Ulceration and stricture of the right dorsal colon after phenylbutazone administration in four horses

Four cases of ulceration and stricture of the right dorsal colon were encountered. Ulceration of the right dorsal colon is generally associated with nonsteroidal anti-inflammatory drug (NSAID) toxicosis but there are few reports of stricture following ulceration. All four horses had recent phenylbutazone use: three had been given doses well in excess of the recommended dose and in one the dose was marginally above those recommended but was combined with administration of other NSAIDs. All four horses presented with intermittent low-grade colic, weight loss and ventral oedema. Diarrhoea was also seen in three of them. All had hypoproteinaemia due to severe hypoalbuminaemia, and hyperfibrinogenaemia. Hypoalbuminaemia was less severe in one horse and this horse was successfully managed medically. Two cases were definitively diagnosed at exploratory celiotomy and two at necropsy. Exploratory celiotomy was performed in two horses: one was euthanased at surgery and one was managed successfully with medical treatment and remained normal 1 year after surgery. Medical management included feeding of a low-roughage pelleted ration, corn oil, psyllium mucilloid, and discontinuation of NSAID administration.     

Normal motility of the cecum and right ventral colon in ponies

To study the normal motility of the cecum and right ventral colon (RVC) in 3 mature Shetland ponies, a 6-part, indwelling, intraluminal catheter system was used to measure intraluminal pressure changes. Three catheters were placed in the cecum at 10, 25, and 40 cm from the cecocolic orifice, and 3 catheters were placed in the RVC at 10, 20, and 30 cm from the cecocolic orifice. Recordings were made during the interdigestive period beginning 2 weeks after surgical operation was done. Frequent, low-amplitude peaks (0.35 +/- 0.13 coordinated peaks/min) were seen involving the cecal body and caudal cecal base, which represented a haustra-to-haustra mixing pattern. Coordinated pressure peaks originated in the cecal body and progressed to the cranial cecal base (0.07 +/- 0.01/min) or originated in the cranial cecal base and progressed to the cecal body (0.07 +/- 0.04/min). Associated with a loud rush of ingesta heard on transabdominal auscultation and progression of liquid ingesta confirmed with barium contrast radiography, there was a series of coordinated, progressive pressure peaks which originated in the cecal body, sequentially involved the cecal base, traversed the cecocolic orifice, and extended into the RVC (0.36 +/- 0.05/min). It seemed that a pacemaker region existed in the cecal body and initiated the important aborally propagated progressive pattern responsible for the transit of ingesta from the cecum to the RVC. A separate mechanism for the transit of gas was not identified. In the RVC, infrequent, nondirectional, low-amplitude segmental pressure peaks (0.12 +/- 0.06/min), and aborally progressive coordinated pressure peaks originating at the beginning of the RVC (0.09 +/- 0.02/min), occurred.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of phenylbutazone, indomethacin, prostaglandin E2, butyrate, and glutamine on restitution of oxidant-injured right dorsal colon of horses in vitro

OBJECTIVE: To study the effects of phenylbutazone, indomethacin, prostaglandin E2 (PGE2), glutamine, and butyrate on restitution of oxidant-injured right dorsal colon of horses in vitro. SAMPLE POPULATION: Right dorsal colon from 9 adult horses euthanatized for reasons other than gastrointestinal tract disease. PROCEDURES: Mucosal segments from the right dorsal colon were injured via exposure to HOCl and incubated in Ussing chambers in solutions containing phenylbutazone, indomethacin, indomethacin and PGE2, glutamine, and butyrate. Transepithelial resistance and mucosal permeability to mannitol were measured, and all mucosal segments were examined histologically. RESULTS: The HOCl-injured mucosa had lower resistance and higher permeability to mannitol, compared with control tissue. Histologic changes were also evident. Resistance of HOCl-injured mucosa recovered partially during the incubation period, and glutamine improved recovery. Phenylbutazone and indomethacin increased resistance, but these increases were not significant. Butyrate and PGE2 had no effects, compared with nontreated HOCl-injured tissues. Mucosal permeability to mannitol was lower in glutamine-treated tissue, compared with nontreated tissue. Histologic changes reflected the resistance and permeability changes. CONCLUSIONS AND CLINICAL RELEVANCE: According to our findings, phenylbutazone and indomethacin do not seem to interfere with restitution of oxidant-injured mucosa of equine colon in vitro, and glutamine could facilitate mucosal restitution.     

