Paralytic or adynamic ileus describes a functional motor paralysis of the digestive tract secondary to neuromuscular failure not associated with mechanical obstruction.1 Paralytic ileus may be commonly observed in the postoperative period following abdominal surgeries (postoperative ileus; POI) or caused by primary inflammatory conditions such as proximal enteritis and septic ileus. Postoperative ileus has a serious impact on equine health, increasing the risk of postoperative complications (ie, adhesions) and hospitalization length and the associated costs as well as increasing mortality.2 Current therapies for POI in horses, including anti-inflammatory and prokinetics drugs, are often considered ineffective as they do not yield consistent clinical response.3,4
A well-recognized pathophysiologic component of paralytic ileus is an overall shift toward an abnormal level of sympathetic tone that inhibits intestinal motility.2 Gastrointestinal motility is regulated through complex interactions between central and autonomic innervation and the enteric nervous system. This communication network includes efferent sympathetic fibers leaving the spinal cord ventral horns, passing through the sympathetic trunk without synapsing, and continuing through a splanchnic nerve to make synaptic connections with the neurons in the prevertebral sympathetic ganglia located in the abdomen: the celiac and the superior and inferior mesenteric ganglia.5 From there, the postganglionic sympathetic neurons project to the digestive tract, where they synapse with neurons of the enteric nervous system, inhibiting excitatory acetylcholine release and consequently suppressing intestinal motility and secretion.6–8 In horses, adrenergic agonists (both α and β agonists) have been found to decrease contraction frequency and amplitude in isolated jejunum portions, with restoration of normal myenteric contractions following adrenergic blockage.9 The role of adrenergic transmission in the development of POI has been confirmed in several experimental models, including the prevention of POI after laparotomy and intestinal manipulation in rats via celiac-mesenteric ganglionectomy.10,11 Adrenergic and dopaminergic stimulation have a central role in the etiology of equine POI, but pharmacologic adrenergic blockade has inconsistent effect in overcoming gut depression, based on action toward α or β receptors.11,12
The prevertebral ganglia also receive sensory fibers from the intestine that crosstalk with the sympathetic neurons, establishing a reflex circuit regulating intestinal motility.13,14 The mediatory function of the sensory spinal afferents passing through the celiac and superior mesenteric ganglia has been also elucidated, confirming the central role of the celiac plexus in mediating the reflex alterations in gastric and intestinal motility in response to POI or obstructive pathologies.15 Taking all these concepts into consideration, a generalized suppression of the sympathetic innervation at the level of the prevertebral celiac-mesenteric ganglia and plexus seems a promising therapeutic option in equine gastrointestinal conditions in regard to its prokinetic effect, as well as afferent nociceptive transmission.
A percutaneous neurolytic celiac plexus block is performed in humans with chronic unrelenting abdominal pain in addition to other conditions, like the median arcuate ligament syndrome, and it is reported to provide analgesia within 15 minutes.16,17 Other effects of the celiac plexus block that have been described in humans include depression of the sympathetic tone with a consequent increase in intestinal motility, resulting in self-limiting diarrhea.18 Moreover, celiac plexus block was proven effective in reversing the sympathetic-mediated decrease in gastric motility in neurosurgical patients.19
Different techniques to infiltrate local anesthetic or neurolytic solutions proximate to the celiac plexus have been described in humans. These may include guidance utilizing different imaging modalities, such as CT, ultrasound, endoscopy, and fluoroscopy.20,21 In horses, a blind transcutaneous celiac plexus block approach following ultrasound-guided identification of the transverse processes of L1 and L2 has been recently described in 9 clinical cases with POI by Rabbogliatti et al.22 The authors reported an increase in small intestinal motility.
Based on the evidence in the human literature and the reported abstract in horses,22 this study aimed at optimizing an ultrasound-guided transcutaneous celiac plexus block in horses. A second aim was to characterize the effect of a transient anesthetic block of the celiac plexus on the motility of different intestinal tracts in healthy horses.
Methods
Study design
During a preliminary phase, dissection was conducted in 4 equine cadavers to verify the major anatomic landmarks in proximity of the celiac plexus. In phase 1, 6 research horses scheduled for euthanasia were enrolled in a dye study to verify the ultrasonographic window and optimize the ultrasound-guided technique to deliver the anesthetic solution near the celiac plexus branches.
Six horses were then enrolled for the experimental study (phase 2) to evaluate the effect of an anesthetic block of the celiac plexus on intestinal motility via a specifically designed ultrasonographic motility score. All procedures were conducted in accordance with the Cornell University IACUC (protocol No. 2021–0118).
Phase 1: dye study
Six research horses scheduled to be euthanized for reasons unrelated to this study were included. A bilateral parasagittal ultrasound scan of the paravertebral area between T17 and L3 was performed using a 2-to-5-MHz curved array transducer (HS60; Samsung Healthcare) in order to identify an appropriate ultrasonographic window. After clipping and aseptic preparation of the skin, the puncture site was infiltrated with 2 mL lidocaine 2% (Lidocaine Hydrochloride Injectable-2%; PHOENIX). A 1% solution of lidocaine (1.3 mg/kg total) in saline mixed with methylene blue (J0324; Jorgensen Laboratories LLC) was prepared and divided into 2 aliquots (1 for each side). After sedation with xylazine (Xylazine Injection; 0.6 mg/kg, IV; Covetrus), bilateral injections were performed aseptically under ultrasound guidance as described below. The horses were monitored for 1 hour following the injections and subsequently euthanized using barbiturate overdose via IV injection of pentobarbital sodium (Fatal-Plus; 85 mg/kg; Vortech Pharmaceuticals). Postmortem dissections were conducted to verify the location and distribution of the dye.
