11 Nov 2025
Joyce Awadalla MVB, MRCVS Carlos Pizarro Del Valle MRCVS discuss how to deal with motility, reduce morbidity and enhance recovery.
Image: nimon_t / Adobe Stock
Postoperative ileus (POI) refers to an abnormal pattern of delayed gastrointestinal motility following abdominal surgery1.
POI can significantly impact patient morbidity, causing clinical signs such as nausea, vomiting, bloating, anorexia and abdominal discomfort. POI can also contribute to additional complications in the critical patient, including reflux, aspiration pneumonia, oesophagitis, delay of nutritional delivery, bacterial overgrowth and abdominal distention/bloating leading to an increased intra-abdominal pressure2,3.
Successful management of POI can not only reduce postoperative morbidity and hospital stays, but also improve patient comfort and enhance recovery. Due to its multifactorial and complex nature, a thorough understanding of the underlying mechanisms and risk factors is crucial to establish effective preventive and management strategies.
The development of POI is influenced by a combination of factors, including inflammation, neurogenic factors, pharmacological effects, and electrolyte imbalances1,2.
Intestinal manipulation during abdominal surgery stimulates resident muscularis macrophages, triggering the release of cytokines and the recruitment of inflammatory cells4. This inflammatory response is believed to impair gastrointestinal motility by causing increased capillary permeability and intestinal wall oedema4,5.
The autonomic nervous system has an essential role in the control of gastrointestinal motility; parasympathetic activity promotes motility by releasing acetylcholine in the myenteric plexus, while sympathetic activity suppresses acetylcholine release, thereby inhibiting gastrointestinal motility6.
Gastrointestinal inflammation secondary to surgical manipulation stimulates afferent nerves, activating splanchnic and vagal pathways, enhancing sympathetic activity and, ultimately, reducing gut motility2,4,5.
Additionally, pharmacological effects of drugs such as opioids, commonly administered perioperatively for pain management, further contribute to POI through activation of µ-opioid receptors and inhibition of acetylcholine release from myenteric neurons4.
Electrolyte disturbances can have a significant impact on the development of POI. Potassium is crucial for maintaining the resting membrane potential and muscle contractility, with hypokalaemia impairing smooth muscle excitability and reducing gastrointestinal motility7.
Calcium plays a vital role in neuromuscular transmission and smooth muscle contraction, and its deficiency can hinder gut peristalsis7. Magnesium has an important role in regulation of peristalsis and parathyroid hormone function; its deficiency can cause hypocalcaemia and impair gastrointestinal motility8. Hypomagnesaemia has been associated with hypomotility, with its role well documented in horses and sheep9,10. In horses, low postoperative magnesium levels are associated with a higher incidence of hypomotility, making magnesium supplementation a common first-line treatment for POI10.
While hypomagnesaemia is commonly implicated, hypermagnesaemia has also been observed in POI, potentially due to its antagonistic effect on calcium and its role in reducing muscle excitability7. Sodium is an important contributor to plasma osmolality; hyponatraemia causes fluid to shift intracellularly, causing cellular oedema and swelling, contributing to POI11.
While various diagnostic modalities are available, no single diagnostic technique can definitively confirm POI. Clinical signs such as nausea, vomiting, bloating, anorexia, abdominal discomfort and absence of defecation can provide only a subjective means of assessing gastrointestinal motility2.
Each of these diagnostic tests has its own advantages and limitations.
Abdominal ultrasound (AUS) and point-of-care ultrasound (POCUS) allow for the assessment of gastrointestinal motility through visualisation of the gut, counting the number of intestinal contractions within a one-minute period.
The normal frequency of these contractions varies depending on the section of digestive tract being evaluated; in the stomach and proximal duodenum, peristaltic contractions typically occur at a rate of four to five per minute, whereas in other parts of the small intestine, the frequency varies more from one to six contractions per minute12.
Delayed gastric emptying may be indicated by prolonged retention of fluids in the stomach, gastric distention and reduced movement of gastric contents13. The absence of gastrointestinal peristalsis in the presence of food may be indicative of ileus.
The advantage of POCUS is that it is easily accessible in an ICU setting, it is a non-invasive tool that can be used to assess gastric emptying and antral contraction in real time, and may require minimal restraint13.
However, this is a subjective measurement that may vary with the operator and has poorly defined reference ranges.
Contrast radiography and fluoroscopy offer a more definitive assessment of gastrointestinal motility by enabling monitoring of the movement of ingested radiopaque substances over time2.
Conventional radiography generally gives little information on gastrointestinal motility; however, serial abdominal radiographs can be helpful to see progression of gas or intestinal contents between two points in time14.