Myoelectric activity of the cecum and right ventral colon in female ponies

The myoelectric activity of the cecum and right ventral colon (RVC) was studied in 4 female ponies. Eight, bipolar Ag-AgCl electrodes were sequentially placed on the seromuscular layer of the cecum (6 electrodes) and RVC (2 electrodes), and recordings were begun 14 days after surgery. The myoelectric activity for each pony was recorded during 12, 60-minute recording sessions done during the interdigestive period (3 to 7 hours after the morning feeding). Coordinated series of spike bursts were recognized as independent motility patterns in the cecum and in the RVC. Local haustra-haustra myoelectric activity involving approximately 40 cm of the cecal body (0.45 +/- 0.03 spike bursts/min) were detected. A series of spike bursts started at the cecal apex and progressed to, but stopped at, the caudal cecal base (0.40 +/- 0.03 spike bursts/min). Infrequently, a series of spike bursts started at the apex and progressed to the cranial cecal base (0.09 +/- 0.01 spike bursts/min). More commonly, a series of spike bursts with a conduction velocity of 3.8 +/- 0.07 cm/s, began in the cranial base and progressed orally to the cecal apex (0.46 +/- 0.03 spike bursts/min). Spike bursts conducted aborally (propulsion) beginning at the origin of the RVC (0.05 +/- 0.007 spike bursts/min) and spike bursts conducted orally (retropulsion; 0.15 +/- 0.02 spike bursts/min) were seen independent of cecal myoelectric activity. A progressive series of coordinated spike bursts, which began at the cecal apex, were conducted through the cecolic orifice and continued into the RVC (0.42 +/- 0.02 spike bursts/min), representing the only pattern common to the cecum and RVC.(ABSTRACT TRUNCATED AT 250 WORDS)     

Absorption and pharmacokinetics of phenylbutazone in Welsh Mountain ponies

The disposition of phenylbutazone (4.4 mg/kg), administered intravenously to six Welsh Mountain ponies, was described by a two-compartment open model. Pharmacokinetic parameters were not significantly different after morning dosing in comparison with afternoon dosing. When phenylbutazone (4.4 mg/kg) was administered orally to the same ponies, marked variations in time to peak concentrations were produced with different feeding schedules. When access to hay was permitted before and after dosing, the mean time to peak concentration was 13.2 +/- 1.2 h and double peaks in the plasma concentration-time curve were common. Double peaks were also encountered when phenylbutazone was given to ponies deprived of food prior to, and allowed access to hay after, dosing. In this circumstance, mean times to peak concentration were much shorter (3.8 +/- 1.3 h after morning dosing and 5.3 +/- 1.5 h followed afternoon dosing). Absorption was more regular and double peaks were less apparent when food was withheld both before and after dosing. In order to explain these findings, it is tentatively postulated that, whereas some of the administered dose of phenylbutazone may be absorbed quickly, some may become adsorbed on to the feed and subsequently released by fermentative digestion in the large intestine and/or caecum. The consequences of delayed absorption in fed animals for toxicity and clinical efficacy, and for the use of phenylbutazone in equestrian sports, are considered. Delayed absorption in ponies given access to hay was not accompanied by a significant reduction in total absorption. Bioavailability was estimated to be approximately 69% in fed and 78% in unfed ponies. Estimates of bioavailability gave similar values for morning (72%) and afternoon (71%) dosing.     

Effects of phenylbutazone on thiamylal disposition and anaesthesia in ponies

Phenylbutazone given during the perisurgical period has been reported to increase the intensity and duration of thiamylal anaesthesia in horses. A possible mechanism of competitive plasma protein binding has been suggested. The purpose of the present study was to experimentally reproduce the phenomenon of increased intensity and/or duration of thiamylal anaesthesia and to determine if there is competitive displacement of plasma protein bound thiamylal by phenylbutazone. Six ponies each received one of three treatments, 11 mg/kg intravenous (i.v.) thiamylal; 8.8 mg/kg i.v. phenylbutazone; and 11 mg/kg i.v. thiamylal with 8.8 mg/kg i.v. phenylbutazone given 9 min later. Thirteen blood samples were collected from 0 time through 600 min following drug administration and plasma drug concentrations quantified by high performance liquid chromatography. The pharmacokinetics of thiamylal and phenylbutazone were best described by three- and two-compartment models, respectively. There were no significant differences in pharmacokinetic parameters for thiamylal in the presence of phenylbutazone. However, there were differences in phenylbutazone pharmacokinetics when preceded by thiamylal administration. Unbound phenylbutazone concentrations were increased at 171, 231 and 351 min when given with thiamylal, accompanied by decreases in per cent bound phenylbutazone (P < 0.05). There were also significant (P < 0.05) changes in per cent plasma protein binding of thiamylal and phenylbutazone between 120 and 360 min, when in combination. No changes in intensity or duration of anaesthesia were observed.     