Ultrasound-guided celiac plexus injection technique
The celiac plexus, constituted by the celiac and cranial mesenteric ganglia (semilunar ganglia) variably fused in a dense network of fibers, in the horse is located in the retroperitoneum, intermingled with the roots of the celiac trunk and superior mesenteric arteries, branching at the level of the first lumbar vertebra, and continuing caudally with the caudal mesenteric plexus.5,23 The celiac-mesenteric ganglia are situated ventral to the abdominal aorta and covered by the caudal vena cava and adrenal glands. Based on the location and the major anatomical landmarks, we optimized an ultrasound-guided technique to deposit the anesthetic solution within the adipose tissue surrounding the aorta/vena cava and the adrenal glands.
A transcutaneous ultrasound of the paravertebral area between T17 and L3 was performed on each side using a 2-to-5-MHz curved array transducer (HS60; Samsung Healthcare). After an initial screening of the area holding the probe in parasagittal orientation, the spaces between the transverse processes of vertebrae T18 and L1, L1 and L2, were examined after rotating the probe in a transverse orientation. An 18-gauge X 20-cm spinal needle was advanced in a ventromedial direction through the epaxial musculature and psoas muscles using the abdominal aorta (on the left) and caudal vena cava (on the right), the adrenal gland, and the dorsomedial border of the kidney as anatomical references (Figure 1). When the tip of the needle was observed in proximity to the ventral border of the psoas minor muscle, the stylet was removed, and a drop of solution was applied to the hub of the needle. The needle was then further advanced slowly with steady pressure until a positive hanging drop technique was observed (the fluid in the hub was sucked in) as the needle tip was located ventral to the psoas minor muscle (Figure 2). Local anesthetic solution was then injected slowly over approximately 30 seconds.
Ultrasonographic window showing the approximative anatomical location of the celiac plexus. Longitudinal parasagittal (A) and transverse (B) view of the intervertebral space between L1 and L2 on the left side. The celiac-mesenteric ganglia and plexus (yellow area) are situated ventral to the abdominal aorta (Ao), in proximity of the adrenal gland (arrow) and the left kidney (LK). These anatomical references were identified on cadaver dissection and utilized to develop an ultrasound-guided technique to deposit anesthetic solution in proximity of the celiac plexus. The study, conducted from January 2022 through June 2022, included a dye study in 6 horses to verify the technique, followed by an experimental study to investigate the effects of the celiac plexus anesthetic block on intestinal motility in 6 healthy, sedated horses. Intestinal motility was recorded via transcutaneous ultrasound and afterward blindly scored using a specifically designed motility scoring system. L1 and L2 indicate the transverse processes, respectively, of the first and second lumbar vertebrae; color-flow mapping (blue; A) highlights blood flow within the aorta.
Citation: American Journal of Veterinary Research 86, 3; 10.2460/ajvr.24.11.0328
Ultrasound-guided celiac plexus injection technique and the anatomical references described in Figure 1. Holding the probe in transverse orientation between L1 and L2, the needle is advanced in a dorsolateral/ventromedial direction through the longissimus dorsi, psoas major, and psoas minor muscles, aiming to deposit the solution ventrally to the psoas muscle, as close as possible to the aorta. Illustration by Allison Buck, MFA, CMI, Medical Illustrator, Educational Support Services, Cornell University College of Veterinary Medicine.
Citation: American Journal of Veterinary Research 86, 3; 10.2460/ajvr.24.11.0328
Phase 3: experimental study
Six healthy research horses were enrolled for the experimental study to evaluate the effect of an anesthetic block of the celiac plexus on intestinal motility in healthy and sedated horses. The health status of the horses was based on normal physical examination. Before any experiment, the horses were acclimated for 4 days in the research barn, where they remained housed for the duration of the study; they were fed free-choice hay and grain twice daily, with daily turnout in a dry lot.
Considering the need for sedation to perform the celiac plexus block injection and aiming to account for the effect of the sedation on the intestinal motility when performing the block, the study included 2 sequential experiments. The first experiment to record the effect of an α2 agonist on intestinal motility and the second experiment to evaluate the effect of the celiac plexus block on intestinal motility in horses that were sedated for the procedure. Motility was assessed via ultrasonography using a specifically designed ultrasonographic motility score (Supplementary Table S1), ranging from 0 (no detectable contractions in any visualized intestinal segment) to 20 (frequent and strong contractions of all the intestinal segments evaluated).
Experiment 1 (effect of sedation on motility)
The horses were fasted for 12 hours, maintaining free access to water, then sedated with xylazine (0.6 mg/kg, IV). After sedation, the horses remained fasted for 6 hours, and then hay was reintroduced. Intestinal motility was assessed at different time points via transcutaneous abdominal ultrasounds performed presedation (baseline) and at times 15, 30, and 45 minutes and 1, 2, 3, 4, and 6 hours postsedation as well as 1 hour post refeeding. Multiple ultrasound video clips (each 30 seconds in length) were recorded from each intestinal ultrasonographic window at each time point.
