Residency · Residency · Gastroenterology

GI Motility - Gastroparesis and Chronic Intestinal Pseudo-Obstruction

Gastroparesis

Definition

Gastroparesis is a syndrome of objectively delayed gastric emptying in the absence of mechanical obstruction. The distinction between objective documentation of delayed emptying and symptomatic overlap with functional dyspepsia is critically important, as many patients with upper gastrointestinal symptoms attributed to gastroparesis actually have normal gastric emptying and require a different therapeutic approach. Confirmation of the diagnosis requires formal testing by gastric emptying scintigraphy, wireless motility capsule, or gastric emptying breath test.

Etiology

Diabetic gastroparesis accounts for 30 to 50% of cases, with type 1 diabetes more commonly affected than type 2. The pathogenesis in diabetes involves autonomic neuropathy with vagal nerve dysfunction, loss of interstitial cells of Cajal, and impairment of inhibitory nitrergic neurons. Glycemic control directly affects gastric motility, as hyperglycemia exceeding 200 mg/dL independently delays gastric emptying, creating a vicious cycle in which gastroparesis impairs glycemic control and hyperglycemia worsens gastroparesis.

Idiopathic gastroparesis accounts for another 30 to 50% of cases and may follow a viral illness (post-infectious gastroparesis associated with cytomegalovirus, Epstein-Barr virus, herpes simplex virus, or norovirus). It predominantly affects younger women and demonstrates significant symptomatic overlap with functional dyspepsia.

Post-surgical gastroparesis accounts for 5 to 10% of cases and results from vagal nerve injury during fundoplication, bariatric surgery, or esophagectomy, or from pyloric damage. Before establishing a diagnosis of gastroparesis, medication-induced delayed gastric emptying must be rigorously excluded. Opioids are the most common cause of secondary delayed emptying. GLP-1 receptor agonists, including semaglutide and tirzepatide, produce dose-dependent delay in gastric emptying that is integral to their mechanism of action. Anticholinergic agents, calcium channel blockers, and tricyclic antidepressants can also impair gastric motility.

Additional causes include Parkinson disease, amyloidosis, systemic sclerosis, hypothyroidism, chronic mesenteric ischemia, Ehlers-Danlos syndrome and other connective tissue disorders, and myotonic dystrophy.

Pathophysiology

The loss of interstitial cells of Cajal is central to the pathogenesis of gastroparesis across all etiologies. These pacemaker cells generate the slow wave electrical activity that coordinates gastric contractions, and their reduced density in the gastric body disrupts the normal propagation of peristaltic contractions. Vagal neuropathy impairs gastric accommodation (the reflex relaxation of the fundus to receive a meal), antral contraction strength, and pyloric relaxation during the emptying phase. Impairment of inhibitory nitrergic neurons reduces pyloric relaxation, and pyloric dysfunction with elevated pyloric pressures has become an increasingly recognized therapeutic target.

Clinical Presentation

The cardinal symptoms of gastroparesis include nausea (present in 92% of patients), vomiting (68 to 84%), early satiety (60%), postprandial fullness, bloating, and epigastric pain (50 to 90%). Pain is frequently the most bothersome and functionally limiting symptom, though it is often underappreciated in the traditional understanding of the disease. The Gastroparesis Cardinal Symptom Index quantifies symptoms across three domains (nausea/vomiting, post-prandial fullness/early satiety, and bloating) on a 0 to 5 scale and is validated for symptom assessment and treatment monitoring.

In severe cases, patients develop weight loss, malnutrition, and dehydration requiring hospitalization. Bezoar formation, the accumulation of undigested food material in the stomach, occurs particularly in diabetic gastroparesis and can cause complete gastric outlet obstruction.

Diagnosis

Gastric Emptying Scintigraphy (GES) -- Gold Standard

Gastric emptying scintigraphy using the standardized low-fat egg white meal (Tougas protocol) with technetium-99m sulfur colloid labeling is the gold standard diagnostic test. Images are obtained at 0, 1, 2, and 4 hours after meal ingestion. Delayed gastric emptying is defined as greater than 90% retention at 1 hour, greater than 60% retention at 2 hours, or greater than 10% retention at 4 hours, with the 4-hour measurement being the most diagnostically valuable.

Proper test preparation is essential for accurate results. Prokinetic medications must be held for at least 3 days before testing, and opioid medications must also be held for at least 3 days. Blood glucose should be below 275 mg/dL at the time of the study, as hyperglycemia independently delays gastric emptying and produces false-positive results.