Experimentally induced phenylbutazone toxicosis in ponies: description of the syndrome and its prevention with synthetic prostaglandin E2

Phenylbutazone (PBZ) toxicosis was induced in 9 ponies to further define the clinical and pathologic changes occurring with this syndrome. Six additional ponies were treated with PBZ and a synthetic prostaglandin E2 to determine the role of prostaglandins in the pathogenesis of PBZ toxicosis. Ponies given only PBZ exhibited CNS depression, anorexia, weight loss, diarrhea, cyanotic mucous membranes, and oral ulcers. Total serum protein concentration gradually decreased during the 10-day treatment period. Marked mucosal atrophy, focal erosions, and ulcers characterized the lesions in the alimentary tract. Ponies given PBZ and prostaglandin E2 remained clinically healthy and did not develop hypoproteinemia or mucosal atrophy. A few erosions were seen, but ulcers were not observed. The results of the present study indicate that mucosal atrophy is a characteristic lesion of PBZ toxicosis. It is also evident that inhibition of prostaglandin synthesis has an important role in the development of this syndrome.     

Diagnosis and surgical treatment of functional obstruction of the right dorsal colon in a horse

Functional obstruction of the right dorsal colon was found at surgery in a 6-year-old American Saddlebred gelding with a history of anorexia, depression, weight loss, and intermittent colic. Side-to-side anastomosis of the right dorsal colon to the small colon was done to bypass the obstruction. Histopathologic findings of the right dorsal colon and regional colonic lymph nodes were unremarkable. Surgical treatment was successful.     

In vitro investigation of the effects of cyclooxygenase-2 inhibitors on contractile activity of the equine dorsal and ventral colon

OBJECTIVE: To evaluate the effect of 2 cyclooxygenase (COX)-2 inhibitors on contractile activity of the circular smooth muscle layer of the equine dorsal and ventral colon. SAMPLE POPULATION: Samples of the dorsal and ventral colon obtained from 10 healthy horses. PROCEDURE: Full-thickness tissue samples were collected from the dorsal colon in the area of the diaphragmatic flexure and the ventral colon in the area of the sternal flexure. Samples were cut into strips oriented along the fibers of the circular muscle layer and mounted in a tissue bath system for determination of contractile strength. Incremental amounts of etodolac, nabumetone, and indomethacin were added, and contractile activity was recorded. RESULTS: Response of the dorsal and ventral colon to nonsteroidal anti-inflammatory drugs (NSAIDs) was variable. Indomethacin induced the greatest reduction in contractile activity, followed by nabumetone. For etodolac, the difference from baseline values was only significantly reduced at the highest concentration used (1 X 10(5)M) for the ventral colon. CONCLUSIONS AND CLINICAL RELEVANCE: The NSAIDs that are designed to target the COX-2 isoform appeared to have variable effects on the contractile activity of the equine dorsal and ventral colon. Etodolac appeared to have the least effect on contractile activity, compared with the effects attributable to nabumetone, and would potentially have the fewest adverse effects relative to motility of the dorsal and ventral colon.     

Effects of acetylcysteine and migration of resident eosinophils in an in vitro model of mucosal injury and restitution in equine right dorsal colon