Experiment 2 (effect of celiac plexus block on motility)
A washout period of at least 3 days, during which the horses were routinely fed and turned out, was allowed before starting the second experiment. On the day of experiment 2, the horses were fasted for 12 hours, maintaining free access to water. After identification of the ultrasonographic window to perform the celiac plexus block, the area was clipped and prepared aseptically. The horses were then sedated with xylazine (0.6 mg/kg, IV), and ultrasound-guided bilateral celiac plexus block was performed immediately after IV sedation as described in the technique paragraph. The solution injected consisted of 1.3 mg/kg lidocaine at 1% concentration, and the final volume was divided equally into 2 syringes (1 for each side). Transcutaneous abdominal ultrasound was performed and multiple video clips recorded from each intestinal ultrasonographic window before sedation (baseline) and at 15, 30, and 45 minutes and 1, 2, 3, 4, and 6 hours postsedation as well as 1 hour post refeeding. Hay was reintroduced after the ultrasonographic exam of the 6 hours postsedation time point.
The horses were closely monitored for 3 days after the experiment. The left and right celiac plexus block sites were monitored ultrasonographically for possible complications at 30 minutes and 1, 3, 6, 12, 24, and 72 hours after the procedure.
Intestinal motility evaluation
Intestinal motility was assessed via transcutaneous abdominal ultrasound using a 2-to-5-MHz curved array transducer (HS60; Samsung Healthcare). Segments of the duodenum, jejunum, cecum, and large colon were consistently examined in preclipped areas at the listed time points: presedation (baseline) and 15, 30, and 45 minutes and 1, 2, 3, 4, and 6 hours postsedation as well as 1 hour post refeeding. At each time point, each intestinal segment was evaluated for about 2 to 3 minutes, and multiple 30-second video clips were recorded. A semiquantitative motility scoring system was designed to evaluate the motility of the duodenum, jejunum, cecum, and colon independently. The score was based on the evaluation of the degree of contractility and number of contractions visualized in each segment. The sum of the score of each intestinal segment provided a total score ranging from 0 (no motility) to 20 (strong and frequent contractions in all the visualized segments; Supplementary Table S1). The recorded ultrasound video clips were retrospectively evaluated after being blinded of horse identity, experiment, date, and timing and randomized in order (computer-generated sequence). Two assessors (BD and JMC) consensus scored the blinded video clips. For each intestinal segment, the median value of the scores assigned at each corresponding video clip was calculated for each time point and used for subsequent analysis.
Statistical analysis
A priori power analysis calculated a minimum sample size of 5 horses to detect clinically significant changes in intestinal motility, estimated as an increase from 4 ± 3 SD baseline score in fasted horses to 12 ± 5 SD after the celiac plexus block (2-tailed matched pairs test for repeated measures; error level α, 0.05; power, 0.8; δ, 1.84; actual power, 0.86; G*Power, version 3.1.9.6; Universität Kiel). Descriptive data are expressed as mean with SD or median with range (or IQR) based on their distribution and central tendency, assessed using the Shapiro-Wilk test. A restricted maximum likelihood mixed-effects model analysis was conducted to identify differences in intestinal motility score based on the fixed effects of time, condition (sole sedation vs celiac plexus block after sedation), and their interaction (time*condition); horse was set as a random effect. The Fisher F ratio was calculated for each fixed effect and their interaction and reported as F value [F(DFn, DFd), where DFn is degrees of freedom for the numerator, and DFd is degrees of freedom for the denominator]. Tukey post hoc multiple comparison tests were used as appropriate. All statistical analyses were performed using JMP, version 16 (SAS Institute), and GraphPad Prism, version 10 (GraphPad Software Inc), with significance set at P < .05.
Results
Dye study (phase 1)
A potential ultrasonographic window to carry out the injection was considered when the aorta on the left side or caudal vena cava on the right side, the adrenal gland, and the dorsomedial border of the kidney were localized in the same field of view (Figure 1).
Six horses were included in this phase (4 mixed breed, 1 Warmblood, and 1 Thoroughbred; median age, 6 years, range, 5 to 21; median weight, 516 kg; range, 476 to 580; 5 mares and 1 gelding). The ultrasonographic window for the injection was most consistently identified between the L1 and L2 intervertebral space. However, in 1 horse, the injection was performed between T18 and L1 since the L1 and L2 space was found excessively narrow due to an abnormal angle of the L1 transverse process. The overall procedure to inject the celiac plexus on both sides in this group of horses was completed within 20 minutes. No complications or short-term adverse effects during or after the celiac plexus injection were observed. Postmortem dissections found dye staining the caudal and lateral branches of the celiac plexus and the ventral surface of the psoas minor in all 6 horses (Figure 3). No signs of hemorrhage or puncture lesions of the adrenal glands or kidneys were observed.
Ultrasound-guided celiac plexus injection technique and dye study described in Figures 1 and 2. A—Ultrasound-guided needle placement through the psoas muscles directed in proximity of the Ao, dorsal to the kidney (K). Color-flow mapping highlights blood flow within the aorta, and arrowheads indicate the needle artifact. B—Representative photograph of postmortem dissection in 1 of the 6 horses enrolled in the dye study. Methylene blue deposited on the branches of the celiac plexus (yellow arrows) caudal to the celiac and cranial mesenteric ganglia (yellow stars) after ultrasound-guided celiac plexus dye injection. The left adrenal gland (AG) and ventral aspect of the right psoas minor (PM) are indicated.
Citation: American Journal of Veterinary Research 86, 3; 10.2460/ajvr.24.11.0328
Experimental study (phase 2)
The experimental study was conducted on 6 healthy horses (3 Thoroughbreds, 2 Warmbloods, and 1 Quarter Horse; 4 females and 2 geldings; median age, 17 years; range, 9 to 29 years; median weight, 560 kg; range, 476 to 612 kg). Significant effects of time [F(4.3, 43.06) = 12.95; P < .0001], condition [F(1, 10) = 9.75; P < .01), and their interaction [F(9, 90) = 2.99; P < .036] were found on the intestinal motility score.