Wireless Motility Capsule (SmartPill)

The wireless motility capsule is a swallowed device that measures pH, pressure, and temperature as it traverses the entire gastrointestinal tract. Normal gastric emptying time is less than 5 hours (median 3.5 hours). This technology offers the additional advantage of simultaneously measuring small bowel and colonic transit times, providing a comprehensive pan-GI motility assessment in a single test. It is contraindicated in patients with strictures, mechanical obstruction, or swallowing disorders.

Gastric Emptying Breath Test (GEBT)

The gastric emptying breath test uses a carbon-13-labeled spirulina meal, with carbon-13 carbon dioxide measured in exhaled breath as the labeled substrate is absorbed and metabolized. It is FDA-approved, correlates well with scintigraphy, requires no radiation exposure, and can be performed in an office setting. The test duration is 4 hours.

Differential Diagnosis

The differential diagnosis of gastroparesis symptoms is critically important, as several conditions present with overlapping symptoms but require fundamentally different management. Functional dyspepsia, defined by Rome IV criteria, shares many symptoms with gastroparesis but demonstrates normal gastric emptying. The dominant pathophysiologic mechanisms in functional dyspepsia are visceral hypersensitivity and impaired gastric accommodation rather than delayed transit. Many patients initially labeled with gastroparesis actually have functional dyspepsia.

Rumination syndrome is characterized by effortless regurgitation of recently ingested food within 15 minutes of eating, without the nausea that precedes vomiting in gastroparesis. Diagnosis is made by high-resolution impedance manometry, which demonstrates an abdominal pressure spike preceding each regurgitation event. Treatment consists of diaphragmatic breathing retraining and behavioral therapy.

Cyclic vomiting syndrome presents with stereotypical episodes of severe nausea and vomiting lasting 24 to 72 hours, separated by symptom-free intervals. It is associated with migraine headaches and cannabis use. Treatment involves amitriptyline for prophylaxis and ondansetron or sumatriptan for acute episodes.

Cannabinoid hyperemesis syndrome occurs in the setting of chronic cannabis use and is characterized by recurrent episodes of severe vomiting with compulsive hot bathing, peri-umbilical pain, and relief with hot showers. The condition resolves with sustained cannabis cessation.

<image>A diagnostic algorithm for suspected gastroparesis. Start with "Chronic nausea, vomiting, early satiety, postprandial fullness." First step: "Exclude mechanical obstruction: EGD (rule out pyloric stenosis, ulcers, malignancy, bezoar)." If normal EGD: "Review medications: hold opioids, GLP-1 RAs, anticholinergics >= 3 days. Control blood glucose < 275 mg/dL." Next: "Gastric emptying scintigraphy (gold standard): standardized egg white meal, images at 0, 1, 2, 4 hours." Result: ">10% retention at 4 hours = delayed gastric emptying = gastroparesis confirmed." If normal GES: "Consider: functional dyspepsia (overlap syndrome), rumination syndrome (HRIM), cyclic vomiting syndrome, superior mesenteric artery syndrome. Functional dyspepsia: trial of neuromodulator or accommodative agent." If gastroparesis confirmed: "Classify etiology: diabetic (optimize A1c), idiopathic, post-surgical, medication-induced." Include GCSI symptom score components in a sidebar box. Add a "Severity classification" panel: mild (symptoms maintained with diet modification), moderate (symptoms partially controlled with medications + dietary modification), severe (refractory symptoms, frequent ER visits/hospitalizations, unable to maintain nutrition orally — consider enteral feeding or advanced interventions). Use green for diet/lifestyle, yellow for pharmacotherapy, red for advanced/refractory interventions.</image>

Treatment

Dietary Modification

Dietary modification is the foundation of gastroparesis management across all severity levels. Patients should eat small, frequent meals, typically 4 to 6 per day, to reduce the volume of gastric content at any one time. A low-fat, low-fiber diet is recommended, as fat delays gastric emptying and fiber increases the risk of bezoar formation. In severe cases, pureed or liquid-consistency meals may be necessary, as liquids empty from the stomach primarily by gravity and are less dependent on coordinated antral contractions. Patients should avoid carbonated beverages, limit alcohol consumption, and sit upright during meals and for 1 to 2 hours afterward to facilitate gravity-assisted emptying.