OBJECTIVES: To evaluate the in vitro protective effects of acetylcysteine and response of resident mucosal eosinophils in oxidant-induced injury to tissues of right dorsal colon of horses. ANIMALS: 9 adult horses. PROCEDURE: Gastrointestinal mucosa was damaged in vitro with 3 mM hypochlorous acid (HOCl), with and without prior exposure to 6mM acetylcysteine. Control tissues were not exposed to HOCl or acetylcysteine. Control and damaged tissues were incubated in Krebs-Ringer-bicarbonate solution and tissue resistance measured during 240 minutes. Tissue permeability to radiolabeled mannitol was also used to assess mucosal barrier integrity. Tissues were examined by light microscopy before and after HOCl exposure and during and after incubation. RESULTS: Exposure to HOCl caused tissue damage and decreased tissue resistance. Restitution did occur during the incubation period. Eosinophils were located near the muscularis mucosae in freshly harvested tissues and migrated towards the luminal surface in response to HOCl-induced injury. Compared with tissues treated with HOCl without acetylcysteine, pretreatment with acetylcysteine prevented HOCl-induced tissue damage, changes in resistance, and histologically detectable eosinophil migration. The permeability to mannitol increased to the same extent in tissues treated with HOCl alone or with acetylcysteine and HOCl. CONCLUSIONS AND CLINICAL RELEVANCE: Eosinophils migrated toward the mucosal surface in equine colon in response to oxidant-induced damage in vitro. This novel finding could be relevant to inflammation in equine colon and a pathophysiologic feature of many colonic diseases. Acetylcysteine protected the mucosa against oxidant-induced injury and may be useful as a treatment option for various gastrointestinal tract disorders in horses.     

In vitro transport of L-alanine by equine cecal mucosa

When sheets of mucosa from the cecum of clinically normal horses were incubated in vitro with radiolabeled L-alanine, they could accumulate this amino acid against an apparent concentration gradient after 60 to 150 minutes of incubation. The active transport system for L-alanine was on the serosal surface of the mucosal sheet only. L-Alanine accumulation at 60 minutes was partly inhibited by 20 mM glycine (P less than 0.01), 0.5 mM ouabain (P less than 0.05), and Na deprivation (P less than 0.02). Anoxia for 60 minutes increased L-alanine accumulation, but had adverse effects on cell structure and intracellular cation distributions. Transmucosal fluxes induced a small, but significant (P less than 0.05), net secretion of L-alanine, and the mean (+/- SEM) transmucosal potential difference was 7.3 +/- 0.7 mV over the period of flux measurement. It was concluded that L-alanine was accumulated by the serosal surface of the cecal mucosa, possibly to provide substrate for tissue metabolism. There was no evidence that the cecal mucosa could actively transport this amino acid from the luminal bathing medium.     

In vitro transport of cycloleucine by equine cecal mucosa

Mucosa obtained from the cecum of healthy horses and incubated in vitro with 0.1 mM cycloleucine could accumulate this amino acid against an apparent concentration gradient after 60 and 120 minutes. Accumulation by the serosal (antiluminal) surface of the tissue was 3 times greater than accumulation by the mucosal (luminal) surface after 120 minutes (P less than 0.001). Cycloleucine accumulation was significantly reduced by Na deprivation after 60 minutes (P less than 0.05) and 120 minutes (P less than 0.01) and by anoxic conditions after 120 minutes (P less than 0.05). Transmucosal flux from mucosal to serosal surface of the tissue was significantly (P less than 0.05) greater than the opposing flux, but both unidirectional fluxes were small and were largely attributed to passive processes. It was concluded that the most avid transport system for cycloleucine was on the serosal surface of the horse's cecal mucosa, and an active transport system was not evident on the mucosal surface. An active transport system for amino acids on the serosal surface could be explained by the need for crypt cells, the predominant epithelial cell type in the cecum, to obtain nutrients from blood, rather than from the intestinal lumen.     

In vitro and in vivo binding of phenylbutazone and related drugs to equine feeds and digesta

In vitro and in vivo studies of phenylbutazone binding to equine ingesta and digesta were undertaken. In vitro binding to chopped hay and powdered pony nuts in buffer solutions at 37 degrees C was found to be time-, concentration- and pH-dependent. Percentage binding generally increased with time, decreased with concentration and varied with buffer pH in an unpredictable manner. Other non-steroidal anti-inflammatory drugs (NSAIDs) also bound to hay, the degree of binding being less for meclofenamate and least for flunixin in comparison with phenylbutazone. Phenylbutazone became bound to digesta collected from eight regions of the gastrointestinal tract when they were spiked with a concentration of 1 mg.10 g-1 digesta, the amounts ranging from 80.0 per cent (duodenum) to 99.6 per cent (stomach). Binding also occurred to equine digesta following the oral administration of phenylbutazone (4.4 mg.kg-1) to three ponies. It was concluded that drug uptake by and release from equine ingesta and digesta were probably adsorptive and desorptive processes. The clinical significance of the findings for the use of NSAIDs in equine medicine was considered.     