In experiment 1
The intestinal motility score before sedation was 7 ± 2, and xylazine administration suppressed the overall intestinal motility already at 15 minutes, causing the score to drop to a minimum of 2 ± 1.4 after 30 minutes (P = .04). The motility scores then returned to the baseline values within 1 hour (7.2 ± 4.3) and remained stable for about 6 hours, showing a nonsignificant increase only after the horses were fed (intestinal motility score of 8.3 ± 2.8, 1 hour after refeeding).
In experiment 2
After the celiac plexus block was performed, the overall motility score showed a significant increase from baseline (3.8 ± 2.4) after 1 hour (12.1 ± 2.9; P = .02) and remained significantly elevated until the 4-hour time point, when the motility score was still 10.3 ± 3 (P = .01; Figure 4).
Results of the experimental study investigating the effect on intestinal motility of the celiac plexus anesthetic block detailed in Figures 1 and 2. A—Box plot graph showing the overall intestinal motility score at different time points pre- and postsedation (xylazine) with celiac plexus block (CPB). Box plots indicate the median, maximum, and minimum values and the IQR, with individual data points for each horse. Time points with uncommon superscript letters are significantly different (P < .05). B—Line graph showing the overall motility score recorded in the horses when receiving sole sedation (red line) and CPB after sedation (black line). A significantly higher score was recorded when CBP was performed compared to sedation alone at 45 minutes and 1, 2, and 3 hours. Data are expressed as median and IQR. *P < .05. **P < .01.
Citation: American Journal of Veterinary Research 86, 3; 10.2460/ajvr.24.11.0328
Comparing the overall intestinal motility score between the 2 conditions, sole sedation and celiac plexus block after sedation, we found that the motility score recorded after the celiac plexus block was higher than the score obtained after sole sedation, with the most significant difference detected at 2 hours (13.6 ± 2.8 vs 8 ± 3, respectively; P = .008; Figure 4). This difference demonstrates that the increase in intestinal motility after the celiac plexus block was not due to the physiologic rebound of intestinal motility after sedation but confirms an additional prokinetic consequence to the anesthetic block of the celiac plexus.
The evaluation of the motility of each individual intestinal segment revealed that after the celiac plexus block, the duodenal motility (score range, 0 to 5) increased from baseline (median, 0.75; range, 0 to 2) to a peak of 3.8 ± 0.4 (median, 3.75; range, 3.5 to 4.5) at 1 hour (P = .01; Figure 5). The motility of the jejunum (score range, 0 to 8) peaked at 2 hours (6.6 ± 1.5 vs 1.1 ± 1.3 baseline; P = .04), whereas the cecum (score range, 0 to 5), from a baseline motility score of 1 ± 1 (median, 0.75; range, 0 to 2.5), reached the highest motility score at 3 hours (median, 3.3; range, 0 to 4; Figure 5). The motility of the cecum remained elevated at 6 hours (2.7 ± 0.6; P = .048) and 1 hour post refeeding, reaching a score of 3.2 ± 1.7 (median, 3.5; range, 0 to 4.5). No significant change in the motility score of the large colon was detected.
Graphs representing the effect on the motility of distinct intestinal portions of the CPB detailed in Figures 1 and 2. Box plot graphs showing motility scores of specific portions of the intestine at different time points pre- and post-CPB. A significant increase in motility was recorded between 1 and 3 hours in the duodenum (A), jejunum (B), and cecum (C) but not in the large colon (D). Box plots indicate the median, maximum, and minimum values and IQR, with individual data points for each horse. Time points with uncommon superscript letters are significantly different (P < .05).
Citation: American Journal of Veterinary Research 86, 3; 10.2460/ajvr.24.11.0328
In experiment 2, the celiac plexus block procedure was feasible in all 6 horses between L1 and L2, and the bilateral procedure was completed within 10 to 12 minutes. No significant complications were encountered during the procedure. The only side effect detected during the study period was a transient unilateral hindlimb ataxia (grade 3/5 of the Mayhem scale)24 in 1 horse. The ataxia developed about 20 minutes after the celiac plexus block and resolved spontaneously within 1 hour. None of the horses showed signs of discomfort or had any adverse event at the site of injection. No sign of hemorrhage, hematomas, or infection were detected on repeated ultrasonography of the celiac plexus block area soon after the procedure or within the following 72 hours in any of the horses.
Discussion
The results of this study confirm that the anesthetic block of the celiac plexus has a significant stimulatory effect on intestinal motility in the sedated healthy horse.
