to 2 g IV MgSO4 over 1 hour; Calcium: IV calcium gluconate 1 to 2 g for symptomatic hypocalcemia
NOTES
Correct magnesium first if both and are low, because hypomagnesemia causes renal potassium wasting
Opioid minimization
DETAILS
Transition to non-opioid analgesia (ketorolac 15 to 30 mg IV q6h, acetaminophen 1 g IV q6h)
NOTES
The single most impactful modifiable risk factor for postoperative ileus
Early ambulation
DETAILS
Encourage walking at least 3 times daily starting on postoperative day 1
NOTES
Stimulates parasympathetic tone and promotes peristalsis
Alvimopan
DETAILS
12 mg PO 30 minutes to 5 hours preoperatively, then 12 mg PO BID postoperatively for up to 7 days (max 15 doses)
NOTES
Peripheral mu-opioid receptor antagonist; FDA-approved for accelerating GI recovery after bowel resection with primary anastomosis; does not cross the blood-brain barrier, so it does not reverse systemic analgesia
Methylnaltrexone
DETAILS
8 to 12 mg SC every other day as needed
NOTES
Peripheral mu-opioid receptor antagonist for opioid-induced constipation/ileus in patients who cannot take oral medications; contraindicated in known or suspected mechanical bowel obstruction
Neostigmine
DETAILS
2 mg IV over 3 to 5 minutes with continuous cardiac monitoring
NOTES
Reserved for Ogilvie syndrome (acute colonic pseudo-obstruction) with cecal diameter 10 to 12 cm; not standard treatment for generalized ileus; requires atropine at bedside for bradycardia
INTERVENTION | DETAILS | NOTES |
|---|---|---|
NPO status | Strict nil per os until bowel function returns | Resume oral intake gradually once flatus or bowel movements return |
Nasogastric (NG) tube decompression | Low intermittent suction | Relieves gastric distension and reduces vomiting risk; not always necessary in mild cases |
IV fluid resuscitation | Normal saline or lactated Ringer's; volume based on clinical assessment of dehydration | Third-spacing from distended bowel can cause significant intravascular volume depletion |
Electrolyte repletion | Potassium: target mEq/L (IV KCl 10 to 20 mEq/hr via central line or 40 mEq/L via peripheral line); Magnesium: 1 to 2 g IV MgSO4 over 1 hour; Calcium: IV calcium gluconate 1 to 2 g for symptomatic hypocalcemia | Correct magnesium first if both and are low, because hypomagnesemia causes renal potassium wasting |
Opioid minimization | Transition to non-opioid analgesia (ketorolac 15 to 30 mg IV q6h, acetaminophen 1 g IV q6h) | The single most impactful modifiable risk factor for postoperative ileus |
Early ambulation | Encourage walking at least 3 times daily starting on postoperative day 1 | Stimulates parasympathetic tone and promotes peristalsis |
Alvimopan | 12 mg PO 30 minutes to 5 hours preoperatively, then 12 mg PO BID postoperatively for up to 7 days (max 15 doses) | Peripheral mu-opioid receptor antagonist; FDA-approved for accelerating GI recovery after bowel resection with primary anastomosis; does not cross the blood-brain barrier, so it does not reverse systemic analgesia |
Methylnaltrexone | 8 to 12 mg SC every other day as needed | Peripheral mu-opioid receptor antagonist for opioid-induced constipation/ileus in patients who cannot take oral medications; contraindicated in known or suspected mechanical bowel obstruction |
Neostigmine | 2 mg IV over 3 to 5 minutes with continuous cardiac monitoring | Reserved for Ogilvie syndrome (acute colonic pseudo-obstruction) with cecal diameter 10 to 12 cm; not standard treatment for generalized ileus; requires atropine at bedside for bradycardia |
Acute management follows a supportive algorithm. The initial steps are simultaneous: place the patient NPO, insert an NG tube if there is significant vomiting or distension, begin IV fluids, and draw a metabolic panel. Electrolyte repletion is the first targeted therapy and should be aggressive. If the patient is on opioids, transitioning to multimodal non-opioid analgesia (IV ketorolac, IV or PO acetaminophen, regional nerve blocks) is the single highest-yield intervention and the most commonly tested "next best step."
Early ambulation is consistently supported by evidence and is a favorite answer choice on exams. Mobilizing the patient out of bed promotes vagal tone and helps restore peristalsis.
For postoperative ileus prevention, alvimopan is the only FDA-approved pharmacologic agent. It selectively blocks mu-opioid receptors in the GI tract without reversing central analgesic effects. Its use is restricted to the inpatient setting (a maximum of 15 doses over 7 days) due to a historical concern for cardiovascular events with long-term use. It is most commonly tested in the context of a patient undergoing elective bowel resection.
When ileus fails to resolve after 5 to 7 days of conservative management, you must reassess the diagnosis. Order a CT scan to rule out mechanical obstruction, abscess, or anastomotic leak. Prolonged ileus is not a benign entity: it increases the risk of aspiration, bacterial translocation, and prolonged hospitalization.
A key contraindication to remember: do not use promotility agents like metoclopramide or erythromycin as a routine treatment for ileus. Their efficacy is not established in this context, and erythromycin's prokinetic effect is primarily on the upper GI tract. Neostigmine is reserved strictly for Ogilvie syndrome and must be administered with cardiac monitoring due to the risk of symptomatic bradycardia.