Effects of xylazine and/or butorphanol or neostigmine on myoelectric activity of the cecum and right ventral colon in female ponies

Effects of xylazine HCl (0.5 mg/kg of body weight, IV) and/or butorphanol tartrate (0.04 mg/kg, IV) or neostigmine methylsulfate (0.022 mg/kg, IV) on myoelectric activity of the cecum and right ventral colon were studied in 4 conscious female ponies. Eight bipolar Ag/AgCl electrodes were sequentially placed on the seromuscular layer of the cecum (6 electrodes) and right ventral colon (2 electrodes). Recordings began 30 minutes before and continued for 90 minutes after drug administration. Each drug or drug combination was studied on 2 occasions in each pony. Two major patterns of coordinated spike bursts were identified. A series of coordinated spike bursts began at the cecal base and was conducted to the cecal apex (pattern I). A series of coordinated spike bursts began at the cecal apex, traversed the cecum, cecocolic orifice, and right ventral colon and was termed a progressive pattern (pattern II). Xylazine administration caused a significant decrease in patterns I and II for 20 minutes (P less than 0.05). Butorphanol tartrate administration caused a significant decrease in the progressive pattern for 10 minutes (P less than 0.05) without affecting the orally directed pattern. Administration of the combination of xylazine/butorphanol significantly decreased the frequency of pattern I for 40 minutes (P less than 0.05) and pattern II for 30 minutes (P less than 0.05). Neostigmine administration caused a significant increase in the frequency of pattern II for 30 minutes (P less than 0.05) without affecting pattern I (P greater than 0.05). Changes in conduction velocity of pattern I or II or the duration of spiking activity were not significantly different because of any treatment.     

In vitro and in vivo effects of corticosteroids on peripheral blood lymphocytes from ponies.

The in vitro and in vivo effects of corticosteroids on peripheral blood lymphocytes (PBL) from ponies were studied. Prednisolone inhibited lymphocyte stimulation by phytohemagglutin (PHA) in a dose-dependent manner, without inducing lysis even at large doses. The PBL from horses heterozygous for the combined immunodeficiency trait responded to corticosteroid treatment the same as did PBL from normal ponies. Removal of the corticosteroid after incubation with PBL from normal ponies partially restored responsiveness of these cells to PHA. Chronic in vivo treatment of ponies with corticosteroids caused a marked decrease in the absolute numbers of circulating lymphocytes. Most remaining lymphocytes had detectable surface immunoglobulin and C3 receptors, suggesting a greater decrease in the T-lymphocyte population. In spite of this, there was little change in the in vitro PHA- or keyhole limpet hemocyanin-sensitized ponies. In general, the corticosteroid effects of lysis, as well as the mitogenic and antigenic responses of PBL from ponies, were similar to those previously reported for human lymphocytes.     

Myoelectric activity of the ileum, cecum, and right ventral colon in ponies during interdigestive, nonfeeding, and digestive periods

Myoelectric activity of the ileum, cecum, and right ventral colon (RVC) was studied in 4 mature ponies. Eight Ag-AgCl bipolar recording electrodes were sutured to the seromuscular layer of the ileum (2 electrodes), cecum (4 electrodes), and RVC (2 electrodes). Myoelectric activity was studied beginning 10 days after surgery. Eight, 60-minute recording sessions were performed in each pony during the interdigestive period, which was the period 3 to 7 hours after the morning feeding. On separate days, food was withheld for 24 hours, and 90-minute recordings were obtained during the nonfeeding period. Ponies were then fed a normal ration, and recordings were continued to obtain data for the digestive (feeding) period. All phases of the migrating myoelectric complex were seen at both ileal electrodes during the interdigestive period, including the periods of no spiking activity (phase 1), irregular spiking activity (phase 2), and regular spiking activity (phase 3). Phase 2 occupied 77% of the total recording time, and the mean duration of phases 1, 2, and 3 was 3.4 +/- 0.2, 12.8 +/- 1.2, and 6.7 +/- 0.7 min, respectively. Frequency of ileal slow waves was 11.8 +/- 0.1/min, and spike burst conduction velocity was 4.7 +/- 0.3 cm/s. A complete migrating myoelectric complex was seen in 11 of 32 tracings (34%) and had a mean duration of 24.2 +/- 2.6 min. The ileal migrating action potential complex, most often seen in phase 2, had a frequency of 4.8 +/- 0.5 spike bursts/h and a conduction velocity of 13.6 +/- 0.4 cm/s.(ABSTRACT TRUNCATED AT 250 WORDS)     

