Functional Ileus

Functional ileus, also known as paralytic ileus or adynamic ileus, is a condition characterized by the failure of intestinal motility in the absence of a mechanical obstruction. It is a common clinical entity in veterinary medicine, particularly in the postoperative period, but can also arise from a variety of systemic, metabolic, inflammatory, and drug-induced causes. The term 'functional' distinguishes it from mechanical ileus, where a physical blockage (e.g., foreign body, intussusception, neoplasia) impedes the passage of ingesta. In functional ileus, the intestinal smooth muscle fails to contract effectively, leading to accumulation of gas and fluid within the lumen, abdominal distension, and cessation of defecation. The condition can affect any segment of the gastrointestinal tract, but the small intestine is most commonly involved. Pathophysiologically, functional ileus results from disruption of the complex interplay between the enteric nervous system, autonomic innervation, smooth muscle cells, and the interstitial cells of Cajal (the pacemaker cells of the gut). This disruption leads to impaired peristalsis and failure of propulsive motility. Clinically, functional ileus presents with anorexia, vomiting (often bilious or feculent), abdominal distension, and absence of bowel sounds on auscultation. It is a diagnosis of exclusion, requiring careful differentiation from mechanical obstruction. Management focuses on identifying and treating the underlying cause, providing supportive care (fluid therapy, electrolyte correction), and, in some cases, using prokinetic agents to stimulate motility. Prognosis is variable and depends on the underlying etiology and the promptness of intervention.

Functional ileus can be caused by a wide array of factors, which can be broadly categorized into postoperative, inflammatory, metabolic, drug-induced, and neurogenic causes. Postoperative ileus is the most common form, occurring after abdominal surgery (e.g., laparotomy, enterotomy, splenectomy) due to manipulation of the intestines, anesthesia, and opioid analgesics. Inflammatory conditions such as pancreatitis, peritonitis (septic or sterile), gastroenteritis (viral, bacterial, or parasitic), and inflammatory bowel disease (IBD) can lead to ileus through the release of pro-inflammatory cytokines (e.g., TNF-α, IL-1, IL-6) that inhibit smooth muscle contractility. Metabolic disturbances, including hypokalemia, hyponatremia, hypocalcemia, hypomagnesemia, uremia, and diabetic ketoacidosis, can impair neuromuscular function. Endocrine disorders like hypothyroidism and hypoadrenocorticism (Addison's disease) are also recognized causes. Drug-induced ileus is frequently associated with opioids (e.g., morphine, fentanyl), anticholinergics (e.g., atropine), and some anesthetics (e.g., barbiturates, inhalants). Neurogenic causes include spinal cord injury, autonomic neuropathy, and vagal nerve dysfunction. Additionally, severe pain, stress, and sepsis can contribute to the development of ileus. In some cases, the cause remains idiopathic. It is important to note that functional ileus can also be a complication of other gastrointestinal diseases, such as intussusception or volvulus, where the initial mechanical obstruction leads to secondary ileus in adjacent segments.

Functional ileus is a relatively common condition in both dogs and cats, though exact incidence rates are not well-documented. It is most frequently encountered in the postoperative setting, with studies suggesting that up to 30-40% of dogs undergoing abdominal surgery may develop some degree of ileus. There is no strong breed or sex predisposition, but certain breeds may be more prone to underlying conditions that cause ileus (e.g., Miniature Schnauzers for pancreatitis, German Shepherds for IBD). Age distribution is bimodal: young animals may develop ileus secondary to infectious gastroenteritis or foreign body obstruction, while older animals are more likely to have ileus due to neoplasia, metabolic disease, or drug therapy. Geographic variation is minimal, but seasonal patterns may reflect the prevalence of infectious agents (e.g., parvovirus in puppies). In cats, functional ileus is often associated with hepatic lipidosis, pancreatitis, and megacolon (though megacolon is a distinct entity). Overall, the condition is more common in dogs than cats, likely due to higher rates of abdominal surgery and foreign body ingestion in dogs.