Pharmacotherapy -- Prokinetics

Metoclopramide is the only FDA-approved medication for gastroparesis. It acts as both a dopamine D2 receptor antagonist and a serotonin 5-HT4 receptor agonist, providing prokinetic and antiemetic effects. It is administered at 5 to 10 mg orally, intravenously, or subcutaneously 15 to 30 minutes before meals and at bedtime. A black box warning exists for the risk of tardive dyskinesia, which occurs in 1 to 10% of patients with prolonged use and increases with cumulative dose and treatment duration. Tardive dyskinesia is irreversible in many cases. Use should be limited to 12 weeks or less when possible, at the lowest effective dose, with monitoring for extrapyramidal symptoms. Additional side effects include drowsiness, depression, prolactin elevation, and QT prolongation.

Domperidone is a peripheral dopamine D2 antagonist that does not cross the blood-brain barrier, resulting in a substantially lower risk of extrapyramidal side effects and tardive dyskinesia. It is administered at 10 to 20 mg three to four times daily before meals. Domperidone is not FDA-approved in the United States but is available through the FDA compassionate use and investigational new drug program. QT prolongation is a concern, necessitating baseline electrocardiogram and periodic monitoring.

Erythromycin acts as a motilin receptor agonist and is a potent gastric prokinetic at doses lower than those used for its antibiotic effects (50 to 100 mg orally or intravenously three times daily before meals). Intravenous erythromycin at 3 mg/kg is particularly useful for acute management of severe gastroparesis flares and bezoar formation. A major limitation is rapid tachyphylaxis developing within 2 to 4 weeks, which may be partially mitigated by intermittent use. QT prolongation, drug interactions through CYP3A4 inhibition, and ototoxicity are additional concerns.

Prucalopride is a selective serotonin 5-HT4 receptor agonist at 1 to 2 mg daily that is FDA-approved for chronic constipation and is used off-label for gastroparesis. It may accelerate gastric emptying and has a favorable safety profile, though gastroparesis-specific data remain limited.

Antiemetics

Ondansetron, a 5-HT3 receptor antagonist at 4 to 8 mg orally, intravenously, or as an orally disintegrating tablet every 8 hours as needed, is the first-line antiemetic. It is safe, well-tolerated, and effective. Promethazine, an antihistamine/phenothiazine at 12.5 to 25 mg every 6 hours, provides additional antiemetic efficacy but is sedating and carries extrapyramidal side effect risk. The granisetron transdermal patch at 3.1 mg per 24 hours changed weekly offers convenience and good tolerability. Aprepitant, an NK-1 receptor antagonist at 40 to 125 mg, may benefit refractory nausea in an off-label capacity. Olanzapine, an atypical antipsychotic at 2.5 to 5 mg daily, has antiemetic properties and is used off-label, though weight gain is a concern.

Neuromodulators (for Pain and Nausea)

Tricyclic antidepressants including nortriptyline and amitriptyline at 10 to 75 mg nightly provide visceral analgesia for the pain component of gastroparesis, though their anticholinergic properties may further delay gastric transit. Mirtazapine at 7.5 to 15 mg nightly is an excellent adjunctive therapy, particularly for gastroparesis patients with predominant nausea and weight loss. Its antiemetic effect is mediated through 5-HT3 antagonism, and it provides appetite stimulation and anxiolysis. Cyproheptadine, an antihistamine and antiserotonergic agent at 4 to 8 mg three times daily, stimulates appetite and is particularly useful in pediatric gastroparesis.

Pyloric-Directed Therapies

Gastric peroral endoscopic myotomy (G-POEM, also called POP for peroral pyloromyotomy) is the most promising procedural intervention for gastroparesis. Using a submucosal tunneling technique analogous to esophageal POEM for achalasia, the procedure divides the pyloric muscle fibers endoscopically. Observational studies report symptom improvement in 70 to 85% of patients, with randomized controlled trials ongoing.

Patient selection is critical for optimal outcomes. The best candidates are those with documented pyloric dysfunction on functional lumen imaging probe (EndoFLIP) assessment, defined as a distensibility index below 7 mm squared per mmHg or a pyloric diameter below 9 mm, or those with elevated pyloric pressures exceeding 40 mmHg on antroduodenal manometry. Complications occur in 3 to 7% and include perforation, bleeding, and capnoperitoneum.

Botulinum toxin injection into the pylorus (100 to 200 units injected into 4 quadrants) demonstrated initial promise in open-label studies but was not superior to placebo in the randomized controlled trials by Friedenberg and Arts. It is not recommended as standard therapy but may serve as a predictive test before committing to G-POEM.