In vitro investigation of the effect of prostaglandins and nonsteroidal anti-inflammatory drugs on contractile activity of the equine smooth muscle of the dorsal colon, ventral colon, and pelvic flexure

OBJECTIVES: To determine the in vitro effect of prostaglandin E2 (PGE2), PGF2alpha, PGI2; and nonsteroidal anti-inflammatory drugs (NSAID; ie, flunixin meglumine, ketoprofen, carprofen, and phenylbutazone) on contractile activity of the equine dorsal colon, ventral colon, and pelvic flexure circular and longitudinal smooth muscle. ANIMALS: 26 healthy horses. PROCEDURE: Tissue collected from the ventral colon, dorsal colon, and pelvic flexure was cut into strips and mounted in a tissue bath system where contractile strength was determined. Incremental doses of PGE2, PGF2alpha,, PGI2, flunixin meglumine, carprofen, ketoprofen, and phenylbutazone were added to the baths, and the contractile activity was recorded for each location and orientation of smooth muscle. RESULTS: In substance P-stimulated tissues, PGE2 and PGF2alpha enhanced contractility in the longitudinal smooth muscle with a decrease or no effect on circular smooth muscle activity. Prostaglandin I2 inhibited the circular smooth muscle response with no effect on the longitudinal muscle. The activity of NSAID was predominantly inhibitory regardless of location or muscle orientation. CONCLUSIONS AND CLINICAL RELEVANCE: In the equine large intestine, exogenous prostaglandins had a variable effect on contractile activity, depending on the location in the colon and orientation of the smooth muscle. The administration of NSAID inhibited contractility, with flunixin meglumine generally inducing the most profound inhibition relative to the other NSAID evaluated in substance P-stimulated smooth muscle of the large intestine. The results of this study indicate that prolonged use of NSAID may potentially predispose horses to develop gastrointestinal tract stasis and subsequent impaction.     

In vitro study of neutrophil apoptosis in dogs

In the present study, to investigate the apoptosis of the polymorphonuclear neutrophil (PMN) from healthy dogs, we carried out TUNEL assay and DNA analysis by electrophoresis on dog PMNs. The TUNEL assay indicated that apoptotic PMNs in dogs were 0.15+/-5% before incubation, 0.3+/-5% at 4h incubation, 1+/-6% at 8h, 9+/-4% at 12h and 28+/-5% at 24h, respectively. The ladder formation was much more clearly observed in DNA from PMNs after 24h incubation at 37 degrees C than that before incubation. The results in this study indicated that healthy dog PMNs undergo apoptosis spontaneously within hours to days, and that the apoptosis of PMNs might be related to the high turnover of these circulating cells in dogs.     

Serum gamma glutamyl transferase activity in horses with right or left dorsal displacements of the large colon

The purpose of this study was to test the hypothesis that horses with right dorsal displacement of the large colon (RDDLC) have elevations in serum gamma glutamyl transferase (GGT) activity when compared with horses with left dorsal displacement of the large colon (LDDLC). Medical records from 37 horses with RDDLC and 48 horses with LDDLC were reviewed. Horses were included for study if the RDDLC or LDDLC was confirmed by exploratory laparotomy or postmortem examination and if a serum GGT measurement was obtained within 24 hours before surgery. The proportion of horses with GGT activity within or above the reference range was determined. Of 37 horses, 18 (49%; exact binomial 95% confidence interval, 32-66%) with RDDLC and, of 48 horses, 1 (2%; 95% CI, 0-11%) with LDDLC had GGT above the reference range. Horses with RDDLC had higher serum GGT than did horses with LDDLC. Of 37 horses, 36 (97%) with RDDLC were discharged with a good prognosis and none returned as a result of hepatic disease. Evaluation of surgical and postmortem examinations revealed that positioning of the colon in horses with RDDLC results in compression of the bile duct, which can cause extrahepatic bile duct obstruction and a subsequent elevation in serum GGT activity.