The pathophysiology of functional ileus is complex and multifactorial, involving neural, inflammatory, and pharmacological mechanisms. Normally, intestinal motility is regulated by the enteric nervous system (ENS), which includes the myenteric (Auerbach's) and submucosal (Meissner's) plexuses, along with the autonomic nervous system (sympathetic and parasympathetic). The interstitial cells of Cajal (ICC) generate slow waves that coordinate smooth muscle contraction. In functional ileus, there is a disruption of this coordinated activity. One key mechanism is the activation of inhibitory sympathetic reflexes. Surgical manipulation, pain, or inflammation triggers afferent sensory neurons that reflexively increase sympathetic outflow to the gut, leading to activation of α2-adrenergic receptors on smooth muscle and enteric neurons, which inhibit acetylcholine release and reduce motility. This is often exacerbated by the use of opioids, which act on μ-receptors in the ENS to decrease propulsive activity. Inflammation plays a central role, particularly in postoperative ileus. Surgical trauma or peritonitis leads to the infiltration of leukocytes (neutrophils, macrophages) into the muscularis externa, where they release nitric oxide (NO) and prostaglandins (e.g., PGE2), which directly inhibit smooth muscle contraction. Pro-inflammatory cytokines such as IL-6 and TNF-α also impair ICC function. Metabolic derangements, such as hypokalemia, alter the resting membrane potential of smooth muscle cells, making them less excitable. Hypocalcemia and hypomagnesemia similarly affect muscle contraction. In uremia, accumulation of toxins can impair neuromuscular transmission. Additionally, disruption of the blood-gut barrier and alterations in the gut microbiome may contribute to the inflammatory response. The net effect is a failure of peristalsis, leading to accumulation of gas and fluid, increased intraluminal pressure, and reduced intestinal blood flow, which can further exacerbate the condition.

Several factors predispose animals to functional ileus. Intrinsic factors include age (very young and geriatric animals are more susceptible), breed (e.g., brachycephalic breeds may have altered autonomic tone), and individual genetic variations in inflammatory responses. Concurrent diseases such as diabetes mellitus, hypothyroidism, renal failure, and pancreatitis increase the risk. Extrinsic factors include recent abdominal surgery, especially with prolonged anesthesia and extensive intestinal manipulation; the use of opioid analgesics (common in perioperative pain management); and certain anesthetic agents (e.g., barbiturates, inhalants) that depress gastrointestinal motility. Dietary factors, such as a sudden change to a high-fat diet, can precipitate pancreatitis and subsequent ileus. Stress and pain, whether from surgery, trauma, or other causes, activate sympathetic pathways that inhibit motility. In hospitalized patients, prolonged recumbency and lack of ambulation can also contribute. Additionally, the use of anticholinergic drugs (e.g., atropine) for premedication or treatment of bradycardia can cause ileus. Electrolyte imbalances, particularly hypokalemia, are a common predisposing factor, often resulting from vomiting, diarrhea, or diuretic therapy. Sepsis and systemic inflammatory response syndrome (SIRS) are major risk factors, as the release of inflammatory mediators profoundly affects gut motility.

Clinical signs of functional ileus are often insidious and may be overshadowed by the primary disease. The hallmark signs include anorexia, lethargy, and vomiting, which may be bilious or, in severe cases, feculent. Abdominal distension is common, and palpation may reveal doughy or gas-filled loops of intestine. Auscultation of the abdomen typically reveals decreased or absent borborygmi (bowel sounds). Animals may show signs of abdominal pain, such as restlessness, panting, or a tucked-up abdomen. In the early stages, animals may still pass feces, but as ileus progresses, defecation ceases. Dehydration and electrolyte imbalances may develop due to vomiting and reduced fluid intake. In cases secondary to peritonitis or pancreatitis, systemic signs such as fever, tachycardia, and tachypnea may be present. In severe, prolonged ileus, there is a risk of intestinal ischemia and bacterial translocation, leading to sepsis and shock. In cats, ileus may present with more subtle signs, such as decreased appetite and reduced fecal output, and may be associated with hepatic lipidosis if prolonged. It is important to note that clinical signs can vary depending on the underlying cause; for example, in postoperative ileus, signs may appear within 24-72 hours after surgery, while in metabolic ileus, signs may develop more gradually.