The celiac plexus is located in the retroperitoneum and is constituted by the celiac and cranial mesenteric ganglia (semilunar ganglia) variably fused in a dense network of fibers.5,23 In humans, several percutaneous techniques have been described to access the celiac plexus under CT, ultrasonographic, fluoroscopic, or MRI-based imaging.21 Recently, a fluoroscopically guided transcutaneous approach has been described in swine cadavers.25 The ultrasound-guided technique we described allows visualization of the anatomical landmarks surrounding the celiac plexus, facilitating reliable deposition of the anesthetic solution as close as possible to the branches of the plexus. This technique involves a level of technical difficulty and expertise similar to other ultrasound-guided needle injections, making the procedure applicable to clinical practice. Considering the localization of the anatomical structures, important limitations are represented by the size of the horse, the amount of SC or intraabdominal fat, and the characteristic of the ultrasound machine (image definition, maximal depth, etc). The proximity of the celiac plexus to great vessels (aorta on the left and vena cava on the right) carries the penetration of these structures as possible complication. For this reason, ultrasound-guided injection is more prudent than a blind injection and allows a more precise anesthetic deposition. In this study, we found consistent infiltration of the anesthetic solution between the most ventral and medial portion of the psoas minor muscle and the adjacent periaortic fat and no evidence of great vessel penetration; however, in case of poor visualization of the needle tip, the risk of such complications needs to be considered. Interestingly, in human medicine, the transaortic approach (involving direct needle penetration of the aorta) is a well-described approach with reports of only rare complications of bleeding or retroperitoneal hemorrhage.21
In humans, the most common side effects reported besides the gastrointestinal ones are hematoma or focal pain at the injection site and hypotension.26 Even if rarely, paraplegia, paraesthesia, and lower extremity weakness have been also reported.27 These complications seem to arise from direct or indirect damage to the spinal cord or other nerves from diffusion of the neurolytic agents and injury or spams of major feeder arteries to the spinal cord.27 The only complication encountered in our study was a temporary and self-resolved unilateral hindlimb ataxia in 1 horse. This ataxia could have been the result of transient vascular insult as suspected in humans or the accidental anesthesia of the lumbar spinal nerves due to broader diffusion of the local anesthetic as reported in cattle undergoing proximal lumbar paravertebral block.28
In our experiments, horses showed minimal intestinal motility when fasted and sedated, whereas after the celiac plexus block the overall motility peaked in 1 to 3 hours and remained above baseline for up to 6 hours. Based on myoelectric studies29 in normal horses, fasting induces a significant decrease in the frequency of ileal and cecal progressive motility pattern followed by a significant increase after the reintroduction of food. The intestinal motility recorded after the celiac plexus block reached higher scores than those obtained 1 hour after refeeding, indicating a vigorous effect of this sympathetic blockade on intestinal motility in healthy horses.
As expected, the intestinal motility decreased soon after sedation. In fasted horses, a decrease in jejunal and cecal activity assessed by ultrasonography has been described after sedation with xylazine.30 As demonstrated via intestinal myoelectrodes and indwelling pressure catheters, the administration of xylazine induces a significant reduction of duodenal, jejunal, cecal, and colonic motility in horses via the activation of presynaptic α-2 adrenergic receptors within the enteric nervous system.31,32 This inhibitory effect on intestinal propulsive motility has been reported to last between 30 and 60 minutes depending on the dose, followed by a gradual return to baseline contraction.33–35 Xylazine has also been reported to reset the cyclic migrating myoelectrical complexes in the duodenum as well as increase the duration of irregular spiking activity in the jejunum.33,35,36 Considering the effects of xylazine administration on intestinal motility and the need for sedation to perform the celiac plexus block injection, we decided to design 2 experiments to compare intestinal motility variation after sole sedation with xylazine and after xylazine and celiac plexus injection. As expected, xylazine induced a decrease in intestinal motility also in our study, with return to baseline activity within the first hour. When the celiac plexus block was performed, intestinal motility similarly decreased within 15 minutes postsedation; however, between 1 and 3 hours it was significantly higher than after sedation alone. This significant difference demonstrates an additional stimulatory effect on intestinal motility to be attributed to the celiac plexus anesthetic injection. The control group in this study received only sedation, therefore we are not able to exclude that in the group receiving the celiac plexus block potential effects have been triggered also by a mechanical stimulation of the celiac plexus from the needle insertion or the volume of solution deposited in its proximity. The aim of this pilot study was to establish if there was any detectable effect following celiac plexus block, ensuring the results were not dependent on sedation; ideally, future studies further evaluating the celiac plexus anesthetic block will include a sham injection performed in the control group.
The different portions of the intestinal tract evaluated in our study showed a peak in their motility at different times, with the duodenum being the fastest to reach peak motility at 1 hour and the cecum being the last to hit peak motility at 3 hours postblock. Based on the sequential, oral-to-aboral response of the different intestinal tracts, we speculated that the difference in peak timing between the duodenum, jejunum, and cecum reflects the cyclic activity of the innate intestinal pacemaker once the sympathetic tone is suppressed. The interstitial cells of Cajal, highly branched cells within the myenteric and submucosal plexuses of the enteric nervous system, initiate the intestinal pacemaker activity, generating slow waves, which determine the maximum frequency of contractions and the propagation characteristics in aboral direction.37–39 The amplitude and frequency of slow waves are modulated by circulating hormones, autocrine and paracrine mediators, and the sympathetic and parasympathetic nervous system.6,9,40–42 Cyclic phases of gastric and small intestinal electrical activity migrate along the small intestine, resulting in aboral movement of ingesta toward the distal intestine.43 Cecal motility is generated by a pacemaker region within the cecal body as well as an association with the ileal migrating action potential complexes that further explain how the cecum was the last segment to show a peak in its motility.29,44,45
We cannot ignore the fact that the intestinal activity may have been influenced in response to systemic absorption of lidocaine from the injection site. It has been demonstrated in vitro that lidocaine increased contractile activity of the proximal duodenum but not the jejunum.46 Despite being commonly used for the management of POI in horses and having overall beneficial effects, an electrophysiologic study in normal horses found that lidocaine at the same dose we used (1.3 mg/kg, IV bolus, followed by 0.05 mg/kg/min as constant infusion) did not change the spiking activity of the jejunum and therefore the rate of its muscular contractions.46,47 Furthermore, there was a trend for lidocaine to lengthen the duration of the jejunal migrating myoelectric complex and decrease the number of phase III events, both effects detrimental to motility.47 This negative effect on the phase III propelling activity of ingesta has been considered a possible explanation for the prolonged intestinal transit time and decreased fecal output recorded during constant rate infusion of lidocaine in healthy horses.48 The study measured barium-filled microspheres’ transit time and defecation frequency to indirectly evaluate the effect of lidocaine on intestinal motility, and the study design did not allow determination of which segment of the intestinal tract was responsible for the increase in the transit time. In our study, the jejunum showed a marked increase in motility that cannot be justified by systemic absorption of the lidocaine.