Gastric Electrical Stimulation (GES, Enterra)

The Enterra gastric electrical stimulation device is an implanted system that delivers high-frequency, low-energy electrical stimulation to the gastric body. It holds FDA humanitarian device exemption status, which is distinct from full FDA approval. The mechanism of action remains uncertain but appears to involve central antiemetic effects rather than true gastric prokinesis, as the device does not significantly accelerate gastric emptying. Open-label trials have shown symptom improvement, particularly for nausea and vomiting, but sham-controlled randomized trials have been largely negative. The device may be considered for medically refractory gastroparesis with predominant nausea and vomiting in carefully selected patients.

Nutritional Support

Enteral feeding is indicated when patients cannot maintain adequate nutrition through oral intake. Nasojejunal tube feeding is appropriate in the acute setting, while percutaneous endoscopic jejunostomy provides long-term nutritional access by bypassing the dysfunctional stomach. Jejunal feeding is preferred over gastrostomy for nutritional support. Parenteral nutrition is the last resort for patients unable to tolerate any enteral nutrition, with awareness of the significant complications of long-term total parenteral nutrition including catheter-related infections and TPN-associated liver disease. A venting gastrostomy may be placed for gastric decompression in patients with refractory symptoms, distinct from its use for feeding.

<image>A comprehensive treatment pyramid for gastroparesis management. Pyramid with five tiers from base to apex. Base (Tier 1, all patients): "Dietary modification: small frequent meals, low-fat, low-fiber, pureed consistency if severe; glycemic optimization (diabetic); medication review (stop offending drugs)." Tier 2: "Prokinetics + Antiemetics: metoclopramide (short-term, lowest dose; monitor for TD), domperidone (if available, FDA IND), erythromycin (intermittent use); ondansetron, granisetron patch." Tier 3: "Neuromodulators: mirtazapine 7.5-15 mg nightly, TCA (nortriptyline/amitriptyline), cyproheptadine; for pain/nausea dominant symptoms." Tier 4: "Pyloric-directed therapy: G-POEM (endoscopic pyloromyotomy) — best for documented pyloric dysfunction (EndoFLIP DI < 7); Gastric electrical stimulation (Enterra) — for refractory nausea/vomiting." Apex (Tier 5): "Nutritional support: jejunal enteral feeding (PEJ), venting gastrostomy for decompression, TPN (last resort); surgical options (subtotal/total gastrectomy — extreme cases)." Include response rates next to each tier where available. Use green for base/lifestyle, yellow for medical, orange for procedural, red for surgical/nutritional support. Include an EndoFLIP measurement inset showing pyloric distensibility assessment.</image>

Chronic Intestinal Pseudo-Obstruction (CIPO)

Definition

Chronic intestinal pseudo-obstruction is a syndrome of recurrent signs and symptoms of bowel obstruction occurring in the absence of mechanical obstruction. It results from severely impaired intestinal motility leading to chronic or recurrent intestinal dilation, stasis, bacterial overgrowth, and malnutrition. CIPO is rare, carries high morbidity, and represents one of the most challenging conditions in gastrointestinal practice.

Etiology

Neuropathic (most common)

Neuropathic CIPO results from damage to the enteric nervous system, specifically the myenteric (Auerbach's) and submucosal (Meissner's) plexuses. Primary forms include familial visceral neuropathy, which may be inherited in autosomal dominant or autosomal recessive patterns. Secondary neuropathic causes are diverse and include diabetes mellitus, amyloidosis, paraneoplastic syndromes (anti-Hu/ANNA-1 antibodies associated with small cell lung cancer), autoimmune conditions (anti-enteric neuronal antibodies), viral infections (cytomegalovirus, Epstein-Barr virus, JC virus), Chagas disease (destruction of myenteric neurons by Trypanosoma cruzi), and Hirschsprung disease.

Myopathic

Myopathic CIPO results from damage to the smooth muscle layers of the intestinal wall. Primary familial visceral myopathy includes disorders caused by ACTG2 gene mutations, which underlie the megacystis-microcolon-intestinal hypoperistalsis syndrome. Secondary myopathic causes include systemic sclerosis (the leading systemic cause of visceral myopathy), dermatomyositis, amyloidosis, radiation enteritis, and celiac axis compression.

Mesenchymopathic

Mesenchymopathic CIPO results from depletion of interstitial cells of Cajal, the intestinal pacemaker cells. This form may occur in isolation or in combination with neuropathic or myopathic changes, reflecting the interrelated nature of the components of the intestinal neuromuscular apparatus.