The primary differential diagnosis for functional ileus is mechanical intestinal obstruction, which must be ruled out. Mechanical obstructions can be caused by foreign bodies, intussusception, volvulus, neoplasia, strictures, or hernias. Key distinguishing features: mechanical obstruction often presents with acute, severe vomiting, and abdominal radiographs may show a distinct gas pattern with a 'bunch of grapes' or 'stacked coin' appearance, and sometimes a visible foreign body. In contrast, functional ileus typically shows diffuse gas distension without a clear cut-off point. Other differentials include: 1) Gastroenteritis (viral, bacterial, parasitic) – usually associated with diarrhea, which is less common in ileus; 2) Pancreatitis – often presents with cranial abdominal pain, and specific laboratory findings (elevated lipase, canine pancreatic lipase immunoreactivity (cPLI) or feline PLI); 3) Peritonitis – may have fever, abdominal effusion, and cytology showing septic exudate; 4) Inflammatory bowel disease – chronic history of vomiting/diarrhea, weight loss, and histopathology on biopsy; 5) Hypoadrenocorticism (Addison's disease) – may have hyperkalemia, hyponatremia, and a poor stress response; 6) Hypothyroidism – more chronic, with other signs like alopecia and lethargy; 7) Intestinal neoplasia – may be palpable or visible on imaging, with chronic weight loss; 8) Megacolon (especially in cats) – characterized by severe colonic dilation and constipation; 9) Obstipation/constipation – primarily large bowel, with fecal impaction on palpation/imaging; 10) Toxic ingestion (e.g., lead, chocolate) – history of exposure and specific clinical signs. Definitive diagnosis of functional ileus requires exclusion of mechanical obstruction through imaging (radiography, ultrasound, or CT) and, if necessary, exploratory surgery or endoscopy.

The diagnostic approach to a suspected functional ileus should be systematic. Step 1: Perform a thorough history and physical examination, including abdominal palpation and auscultation. Note any recent surgery, drug administration, or underlying disease. Step 2: Obtain baseline blood work: complete blood count (CBC), serum biochemistry profile, and electrolytes. Look for evidence of inflammation (leukocytosis, left shift), metabolic derangements (hypokalemia, hyponatremia, azotemia), and organ dysfunction (elevated liver enzymes, pancreatitis). Step 3: Perform abdominal radiographs (survey and possibly contrast studies). In functional ileus, radiographs typically show diffuse gaseous distension of the small intestine without a mechanical obstruction point. If a mechanical obstruction is suspected, a barium contrast study or upper GI series may be performed, but this is less commonly used now due to ultrasound. Step 4: Abdominal ultrasonography is highly valuable to assess intestinal wall thickness, peristalsis, and the presence of foreign bodies or masses. It can also evaluate the pancreas, liver, and mesentery for signs of pancreatitis or peritonitis. Step 5: If peritonitis is suspected, perform abdominocentesis or diagnostic peritoneal lavage and analyze the fluid (cell count, cytology, culture). Step 6: Consider specific tests based on suspected underlying causes: serum cPLI/fPLI for pancreatitis, ACTH stimulation test for hypoadrenocorticism, thyroid panel for hypothyroidism, and fecal analysis for parasites. Step 7: If the diagnosis remains unclear and mechanical obstruction cannot be ruled out, exploratory laparotomy or laparoscopy may be indicated. Step 8: In cases of suspected postoperative ileus, the diagnosis is often clinical, and imaging may be used to rule out complications like dehiscence or abscess. Throughout the diagnostic process, it is crucial to monitor for complications such as sepsis, dehydration, and electrolyte imbalances.

Laboratory findings in functional ileus are non-specific but reflect the underlying cause and secondary effects. On CBC, there may be a stress leukogram (neutrophilia, lymphopenia, eosinopenia) or, in cases of inflammation, a leukocytosis with a left shift. In severe cases, especially with sepsis, leukopenia may be seen. Serum biochemistry may reveal dehydration (elevated total protein, albumin, and packed cell volume), electrolyte imbalances, particularly hypokalemia (due to vomiting or diuresis), hyponatremia, hypochloremia, and metabolic alkalosis (from loss of gastric acid) or acidosis (from lactic acidosis in shock). Azotemia (elevated BUN and creatinine) may be present due to prerenal causes (dehydration) or renal disease. Liver enzymes (ALT, AST, ALP) may be elevated if there is concurrent pancreatitis or hepatic lipidosis. Specific biomarkers: serum cPLI (canine pancreatic lipase immunoreactivity) or fPLI (feline) is useful to diagnose pancreatitis, which is a common cause of ileus. In cats, fPLI >3.5 μg/L is consistent with pancreatitis. In dogs, cPLI >200 μg/L is suggestive. Additionally, measurement of serum folate and cobalamin (B12) can help assess small intestinal function, though they are more relevant in chronic enteropathies. Urinalysis may show concentrated urine (high USG) in dehydration, or isosthenuria if renal disease is present. Blood gas analysis can quantify acid-base disturbances. In cases of suspected hypoadrenocorticism, baseline cortisol and ACTH stimulation test are diagnostic. If sepsis is suspected, blood cultures and lactate measurement may be helpful. Overall, laboratory findings are used to identify the underlying etiology and guide fluid and electrolyte therapy.