Based on the results of our study, the use of lidocaine as anesthetic for the celiac plexus injection maintained an increase in intestinal activity for at least 6 hours. Significant effects beyond 6 hours may be unlikely since the duration of lidocaine as a local anesthetic has been reported to be up to 5 hours when administered as a peripheral nerve block.49 For our experiment we elected to use lidocaine for its shorter duration of effect compared to other anesthetics, that allowed us to trace the changes in intestinal motility through the sedation, the lidocaine peak of action and during its wearing off period. The dose of lidocaine we used is the most frequently administered as an IV bolus and has been shown to achieve serum levels in the therapeutic but not toxic range.50 However, more studies in both healthy horses and horses affected by naturally occurring paralytic ileus are needed to establish the ideal local anesthetic to use and the relative redosing interval as the duration of the anesthetic block can be influenced by many factors, such as the health status of the patient and amount of intrabdominal adipose tissue. Rabbogliatti et al22 reported celiac plexus blocks performed using a mixture of lidocaine 1% (40 mL) and ropivacaine 1% (10 mL) bilateral, repeated every 6 hours for 48 hours. To establish guidelines for clinical use of the celiac plexus block, more data are needed in regard of its potential in preventing and not only treating POI, about the most effective timing to perform the block after surgery, and understand if bilateral (vs unilateral) or repeated injections are required and how frequently.
The main limitation of this study resides in the use of only ultrasonographic evaluation to assess the effects on intestinal motility without electrophysiologic studies that could substantiate the actual changes in myenteric activity and confirm or disprove the actual blockade of the celiac plexus branches and ganglia. In the past, there has been an attempt to validate ultrasonography recordings by comparison with a more direct method of assessing motility, and the results have been inconsistent.51 We designed a semiquantitative scoring system for motility assessment and performed a completely blinded evaluation of the recorded videoclips to increase the objectivity of the results. Moreover, it is unknown if the increase in contractility we detected on ultrasound is propulsory or not. Based only on ultrasound, we are not able to differentiate between the activation of the circular and longitudinal muscles layers within the intestine, and while the circular musculature is responsible for mixing ingesta, the synchronous activation of circular and longitudinal muscles is required to promote actual transit (peristalsis).9
In conclusion, ultrasound-guided celiac plexus block is feasible in horses and has a significant stimulating effect on intestinal motility in fasted and sedated healthy horses. This technique can become a fundamental resource in the multimodal management of postoperative colic and paralytic ileus. Further studies are needed to assess the effect on intestinal motility and other parameters, such as comfort level, in horses with experimentally induced and naturally occurring ileus and other intestinal pathologies.
Supplementary Materials
Supplementary materials are posted online at the journal website: avmajournals.avma.org.
Acknowledgments
The authors wish to thank Lisa Mitchell, LVT, for her technical assistance during the experiments and Allison Buck for her Figure 2 illustration .
Disclosures
Dr. Chevalier is a former Associate Editor for AJVR, but was not involved in the editorial evaluation of or decision to accept this article for publication.
No AI-assisted technologies were used in the generation of this manuscript.
Funding
The authors have nothing to disclose.
ORCID
J. M. Chevalier https://orcid.org/0000-0002-7278-5463
M. Cercone https://orcid.org/0000-0002-8922-7927
References
- 2.↑
Hellstrom EA, Ziegler AL, Blikslager AT. Postoperative ileus: comparative pathophysiology and future therapies. Front Vet Sci. 2021;8:714800. doi:10.3389/fvets.2021.714800
- 3.↑
Burke M, Blikslager A. Advances in diagnostics and treatments in horses with acute colic and postoperative ileus. Vet Clin North Am Equine Pract. 2018;34(1):81–96. doi:10.1016/j.cveq.2017.11.006
- 4.↑
Freeman DE. Is there still a place for lidocaine in the (postoperative) management of colics? Vet Clin North Am Equine Pract. 2019;35(2):275–288. doi:10.1016/j.cveq.2019.03.003
- 5.↑
Getty R. Equine nervous system. In: Sisson and Grossman’s the Anatomy of the Domestic Animals. 5th ed. Saunders Company; 1975:697–701.
- 6.↑
Nieto JE, Rakestraw PC. Intestinal motility and transit. In: Blikslager AT, White NA, Moore JN, Mair T, eds. The Equine Acute Abdomen. 3rd ed. Wiley Blackwell; 2017:78–95.
- 7.