Clinical Presentation

Abdominal distension is the most common presenting symptom, accompanied by nausea, vomiting, abdominal pain, constipation (or paradoxically diarrhea from small intestinal bacterial overgrowth), weight loss, and progressive malnutrition. The clinical course may be episodic with acute exacerbations or continuously symptomatic. Acute episodes may present as apparent bowel obstruction, and it is essential to distinguish acute pseudo-obstruction from true mechanical obstruction. It is important to note that Ogilvie syndrome (acute colonic pseudo-obstruction) is a distinct entity from CIPO.

A particularly important clinical pitfall is the frequent misdiagnosis of CIPO as mechanical obstruction, leading to unnecessary exploratory surgeries that worsen the condition through adhesion formation and further disruption of intestinal motility. Any segment of the gastrointestinal tract may be involved, including the esophagus, stomach, small bowel (most commonly affected), and colon, or the entire tract may be affected. Associated urinary tract involvement with megacystis occurs in some familial forms.

Diagnosis

Imaging

Abdominal radiography and CT demonstrate dilated loops of small bowel and/or colon with air-fluid levels without an identifiable transition point or mechanical obstruction. CT enterography is essential to definitively exclude mechanical obstruction before establishing the diagnosis of CIPO. Upper gastrointestinal series with small bowel follow-through may demonstrate dilated loops, delayed transit, and small bowel diverticulosis.

Motility Testing

Antroduodenal manometry is the gold standard for diagnosing CIPO and provides critical information about the type of dysmotility. Neuropathic CIPO is characterized by disorganized contractions of normal amplitude with absence of the phase III migrating motor complex. Myopathic CIPO demonstrates low-amplitude contractions with preserved contractile patterns. This distinction has implications for treatment approach and prognosis.

The wireless motility capsule (SmartPill) measures transit times throughout the gastrointestinal tract and can identify pan-GI dysmotility in a single study. Colonic manometry is indicated when colonic involvement is suspected, to assess for colonic neuropathy or myopathy.

Full-Thickness Biopsy

Laparoscopic full-thickness small bowel biopsy provides the definitive histopathologic diagnosis. The specimen is evaluated for myenteric plexus integrity (neuronal degeneration, inflammatory infiltrate), smooth muscle layer architecture (fibrosis, vacuolar degeneration), and ICC density. This invasive procedure is not routinely performed and is reserved for cases of diagnostic uncertainty or for research purposes.

Paraneoplastic Evaluation

Anti-Hu (ANNA-1) antibodies should be tested in all patients with unexplained CIPO, as paraneoplastic intestinal pseudo-obstruction may be the presenting manifestation of small cell lung cancer. CT of the chest, abdomen, and pelvis, and PET-CT when clinical suspicion is high, should be obtained. Treatment of the underlying malignancy is paramount, and immunotherapy with intravenous immunoglobulin or corticosteroids may improve intestinal motility.

Treatment

Nutritional Support (Central to Management)

Nutritional support is the cornerstone of CIPO management. Enteral nutrition is preferred whenever tolerable, typically via jejunal feeding. Home total parenteral nutrition is frequently necessary, required in 40 to 80% of CIPO patients for long-term nutritional support. Patients on TPN require monitoring for TPN-associated liver disease and catheter-related bloodstream infections, which are the most common serious complications. Unnecessary periods of nothing-by-mouth should be minimized, and oral intake should be encouraged in small amounts whenever tolerated.

Prokinetics

Prokinetic agents have limited efficacy in CIPO compared with their performance in gastroparesis. Erythromycin, metoclopramide, and prucalopride may be trialed, though response rates are lower than in gastroparesis. Pyridostigmine, an acetylcholinesterase inhibitor at 60 mg three times daily, may improve motility in neuropathic CIPO, though cramping and diarrhea can limit tolerability. Octreotide at 50 to 100 micrograms subcutaneously two to three times daily, or at bedtime, stimulates phase III migrating motor complexes in neuropathic CIPO and reduces small intestinal bacterial overgrowth by promoting small bowel clearance.

SIBO Management

Small intestinal bacterial overgrowth is extremely common in CIPO due to intestinal stasis and represents a major contributor to symptoms including bloating, diarrhea, and malabsorption. Management requires cyclical antibiotics using rotating regimens of rifaximin, ciprofloxacin, metronidazole, and doxycycline. Prokinetic agents, particularly octreotide and erythromycin, provide complementary benefit by improving small bowel clearance.