In dogs and cats, gastric emptying occurs in both a solid and liquid phase. However, disorders affecting gastric emptying primarily impact the solid phase, and abnormalities are less detectable in the liquid phase13. Several methods exist for assessing gastric emptying with contrast radiography, including liquid barium, barium mixed with food, or radiopaque indigestible solids13.
The limitations of these methods include barium separating from food and being emptied in the liquid phase, giving inaccurate results; variability in emptying rates of indigestible solids; and challenges of administering radiopaque meals to anorexic patients at risk of regurgitation and aspiration13.
Radiographic equipment is readily available in most small animal practices; therefore, these methods remain valuable for assessment of gastric motility disorders in practice.
Gastric residual volume (GRV) refers to the amount of fluid aspirated from the stomach via nasogastric tube at set intervals, prior to administration of the next feeding, and can aid to assess gastric emptying efficiency and tolerance of enteral nutrition2.
While no standardised protocol exists in veterinary medicine, studies in human patients have assessed GRV at four-hour intervals, and this may be applicable to veterinary patients15. In humans, measuring GRV can be used to monitor POI in critically ill patients in ICU; elevated GRV has been associated with an increased risk for regurgitation and aspiration16.
Gastric contents can be aspirated before meals to assess motility: if less than half of the previous meal remains, normal feeding can continue; if more than half remains, hypomotility may be suspected, warranting a reduced meal volume and consideration of prokinetic therapy17.
Repeated aspiration of the gastric contents may cause electrolyte imbalances and acid-base disturbances. Therefore, partially returning residual gastric volume may be considered if aspiration of contents occurs for greater than 24 hours17.
The mainstays of treatment for POI include mobilisation, early enteral nutrition, maintenance of fluid requirements, correction of electrolyte abnormalities, multimodal pain management and pharmacological intervention2.
Early ambulation has been shown to stimulate gastrointestinal motility and can shorten recovery time; however, it does not decrease patient morbidity18.
Early enteral nutrition is believed to enhance intestinal blood flow, promote motility, reduce the risk of bacterial translocation and support the secretion of vital gut hormones2. However, gastric distention can increase patient discomfort; therefore, small feedings that stimulate gastrointestinal function while avoiding over-distension may be recommended6.
Placement of a nasogastric tube can facilitate enteral nutrition while enabling the aspiration of gastric contents for prevention of gastric distention and measurement of GRV, helping to reduce patient discomfort and minimising the risk of regurgitation and aspiration19.
Fluid therapy is crucial in the management of POI. However, excessive fluid administration can lead to bowel oedema, potentially contributing to POI6.
A recent study in people undergoing rectal cancer surgery found that administering large volumes of crystalloids was associated with a higher incidence of POI20. This is likely due to a decrease in the plasma colloid osmotic pressure that reduces the retention of fluid in the vasculature, causing a shift of fluid into the interstitial space – including the gut wall – leading to interstitial oedema21.
Hypertonic saline has been shown to decrease intestinal oedema through shifting fluid from the interstitial space into the intravascular compartment22.
Fluid resuscitation strategies should be aimed towards avoiding fluid overload and intestinal oedema by adjusting fluid composition and volume to the individual needs of the patient, considering factors such as hydration status, electrolyte balance and ongoing losses2.
Serial assessment of electrolytes is essential for identifying and addressing alterations that may compromise gastrointestinal motility.
Correction of these electrolyte imbalances through tailored fluid therapy and electrolyte supplementation is essential for optimising gastrointestinal function and preventing POI.
Postoperative pain management should involve a multimodal analgesia approach. Although opioids are frequently used postoperatively, their negative effects on gastrointestinal motility are a concern in patients with POI. Therefore, minimising opioid use and implementing alternative analgesic strategies should be considered2.
Paracetamol is an effective and well-tolerated option for managing postoperative pain, and can be used as a foundation for a multimodal analgesia approach23.
NSAIDs are effective in the management of postoperative pain while also reducing intestinal inflammation through the inhibition of the cyclooxygenase-2 enzyme. While the use of NSAIDs is beneficial due to their opiate sparing effect, their application is limited in a critical care setting by adverse effects on platelet aggregation, nephrotoxicity and gastric ulceration23.
Ketamine is a non-competitive N-methyl-D-aspartate (NMDA) antagonist, which, when administered as a continuous rate infusion (CRI), is effective in the management of postoperative pain and reduces the need for opioids24. Ketamine also significantly reduced the incidence of POI, nausea and vomiting when compared with traditional opioid analgesia25. However, ketamine may cause adverse effects such as dysphoria.