Martelli D, Yao ST, McKinley MJ, McAllen RM. Reflex control of inflammation by sympathetic nerves, not the vagus. J Physiol. 2014;592(7):1677. doi:10.1113/jphysiol.2013.268573
- 8.↑
Straub RH, Wiest R, Strauch UG, Härle P, Schölmerich J. The role of the sympathetic nervous system in intestinal inflammation. Gut. 2006;55(11):1640–1649. doi:10.1136/gut.2006.091322
- 9.↑
Malone ED, Brown DR, Trent AM, Turner TA. Influence of adrenergic and cholinergic mediators on the equine jejunum in vitro. Am J Vet Res. 1996;57(6):884–890. doi:10.2460/ajvr.1996.57.06.884
- 10.↑
Fukuda H, Tsuchida D, Koda K, Miyazaki M, Pappas TN, Takahashi T. Inhibition of sympathetic pathways restores postoperative ileus in the upper and lower gastrointestinal tract. J Gastroenterol Hepatol. 2007;22(8):1293–1299. doi:10.1111/j.1440-1746.2007.04915.x
- 11.↑
Gerring EEL, Hunt JM. Pathophysiology of equine postoperative ileus: effect of adrenergic blockade, parasympathetic stimulation and metoclopramide in an experimental model. Equine Vet J. 1986;18(4):249–255. doi:10.1111/j.2042-3306.1986.tb03618.x
- 12.↑
Serio R, Zizzo MG. The multiple roles of dopamine receptor activation in the modulation of gastrointestinal motility and mucosal function. Auton Neurosci. 2023;244:103041. doi:10.1016/j.autneu.2022.103041
- 13.↑
Sachdev AH, Gress FG. Celiac plexus block and neurolysis: a review. Gastrointest Endosc Clin N Am. 2018;28(4):579–586. doi:10.1016/j.giec.2018.06.004
- 14.↑
Kambadakone A, Thabet A, Gervais DA, Mueller PR, Arellano RS. CT-guided celiac plexus neurolysis: a review of anatomy, indications, technique, and tips for successful treatment. Radiographics. 2011;31(6):1599–1621. doi:10.1148/rg.316115526
- 15.↑
Holzer HH, Raybould HE. Vagal and splanchnic sensory pathways mediate inhibition of gastric motility induced by duodenal distension. Am J Physiol. 1992;262(4):G603–G608. doi:10.1152/ajpgi.1992.262.4.G603
- 16.↑
Bhatnagar S, Joshi S, Rana SPS, Mishra S, Garg R, Ahmed SM. Bedside ultrasound-guided celiac plexus neurolysis in upper abdominal cancer patients: a randomized, prospective study for comparison of percutaneous bilateral paramedian vs. unilateral paramedian needle-insertion technique. Pain Pract. 2014;14(2):E63–E68. doi:10.1111/papr.12107
- 17.↑
Barbon DA, Hsu R, Noga J, Lazzara B, Miller T, Stainken BF. Clinical response to celiac plexus block confirms the neurogenic etiology of median arcuate ligament syndrome. J Vasc Interv Radiol. 2021;32(7):1081–1087. doi:10.1016/j.jvir.2021.04.003
- 18.↑
Weinstabl C, Porges P, Plainer B, Werba M, Spiss CK. Coeliac plexus block with bupivacaine reduces intestinal dysfunction in neurosurgical ICU patients. Anaesthesia. 1993;48(2):162–164. doi:10.1111/j.1365-2044.1993.tb06860.x
- 19.↑
Vorenkamp KE, Dahle NA. Diagnostic celiac plexus block and outcome with neurolysis. Tech Reg Anesth Pain Manag. 2011;15(1):28–32. doi:10.1053/j.trap.2011.03.001
- 20.↑
Tadros MY, Zaher Elia R. Percutaneous ultrasound-guided celiac plexus neurolysis in advanced upper abdominal cancer pain. Egypt J Radiol Nucl Med. 2015;46(4):993–998. doi:10.1016/j.ejrnm.2015.06.009
- 21.↑
Urits I, Jones MR, Orhurhu V, et al. A comprehensive review of the celiac plexus block for the management of chronic abdominal pain. Curr Pain Headache Rep. 2020;24(8):42. doi:10.1007/s11916-020-00878-4
- 22.↑
Rabbogliatti V, Zani DD, Guglielmetti E, et al. Celiac plexus block in equine ileus: a pilot study. In: Proceedings of the 69° Convegno. SISVet; 2015:216.
- 23.↑
Dyce M. The splanchnic nerves and major abdominal ganglia of the horse. J Anat. 1958;92(1):62–73.
- 24.↑
Mayhew IG, deLahunta A, Whitlock RH, Krook L, Tasker TB. Spinal cord disease in the horse. Cornell Vet. 1978;68(suppl 6):1–207.
- 25.↑
Aprea F, Millan Y, Tomás A, Campello GS, Calvo RN, Granados MM. Percutaneous fluoroscopic-guided celiac plexus approach: results in a pig cadaveric model. Animals (Basel). 2024;14(1):1478. doi:10.3390/ani14101478
- 26.↑
Gupta R, Madanat L, Jindal V, Gaikazian S. Celiac plexus block complications: a case report and review of the literature. J Palliat Med. 2021;24(9):1409–1412. doi:10.1089/jpm.2020.0530
- 27.↑
Erdine S. Complications of splanchnic and celiac plexus block. In: Erdine S, Staats PS, eds. Complications of Pain-Relieving Procedures: an Illustrated Guide. John Wiley and Sons Ltd; 2022:236–245.
- 28.↑
Skarda RT. Local and regional anesthesia in ruminants and swine. Vet Clin North Am Food Anim Pract. 1996;12(3):579–626. doi:10.1016/S0749-0720(15)30390-X
- 29.↑
Ross MW, Cullen KK, Rutkowski JA. Myoelectric activity of the ileum, cecum, and right ventral colon in ponies during interdigestive, nonfeeding, and digestive periods. Am J Vet Res. 1990;51(4):561–566. doi:10.2460/ajvr.1990.51.04.561
- 30.↑
Mitchell CF, Malone ED, Sage AM, Niksich K. Evaluation of gastrointestinal activity patterns in healthy horses using B mode and Doppler ultrasonography. Can Vet J. 2005;46(2):134–140.