Decompression

Nasogastric or nasojejunal decompression provides relief during acute episodes. Venting enterostomy (gastrostomy or jejunostomy) addresses chronic decompressive needs. Surgical intervention should be avoided whenever possible, as adhesions from prior surgeries frequently worsen CIPO.

Surgical

The surgical role in CIPO is limited, and unnecessary explorations for apparent mechanical obstruction must be avoided. Ileostomy or colostomy may be indicated when colonic dilation is the dominant and refractory feature. Small bowel transplantation is considered for TPN-dependent patients who develop liver failure or loss of intravenous access. Survival at 5 years following small bowel transplantation is 50 to 60%, and the procedure is pursued only when TPN complications become life-threatening. Multi-visceral transplantation may be necessary for patients with pan-GI dysmotility accompanied by liver failure.

Acute Colonic Pseudo-Obstruction (Ogilvie Syndrome)

Key Features

Acute colonic pseudo-obstruction, also known as Ogilvie syndrome, is distinct from CIPO and presents as acute, massive colonic dilation without mechanical obstruction. It occurs typically in hospitalized, critically ill patients and is associated with recent surgery, opioid use, and electrolyte imbalances. A cecal diameter exceeding 12 cm is associated with a perforation risk of 4 to 13%, making timely recognition and treatment essential.

Management

Conservative management is appropriate for the initial 24 to 48 hours and includes correction of electrolyte abnormalities (potassium, magnesium, calcium), discontinuation of offending medications (opioids, anticholinergics), ambulation when feasible, nasogastric decompression, and rectal tube placement.

Neostigmine at 2 mg intravenously administered over 3 to 5 minutes is the pharmacologic treatment of choice and has a response rate of 80 to 90%. Administration requires continuous cardiac monitoring because of the risk of bradycardia, and atropine must be available at the bedside. The dose may be repeated once if the initial response is inadequate. Neostigmine is contraindicated in the presence of mechanical obstruction, recent myocardial infarction, or active bronchospasm.

Colonoscopic decompression is indicated when neostigmine fails or is contraindicated and when the cecal diameter exceeds 12 cm with more than 48 hours of persistent dilation. A decompression tube may be placed during the procedure, though recurrence occurs in approximately 30% of cases. Surgical intervention, consisting of cecostomy or right hemicolectomy, is reserved for perforation, ischemia, or failure of all other measures.

Key Clinical Pearls

• Medication-induced delayed emptying (opioids, GLP-1 receptor agonists) must always be excluded before diagnosing gastroparesis. Offending medications should be held for at least 3 days before gastric emptying scintigraphy.
• Gastric emptying scintigraphy: 4-hour retention exceeding 10% is the most diagnostic criterion. The standardized meal protocol is essential for reliable results.
• Metoclopramide is the only FDA-approved prokinetic for gastroparesis but carries tardive dyskinesia risk. The lowest dose for the shortest duration should be used.
• G-POEM (endoscopic pyloromyotomy) is the most promising procedural intervention for gastroparesis, especially when pyloric dysfunction is documented on EndoFLIP.
• Mirtazapine at 7.5 to 15 mg nightly is an excellent adjunctive therapy for gastroparesis with predominant nausea and weight loss.
• CIPO is frequently misdiagnosed as mechanical obstruction, leading to unnecessary and harmful surgeries. CT enterography should definitively exclude obstruction before diagnosis.
• Antroduodenal manometry distinguishes neuropathic (disorganized contractions) from myopathic (low-amplitude contractions) CIPO, guiding the management approach.
• Neostigmine is highly effective (80 to 90% response) for acute colonic pseudo-obstruction (Ogilvie syndrome). It must be administered with cardiac monitoring and atropine at the bedside.

References

1. Camilleri M, et al. ACG Clinical Guideline: Gastroparesis. Am J Gastroenterol. 2022;117(8):1197-1220.
2. Mearin F, et al. Bowel Disorders. Gastroenterology. 2016;150(6):1393-1407. (Rome IV)
3. Khashab MA, et al. Gastric peroral endoscopic myotomy for refractory gastroparesis: results from the first multicenter study on endoscopic pyloromyotomy (G-POEM). Gastrointest Endosc. 2017;85(1):123-128.
4. Ponec RJ, et al. Neostigmine for the treatment of acute colonic pseudo-obstruction. N Engl J Med. 1999;341(3):137-141.
5. Di Lorenzo C, et al. Chronic intestinal pseudo-obstruction: clinical features, diagnosis, and therapy. Curr Gastroenterol Rep. 2020;22:11.

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