05Differential Diagnosis and Distractors
Small bowel obstruction (SBO)
WHY IT IS SIMILAR
Distension, vomiting, constipation, air-fluid levels on X-ray
KEY DISCRIMINATOR
SBO has a transition point on imaging (dilated proximal bowel, decompressed distal bowel); bowel sounds are high-pitched and hyperactive early; pain is colicky and episodic, not diffuse and constant; prior surgical history with adhesions is the classic cause
Large bowel obstruction (LBO)
WHY IT IS SIMILAR
Distension, obstipation, X-ray showing dilated colon
KEY DISCRIMINATOR
LBO shows dilation proximal to the obstruction only (e.g., sigmoid mass); rectal exam may reveal a mass; a contrast enema or CT demonstrates the point of obstruction; ileus dilates both small and large bowel uniformly
Ogilvie syndrome (acute colonic pseudo-obstruction)
WHY IT IS SIMILAR
Functional, non-mechanical colonic dilation; often in hospitalized or postoperative patients
KEY DISCRIMINATOR
Ogilvie syndrome involves only the colon (cecum prominently dilated, often 10 to 12 cm); small bowel is normal; treated with neostigmine if cecal diameter is critical; generalized ileus involves both small and large bowel
Toxic megacolon
WHY IT IS SIMILAR
Colonic dilation, absent bowel sounds, systemic toxicity
KEY DISCRIMINATOR
Occurs in the setting of inflammatory bowel disease (especially ulcerative colitis) or Clostridioides difficile infection; patient is febrile, tachycardic, and acutely ill with bloody diarrhea; the colon wall is edematous and at risk of perforation
Mesenteric ischemia
WHY IT IS SIMILAR
Abdominal distension, ileus on imaging, elderly patient
KEY DISCRIMINATOR
Classically presents with pain out of proportion to exam early on; elevated serum lactate; CT angiography shows vascular occlusion; ileus does not produce significant pain or lactate elevation
Gastroparesis
WHY IT IS SIMILAR
Nausea, vomiting, bloating, postprandial distension
KEY DISCRIMINATOR
Isolated to the stomach; small bowel and colon are normal; associated with longstanding diabetes; diagnosed by a gastric emptying study, not abdominal X-ray
DIFFERENTIAL | WHY IT IS SIMILAR | KEY DISCRIMINATOR |
|---|---|---|
Small bowel obstruction (SBO) | Distension, vomiting, constipation, air-fluid levels on X-ray | SBO has a transition point on imaging (dilated proximal bowel, decompressed distal bowel); bowel sounds are high-pitched and hyperactive early; pain is colicky and episodic, not diffuse and constant; prior surgical history with adhesions is the classic cause |
Large bowel obstruction (LBO) | Distension, obstipation, X-ray showing dilated colon | LBO shows dilation proximal to the obstruction only (e.g., sigmoid mass); rectal exam may reveal a mass; a contrast enema or CT demonstrates the point of obstruction; ileus dilates both small and large bowel uniformly |
Ogilvie syndrome (acute colonic pseudo-obstruction) | Functional, non-mechanical colonic dilation; often in hospitalized or postoperative patients | Ogilvie syndrome involves only the colon (cecum prominently dilated, often 10 to 12 cm); small bowel is normal; treated with neostigmine if cecal diameter is critical; generalized ileus involves both small and large bowel |
Toxic megacolon | Colonic dilation, absent bowel sounds, systemic toxicity | Occurs in the setting of inflammatory bowel disease (especially ulcerative colitis) or Clostridioides difficile infection; patient is febrile, tachycardic, and acutely ill with bloody diarrhea; the colon wall is edematous and at risk of perforation |
Mesenteric ischemia | Abdominal distension, ileus on imaging, elderly patient | Classically presents with pain out of proportion to exam early on; elevated serum lactate; CT angiography shows vascular occlusion; ileus does not produce significant pain or lactate elevation |
Gastroparesis | Nausea, vomiting, bloating, postprandial distension | Isolated to the stomach; small bowel and colon are normal; associated with longstanding diabetes; diagnosed by a gastric emptying study, not abdominal X-ray |
06Traps and High-Yield Pearls
The most common way students lose points on ileus questions is by confusing it with mechanical small bowel obstruction. Both present with distension, vomiting, and air-fluid levels on X-ray. The trap is that students see "dilated bowel" and immediately jump to obstruction without checking whether the dilation involves both the small and large bowel (ileus) or is limited to the small bowel with a visible transition point (SBO). The vignette will always contain a distinguishing clue: in ileus, bowel sounds are absent and the abdomen is diffusely tympanic without tenderness; in SBO, bowel sounds are initially hyperactive and pain is colicky.
A second common trap involves the "next best step" question in a postoperative patient with ileus who is receiving IV morphine. Students often choose NG tube placement or a CT scan. The tested answer is to discontinue or minimize opioids and switch to non-opioid analgesia. This is the most impactful intervention and should be selected before additional imaging or invasive procedures.
Another high-yield pearl: do not confuse ileus with Ogilvie syndrome. If the vignette describes an elderly, hospitalized patient with isolated colonic dilation (cecum 12 cm) and no small bowel involvement, the answer is Ogilvie syndrome and the treatment is IV neostigmine, not conservative management alone. Students who lump these two together will select the wrong treatment.
Finally, remember that ileus is almost never the final diagnosis in a patient with peritoneal signs (rebound, guarding, rigidity). If the vignette includes these findings, the patient has a surgical abdomen (perforation, strangulated obstruction, mesenteric ischemia) and the answer is emergent surgical consultation, not conservative management for ileus. The core competency being tested is the ability to distinguish functional bowel hypomotility from conditions requiring urgent intervention.