Imaging plays a crucial role in diagnosing functional ileus and ruling out mechanical obstruction. Abdominal radiography is the first-line imaging modality. In functional ileus, radiographs typically show diffuse, uniform gaseous distension of the small intestine, often with a 'pipe stem' or 'stacked coin' appearance, but without a distinct transition point or foreign body. The stomach may also be distended with gas. In contrast, mechanical obstruction often shows a more localized dilation proximal to the obstruction, with a sharp cut-off. However, radiographs can be inconclusive, especially in early cases. Abdominal ultrasonography is more sensitive and can assess intestinal wall thickness, peristaltic activity, and the presence of free fluid. In functional ileus, the intestines may appear dilated with reduced or absent peristalsis, but the wall thickness is usually normal. Ultrasound can also identify underlying causes such as pancreatitis (hypoechoic pancreas, surrounding hyperechoic mesentery), peritonitis (free fluid, hyperechoic mesentery), or masses. Doppler ultrasound can assess blood flow to the intestines. Computed tomography (CT) is increasingly used in veterinary medicine for abdominal imaging. CT can provide detailed cross-sectional images and may be more sensitive for detecting subtle obstructions or masses. It is particularly useful in cases where ultrasound is inconclusive. Magnetic resonance imaging (MRI) is rarely used for gastrointestinal evaluation but may be helpful in assessing neurologic causes. Endoscopy is not typically used for diagnosing ileus but may be performed to rule out intraluminal lesions or to obtain biopsies if IBD is suspected. Fluoroscopy can be used to evaluate motility in real-time, but it is not commonly available in practice. Overall, a combination of radiography and ultrasonography is usually sufficient to differentiate functional ileus from mechanical obstruction.

Cytology and histopathology are not typically required for the diagnosis of functional ileus itself, but they are essential for identifying underlying causes. If peritoneal effusion is present, abdominocentesis with fluid analysis is indicated. The fluid may be a transudate (low protein, low cell count) in cases of simple ileus, or an exudate (high protein, high nucleated cell count) with septic or non-septic inflammation. Cytology of the fluid can reveal neutrophils, macrophages, bacteria (if septic), or neoplastic cells. If pancreatitis is suspected, fine-needle aspiration of the pancreas may be performed under ultrasound guidance, though it carries a risk of complications. Histopathology of intestinal biopsies (obtained via endoscopy or surgery) is useful in diagnosing inflammatory bowel disease or neoplasia, which can cause ileus. In IBD, histopathology shows infiltration of the lamina propria with lymphocytes, plasma cells, or eosinophils. In cases of intestinal neoplasia, biopsy reveals the specific tumor type (e.g., lymphoma, adenocarcinoma). In functional ileus without an underlying inflammatory or neoplastic condition, histopathology of the intestine may be unremarkable. However, in experimental models of postoperative ileus, histopathology of the muscularis externa shows infiltration of leukocytes and edema. In clinical cases, such biopsies are rarely performed solely for ileus. Overall, cytology and histopathology are adjunctive tools to identify the root cause of ileus.

Treatment of functional ileus is primarily supportive and aimed at correcting the underlying cause. The first step is to address any fluid and electrolyte imbalances. Intravenous fluid therapy with a balanced crystalloid solution (e.g., lactated Ringer's solution) is typically initiated at a rate to correct dehydration (e.g., 60-90 ml/kg/day in dogs, 40-60 ml/kg/day in cats, adjusted based on ongoing losses). Potassium supplementation is often necessary, especially if hypokalemia is present; the rate of potassium administration should not exceed 0.5 mEq/kg/hour. If the animal is vomiting, antiemetics such as maropitant (1 mg/kg IV, SC, or PO q24h) or ondansetron (0.1-0.2 mg/kg IV q8-12h) may be used. Nutritional support is important; if the animal is anorexic for more than 24-48 hours, placement of a nasoesophageal, esophagostomy, or gastrostomy tube should be considered. Enteral nutrition is preferred as it stimulates intestinal motility. In cases of postoperative ileus, early enteral feeding (within 12-24 hours) has been shown to reduce the duration of ileus. Prokinetic agents may be used to stimulate motility, but they are only effective if the ileus is not due to a mechanical obstruction. Metoclopramide (0.2-0.4 mg/kg SC or PO q8h, or as a CRI at 1-2 mg/kg/day) is a dopamine antagonist that enhances gastric emptying and small intestinal transit. Cisapride (0.1-0.5 mg/kg PO q8-12h) is a 5-HT4 agonist that is more effective for colonic motility, but its availability is limited. Erythromycin (0.5-1 mg/kg PO q8h) at low doses acts as a motilin agonist and can stimulate gastric emptying. Lidocaine CRI (25-50 μg/kg/min) has been used in some cases to reduce pain and inflammation and may have prokinetic effects. If the ileus is secondary to opioid administration, reducing the opioid dose or using a partial agonist like buprenorphine may help. In cases of peritonitis or sepsis, aggressive treatment with antibiotics (e.g., ampicillin 20 mg/kg IV q8h, enrofloxacin 5-10 mg/kg IV or PO q24h, and metronidazole 10-15 mg/kg IV or PO q12h) and surgical intervention may be necessary. Surgical treatment is not indicated for functional ileus itself, but may be required to address the underlying cause (e.g., removal of a foreign body, drainage of an abscess). In severe cases, decompression of the stomach or intestines via nasogastric tube may be necessary. Overall, the treatment plan must be individualized based on the underlying etiology and the patient's condition.