Lidocaine is a sodium-channel blocker that is widely used as a local anaesthetic26. Like ketamine, lidocaine has inhibitory properties on the NMDA receptors and can be used perioperatively to manage pain and reduce inhalant anaesthetic and opioid requirements27.
In horses, administration of lidocaine enhances analgesia and reduces the incidence of POI by improving propulsive motility27.
In dogs, these effects have not been demonstrated, and the observed improvements in motility associated with lidocaine CRI are likely due to reduced opioid usage and decreases in sympathetic nervous stimulation26,27. Lidocaine can cause adverse effects such as sedation and nausea in dogs, and its use in cats is typically not recommended due to their higher risk of toxicity at therapeutic doses27.
Epidural analgesia is another analgesic technique that reduces the incidence of POI, by limiting the use of systemic opioids and improving intestinal motility in the postoperative period through inhibition of pain, and blocking sympathetic reflexes28.
Gastrointestinal motility relies on a dynamic interplay of neural, hormonal and muscular mechanisms, ensuring coordinated peristalsis through the digestive tract. This regulation involves various receptors that influence smooth muscle contraction and intestinal secretion.
These receptors include dopaminergic (D1, D2), serotonergic (5-HT1, 5-HT3), histaminergic (H2), and motilin (M1, M2). In dysmotility disorders, clinicians can optimise the use of prokinetic agents by combining drugs that target different receptors.
Dopaminergic antagonists have both central antiemetic and peripheral prokinetic properties29. They enhance gastrointestinal motility by indirectly stimulating acetylcholine release from post-ganglionic neurons, which promotes smooth muscle contraction and facilitates peristalsis2.
Metoclopramide enhances upper gastrointestinal motility by blocking dopamine (D2) receptors and stimulating serotonin (5-HT4) receptors, increasing acetylcholine release. This strengthens the lower oesophageal sphincter, decreases postprandial fundus relaxation and improves antroduodenal contractions, accelerating gastric emptying30.
Additionally, metoclopramide has anti-emetic effects through inhibition of D2 and 5-HT3 receptors in the chemoreceptor trigger zone30. Metoclopramide can cross the brain-blood barrier, causing adverse effects such as extrapyramidal symptoms, manifesting as involuntary muscle contractions, motor agitation, and uncharacteristic aggressive behaviour2.
Domperidone is another D2-receptor antagonist, which enhances oesophageal motor activity, strengthens duodenal contractions and synchronises peristalsis across the pylorus to promote efficient gastric emptying31.
Unlike metoclopramide, domperidone has minimal ability to cross the blood-brain barrier and, therefore, does not cause central nervous adverse effects31. Domperidone has been associated with an adverse risk of QT prolongation in people32.
The serotonergic receptor 5-HT4 plays a key role in regulating gut motility; when activated, it enhances acetylcholine release from post-ganglionic cholinergic neurons, which subsequently triggers smooth muscle contractions2.
Cisapride enhances gastrointestinal motility through cholinergic pathways and has effects in the lower oesophageal sphincter, gastric antrum and colon33.
Cisapride was withdrawn from the human market due to documentation of adverse effects such as ventricular arrhythmias caused by QT interval prolongation33. However, such effects have not been documented in veterinary medicine29.
Erythromycin, a macrolide antibiotic with motilin-like properties (M1 and M2), stimulates the release of motilin from enterochromaffin cells, promoting contractions in the duodenum and gastric fundus and antrum while reducing pyloric contractility34. Erythromycin has species-dependent effects on colonic motility, enhancing smooth muscle contractions in dogs, but not in cats29.
Ranitidine and cimetidine are H2 receptor antagonist drugs which inhibit gastric acid secretion through H2-receptor antagonism on gastric parietal cells, reducing stomach pH35.
Ranitidine, however, also exhibits prokinetic properties due its anti-cholinesterase inhibition in smooth muscle, stimulating intestinal and colonic motility29,35.
In cats, intravenous administration of ranitidine may cause transient hypotension36.
POI remains a clinically significant yet often under-recognised complication in companion animals following abdominal surgery.
While its multifactorial and complex pathophysiology makes recognition of POI a challenge, early identification and proactive management are essential to reducing morbidity and improving patient outcomes.
Current evidence supports combination strategies for treatment, including a multimodal pharmacological approach and early enteral nutrition and mobilisation.
Future research is needed to establish more specific diagnostic criteria, better define risk factors and evaluate targeted therapeutic interventions.
By fostering a greater understanding of POI and incorporating evidence-based practices into perioperative protocols, veterinary professionals can enhance recovery and quality of care in their surgical patients.
