Motility describes the spontaneous movement of cells or organs through metabolic activity, such as the contractions of the gastrointestinal (GI) tract. It is important to understand how anesthesia, a key component of smooth surgical operation, affects digestive motility. These analyses can help prevent intraoperative and postoperative complications, such as increased surgical time, bowel distension, or delayed gastric emptying (i.e., gastric aspiration).

Fentanyl is a liver-metabolized synthetic opioid that acts on μ-opioid receptors with a long duration of action. Although fentanyl is among the commonly used drugs in anesthesia, a known side effect of it and other opioids is constipation, which can lead to decreased digestive motility. In a 2020 clinical study, researchers sought to examine the impact of fentanyl on digestive motility. The study included 19 adult patients undergoing high-resolution impedance manometry and found increased supine integrated relaxation pressure (a measure of GI motility). Despite the significant difference in these measurements for patients receiving either fentanyl or saline, the final diagnosis of normal esophageal motility remained the same for all patients.²

Halogenated inhaled anesthetics act via GABA-A agonism and NMDA antagonism, with their potency and uptake influenced by solubility. These anesthetic agents are often used due to their rapid tissue action and predictable cerebral uptake.³ A clinical study investigated the effect of halothane and enflurane on the lower esophageal sphincter (LOS) and found a significant decrease in the resting pressure of the LOS following the administration of nitrous oxide, halothane, or enflurane.⁴ A subsequent study in children confirmed the finding of a concentration-dependent decrease in LOS resting pressure and gastroesophageal pressure after sevoflurane or enflurane administration.⁵ In another study, researchers used a canine model to demonstrate sevoflurane anesthesia decreased gastric and small bowel motility, without changes in luminal pH. Mean gastric contraction force decreased from 11 to 3 mmHg (p < 0.01), while gastric motility index measures decreased from 0.63 to 0 (p = 0.01). While gastric motility returned to normal levels 12-15 hours post-anesthesia, gastric emptying was delayed until 49 hours (compared to 12 hours in animals that did not receive sevoflurane anesthesia). Delayed gastric emptying can lead to ileus, or content buildup of the GI tract, which can cause intestinal blockage, tissue death, perforation, or infection.⁶

The intravenous anesthetic agent propofol also works through GABA-A receptor agonism and has a rapid onset of action, elimination half-life, and distribution rate. Dexmedetomidine, the a2-adrenergic agonist, is another agent similarly valued for its anxiolytic, analgesic, and mild respiratory effects.³ In a randomized, double-blind, cross-over study, 11 healthy volunteers were sedated with different quantities of either dexmedetomidine or propofol. For both agents, the LOS resting pressure decreased proportionally with increasing dosage. On the other hand, the gastroesophageal pressure gradient was preserved across dosage levels and anesthetic drug type.⁷ To assess sepsis-induced ileus, researchers injected either propofol or dexmedetomidine in endo-toxemic mice. Dexmedetomidine significantly delayed gastric emptying (P = 0.006), small intestinal transit (P = 0.006), colonic transit (P =0.0006), gastrointestinal transit (P = 0.0001) and whole gut transit (P = 0.034), whereas propofol showed no depression across these measurements. The inhibitive effects of dexmedetomidine vanished 24 hours after anesthesia administration.⁸

Understanding the impact of anesthesia drugs on digestive motility is essential. While agents like fentanyl, sevoflurane, propofol, and dexmedetomidine can effectively induce anesthesia, each agent uniquely affects GI function, highlighting the importance of tailored anesthetic treatment plans to optimize patient outcomes and minimize perioperative risk.

References

1. Hernandez, Matthew C., et al. “GI Surgical Emergencies: Scope and Burden of Disease.” Journal of Gastrointestinal Surgery, 23(4), 2019, 827–36.  https://doi.org/10.1007/s11605-018-3992-6
2. Su, Hui, et al. “Performing High-Resolution Impedance Manometry After Endoscopy With Conscious Sedation Has Negligible Effects on Esophageal Motility Results.” Journal of Neurogastroenterology and Motility, 26(3), 2020, 352-361. https://doi.org/10.5056/jnm20006
3. Renard, Domitille, et al. “Impact of Anesthesia Drugs on Digestive Motility Measurements in Humans: A Systematic Review.” Neurogastroenterology & Motility, 36(9), 2024, e14855.  https://doi.org/10.1111/nmo.14855
4. Sehhati, G., et al. “The Action of Inhalation Anesthetics upon the Lower Oesophageal Sphincter.” Acta Anaesthesiologica Belgica, 31(2), 1980, 91–98
5. Kohjitani, Atsushi, et al. “Effects of Sevoflurane and Enflurane on Lower Esophageal Sphincter Pressure and Gastroesophageal Pressure Gradient in Children.” Journal of Anesthesia, 13(1), 1999, 1–7.  https://doi.org/10.1007/s005400050013
6. Boscan, Pedro, et al. “Effect of Prolonged General Anesthesia with Sevoflurane and Laparoscopic Surgery on Gastric and Small Bowel Propulsive Motility and pH in Dogs.” Veterinary Anaesthesia and Analgesia, 41(1), 2014, 73–81. https://doi.org/10.1111/vaa.12093
7. Turan, A., Wo, J., Kasuya, Y., Govinda, R., Akça, O., Dalton, J. E., and Rauch, S. “Effects of dexmedetomidine and propofol on lower esophageal sphincter and gastroesophageal pressure gradient in healthy volunteers.” Anesthesiology, 112(1), 2010, 19-24.
8. Chang, Haiqing, et al. “Effect of Sedation with Dexmedetomidine or Propofol on Gastrointestinal Motility in Lipopolysaccharide-Induced Endotoxemic Mice.” BMC Anesthesiology, 20(1), 2020, 227. https://doi.org/10.1186/s12871-020-01146-z