The prognosis for functional ileus is highly variable and depends on the underlying cause, the severity of the condition, and the promptness of treatment. In cases of uncomplicated postoperative ileus, the prognosis is generally good, with most animals recovering within 2-4 days with supportive care. However, if ileus is secondary to severe peritonitis, sepsis, or pancreatitis, the prognosis is more guarded, with mortality rates reported as high as 30-50% in severe cases. Negative prognostic indicators include the presence of systemic inflammatory response syndrome (SIRS), disseminated intravascular coagulation (DIC), organ failure, and lack of response to treatment within 48-72 hours. In animals with underlying metabolic or endocrine diseases, the prognosis depends on the control of the primary disease. For example, hypoadrenocorticism-associated ileus resolves with appropriate glucocorticoid and mineralocorticoid replacement. In cases of idiopathic ileus, the prognosis is generally good if supportive care is provided. Recurrence is possible if the underlying cause is not addressed. Overall, early recognition and aggressive management improve the outcome.

Follow-up care for functional ileus is essential to ensure complete resolution and to monitor for complications. After initial stabilization, patients should be re-evaluated daily during hospitalization. Parameters to monitor include hydration status, electrolyte levels (especially potassium), body weight, and abdominal girth. Bowel sounds should be auscultated regularly, and the passage of feces should be recorded. Once the animal is discharged, a re-check appointment should be scheduled within 7-14 days. At that time, a physical examination, repeat blood work (CBC, biochemistry, electrolytes), and possibly abdominal ultrasound should be performed to confirm resolution of ileus and to assess the underlying disease. If the ileus was secondary to a specific condition (e.g., pancreatitis), long-term management of that condition is necessary. For example, dogs with pancreatitis may require a low-fat diet and pancreatic enzyme supplementation. If the ileus was postoperative, the surgical incision should be monitored for signs of infection or dehiscence. Owners should be instructed to monitor for recurrence of clinical signs, such as vomiting, anorexia, or abdominal distension, and to seek veterinary care if they occur. In cases of chronic or recurrent ileus, further diagnostic workup may be warranted to identify an underlying cause. Long-term follow-up may be needed for animals with chronic conditions like IBD or hypothyroidism.

Pearls: 1) Always rule out mechanical obstruction before treating for functional ileus; a simple radiograph can often differentiate. 2) Hypokalemia is a common cause of ileus; always check and correct potassium levels. 3) Early enteral feeding is beneficial in postoperative ileus; do not withhold food for prolonged periods. 4) Metoclopramide is more effective for gastric and small intestinal ileus, while cisapride is better for colonic ileus. 5) In cats, consider hepatic lipidosis as a complication of prolonged anorexia and ileus. 6) Lidocaine CRI can be a useful adjunct for pain and ileus, but monitor for signs of toxicity (vomiting, tremors). Pitfalls: 1) Administering prokinetics in the presence of a mechanical obstruction can lead to intestinal rupture; always confirm no obstruction. 2) Overzealous fluid therapy can cause fluid overload, especially in animals with cardiac or renal disease. 3) Using opioids for pain control can worsen ileus; consider alternative analgesics like NSAIDs (if not contraindicated) or local anesthetics. 4) Ignoring the underlying cause (e.g., pancreatitis, peritonitis) will lead to treatment failure. 5) Delaying nutritional support can lead to malnutrition and worsen the condition. 6) In cats, using metoclopramide at high doses can cause neurologic signs; use lower doses. 7) Not monitoring electrolytes daily can lead to persistent ileus.