- 31.↑
Koenig J, Cote N. Equine gastrointestinal motility—ileus and pharmacological modification. Can Vet J. 2006;47(6):551–559.
- 32.↑
Blandizzi C, Tarkovacs G, Natale G, Del Tacca N, Vizi ES. Functional evidence that [3H]acetylcholine and [3H]noradrenaline release from guinea pig ileal myenteric plexus and noradrenergic terminals is modulated by different presynaptic alpha-2 adrenoceptor subtypes. J Pharmacol Exp Ther. 1993;267(3):1054–1060.
- 33.↑
Adams SB, Lamar CH, Masty J. Motility of the distal portion of the jejunum and pelvic flexure in ponies: effects of six drugs. Am J Vet Res. 1984;45(4):795–799.
- 34.
Merritt AM, Burrow JA, Hartless CS. Effect of xylazine, detomidine, and a combination of xylazine and butorphanol on equine duodenal motility. Am J Vet Res. 1998;59(5):623–629.
- 35.↑
Lester GD, Merritt AM, Neuwirth L, Vetro-Widenhouse T, Steible C, Rice B. Effect of alpha-2 adrenergic, cholinergic, and nonsteroidal anti-inflammatory drugs on myoelectric activity of ileum, cecum, and right ventral colon and on cecal emptying of radiolabeled markers in clinically normal ponies. Am J Vet Res. 1998;59(3):320–327. doi:10.2460/ajvr.1998.59.03.320
- 36.↑
Merritt AM, Campbell-Thomson ML, Lowrey S. Effect of xylazine treatment on equine proximal gastrointestinal tract myoelectrical activity. Am J Vet Res. 1998;50(6):945–949.
- 37.↑
Huizinga JD. Gastrointestinal peristalsis: joint action of enteric nerves, smooth muscle, and interstitial cells of cajal. Microsc Res Tech. 1999;47(4):239–247. doi:10.1002/(SICI)1097-0029(19991115)47:4<239::AID-JEMT3>3.0.CO;2-0
- 38.
Phaneuf LP, Grivel ML, Ruckebusch Y. Electromyoenterography during normal gastrointestinal activity, painful or non-painful colic, and morphine analgesia in the horse. Can J Comp Med. 1972;36(2):138–144.
- 39.↑
Davies JV, Gerring EL. Electromechanical activity of the equine small intestine and its correlation with transit of fluid through Thiry-Vella loops. Res Vet Sci. 1983;34(3):327–333. doi:10.1016/S0034-5288(18)32232-X
- 40.↑
Sasaki N, Yoshihara T. The effect of motilin on the regulation mechanism of intestinal motility in conscious horses. J Vet Med Sci. 1999;61(2):167–170. doi:10.1292/jvms.61.167
- 41.
King JN, Gerring EL. The action of low dose endotoxin on equine bowel motility. Equine Vet J. 1991;23(1):11–17. doi:10.1111/j.2042-3306.1991.tb02705.x
- 42.↑
Malone ED, Kannan MS, Brown DR, Turner TA, Trent AM. Adrenergic, cholinergic, and nonadrenergic-noncholinergic intrinsic innervation of the jejunum in horses. Am J Vet Res. 1999;60(7):898–904. doi:10.2460/ajvr.1999.60.07.898
- 43.↑
Wong DM, Davis JL, White NA. Motility of the equine gastrointestinal tract. Equine Vet Educ. 2011;23(2):88–100.
- 44.↑
Ross MW, Donawick WJ, Sellers AF, Lowe JE. Normal motility of the cecum and right ventral colon. Am J Vet Res. 1986;47(8):1756–1762.
- 45.↑
Lester GD, Merritt AM, Neuwirth L, et al. Myoelectric activity of the ileum, cecum, and right ventral colon, and cecal emptying of radiolabeled markers in clinically normal ponies. Am J Vet Res. 1998;59:313–319. doi:10.2460/ajvr.1998.59.03.313
- 46.↑
Nieto JE, Rakestraw PC, Snyder JR, Vatistas NJ. In vitro effects of erythromycin, lidocaine, and metoclopramide on smooth muscle from the pyloric antrum, proximal portion of the duodenum, and middle portion of the jejunum of horses. Am J Vet Res. 2000;61(4):413–419. doi:10.2460/ajvr.2000.61.413
- 47.↑
Milligan M, Beard W, Kukanich B, Sobering T, Waxman S. The effect of lidocaine on postoperative jejunal motility in normal horses. Vet Surg. 2007;36(3):214–220. doi:10.1111/j.1532-950X.2007.00255.x
- 48.↑
Rusiecki KE, Nieto JE, Puchalski SM, Snyder JR. Evaluation of continuous infusion of lidocaine on gastrointestinal tract function in normal horses. Vet Surg. 2008;37(6):564–570. doi:10.1111/j.1532-950X.2008.00421.x
- 49.↑
Weinberg L, Peake B, Tan C, Nikfarjam M. Pharmacokinetics and pharmacodynamics of lignocaine: a review. World J Anesthesiol. 2015;4(2):17–29. doi:10.5313/wja.v4.i2.17
- 50.↑
van Hoogmoed LM, Nieto JE, Snyder JR, Harmon FA. Survey of prokinetic use in horses with gastrointestinal injury. Vet Surg. 2004;3(3):279–285. doi:10.1111/j.1532-950X.2004.04041.x
- 51.↑
Sasaki N, Murata A, Lee I, Yamada H. Evaluation of equine cecal motility by auscultation, ultrasonography, and electrointestinography after jejunocecostomy. Res Vet Sci. 2008;84(2):305–310. doi:10.1016/j.rvsc.2007.04.009