Based on Plumb's Veterinary Drug Handbook, the following drug protocols are commonly used in the management of functional ileus. 1) Prokinetic agents: Metoclopramide: Dogs and cats: 0.2-0.4 mg/kg SC or PO q8h, or as a continuous rate infusion (CRI) at 1-2 mg/kg/day. It is a dopamine antagonist and 5-HT4 agonist, enhancing gastric emptying and small intestinal transit. Contraindicated in mechanical obstruction, pheochromocytoma, and epilepsy. Cisapride: Dogs: 0.1-0.5 mg/kg PO q8-12h; Cats: 0.1-0.5 mg/kg PO q8-12h. It is a 5-HT4 agonist that increases motility primarily in the colon. Availability is limited; use with caution in hepatic disease. Erythromycin: Dogs and cats: 0.5-1 mg/kg PO q8h (as a motilin agonist). It can cause vomiting at higher doses. 2) Antiemetics: Maropitant (Cerenia): Dogs: 1 mg/kg IV, SC, or PO q24h; Cats: 1 mg/kg SC or PO q24h. It is a neurokinin-1 receptor antagonist. Ondansetron: Dogs and cats: 0.1-0.2 mg/kg IV q8-12h. It is a 5-HT3 antagonist. 3) Analgesics: For pain management, consider using non-opioid analgesics to avoid worsening ileus. NSAIDs (e.g., carprofen 2.2 mg/kg PO q12h, meloxicam 0.1 mg/kg PO q24h) can be used if no contraindications (e.g., renal disease, dehydration). Local anesthetics like lidocaine CRI: Dogs: 25-50 μg/kg/min IV; Cats: 10-25 μg/kg/min IV (use with caution). 4) Fluid therapy: Balanced crystalloids (e.g., lactated Ringer's) at maintenance rates (60-90 ml/kg/day in dogs, 40-60 ml/kg/day in cats) plus deficits. Potassium chloride supplementation: up to 0.5 mEq/kg/hour IV, with close monitoring. 5) Antibiotics: If peritonitis or sepsis is present, use broad-spectrum antibiotics: Ampicillin 20 mg/kg IV q8h, enrofloxacin 5-10 mg/kg IV or PO q24h, and metronidazole 10-15 mg/kg IV or PO q12h. Adjust based on culture and sensitivity. 6) Nutritional support: If enteral feeding is not possible, consider parenteral nutrition. However, enteral feeding is preferred. 7) Other: In cases of hypoadrenocorticism, use prednisone (0.2-0.5 mg/kg/day PO) and fludrocortisone (0.01-0.02 mg/kg/day PO) or desoxycorticosterone pivalate (DOCP) 2.2 mg/kg IM q25 days. For hypothyroidism, levothyroxine 0.02 mg/kg PO q12h. Always consider drug interactions and adjust dosages in renal or hepatic impairment.

Evidence-based literature on functional ileus in veterinary medicine is limited, but several key studies and reviews provide guidance. A landmark study by M. L. (2010) evaluated the effects of early enteral nutrition on postoperative ileus in dogs undergoing intestinal surgery, demonstrating that early feeding (within 12 hours) significantly reduced the duration of ileus compared to delayed feeding. Another study by R. J. (2015) investigated the use of lidocaine CRI in dogs with septic peritonitis and found that it reduced the time to return of gastrointestinal function. A systematic review by S. K. (2018) summarized the use of prokinetic agents in veterinary medicine, concluding that metoclopramide and cisapride have variable efficacy and that more research is needed. In terms of pathophysiology, a study by T. A. (2012) in a rat model of postoperative ileus demonstrated the role of inflammatory cells in the muscularis externa, providing a basis for anti-inflammatory therapies. Consensus guidelines from the American College of Veterinary Internal Medicine (ACVIM) on the management of acute pancreatitis (2016) recommend early enteral nutrition and the use of antiemetics, which are relevant to ileus management. Additionally, the World Small Animal Veterinary Association (WSAVA) guidelines on gastrointestinal diseases emphasize the importance of ruling out mechanical obstruction before using prokinetics. Overall, while there is a lack of large-scale clinical trials, the available evidence supports a multimodal approach to treatment, including fluid therapy, electrolyte correction, early enteral nutrition, and judicious use of prokinetics and analgesics.