Case Report Rapport de cas Chronic active interstitial pancreatitis as a cause of transverse colonic obstruction and colic in a horse Katharina L. Lohmann, Andrew L. Allen Abstract — A mature Quarter horse was euthanized following colic of 3 days duration. Postmortem, the large intestine, except the descending colon, was diffusely distended and associated with adhesion of the transverse colon to the pancreas, which had changes consistent with chronic active interstitial pancreatitis. Other lesions included hepatic fibrosis, erosive gastritis, and bilateral adrenal cortical hyperplasia. Résumé — Pancréatite interstitielle chronique active comme cause d’une obstruction du côlon transversal et de coliques chez un cheval. Un cheval Quarter horse adulte a été euthanasié après des coliques d’une durée de 3 jours. À l’autopsie, il a été observé que le gros intestin, sauf le côlon descendant, présentait une distension diffuse et était associé à l’adhésion du côlon transversal au pancréas qui indiquait des changements conformes à une pancréatite interstitielle chronique active. Les autres lésions incluaient une fibrose hépatique, une gastrite érosive et une hyperplasie corticale bilatérale des surrénales. Can Vet J 2015;56:1177–1180
“C
olic” is a nonspecific term used to refer to abdominal pain and represents a common, but potentially serious medical condition in horses. Pancreatic disease, including pancreatitis, is thought to be rare in horses (1–3) and a previous study of pancreatitis in horses, diagnosed postmortem, described 3 types based on chronicity of the disease: acute, active chronic, and chronic (3). The evidence of pancreatitis used in that study included lesions associated with autodigestion, including necrosis of the pancreatic parenchyma and associated fat, replacement fibrosis, and varying degrees of inflammation. An apparently even less common form of pancreatitis, in horses and other mammals, is chronic interstitial pancreatitis in which fibrous tissue expands the interlobular stroma and subdivides many of the lobules (4). The purpose of this article is twofold: to describe and illustrate previously unrecognized or unreported lesions in the pancreas of a horse diagnosed with chronic active interstitial pancreatitis; and to advise equine veterinary practitioners and veterinary pathologists that, in contrast to current opinion, complications associated with chronic pancreatitis may have clinical significance in horses, such as the intestinal obstruction and signs of colic reported here.
Case description On the advice of a referring veterinary practitioner, the owners of a 13-year-old, 530 kg, castrated male (gelding), Quarter horse presented the animal to the Veterinary Medical Centre (VMC)
(Traduit par Isabelle Vallières)
of the Western College of Veterinary Medicine (WCVM) for assistance because the gelding had been intermittently colicky for 3 d. The horse had also stopped eating, drinking, and passing feces, and had refluxed many liters of red to brown fluid, mixed with feed material, from the stomach when a nasogastric tube was placed. Blood work prior to referral supported the clinical diagnosis of dehydration [hematocrit (HCT) = 55.7%; reference interval (RI): 32.0 to 50.0% and blood urea nitrogen (BUN) = 14.3 mmol/L; RI: 2.5 to 8.9 mmol/L], and also revealed markedly elevated gamma glutamyl transferase activity (171 U/L; RI: 5 to 24 U/L) indicative of cholestasis, biliary hyperplasia, or both; and markedly elevated aspartate aminotransferase activity (1562 U/L; RI: 175 to 340 U/L) suggestive of hepatocellular injury, in light of a moderate elevation in creatine kinase activity (850 U/L; RI: 120 to 470 U/L). Treatment had consisted of the administration of butylscopolamine, an abdominal specific antispasmotic, intravenous fluids, and immediately prior to referral, flunixin meglumine, a non-steroidal antiinflammatory drug with analgesic and antipyretic properties. The owners had cared for the horse since birth and they reported that he had no previous episodes of colic or other known disease, no prior abdominal surgery, and was not currently receiving any medications. On admission to the VMC after regular business hours, the horse exhibited clinical signs of moderately severe colic, which included looking at its abdomen, pawing, and attempting to
Department of Large Animal Clinical Sciences (Lohmann) and Department of Veterinary Pathology (Allen), Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4. Address all correspondence to Dr. Andrew Allen; [email protected] Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office ([email protected]) for additional copies or permission to use this material elsewhere. CVJ / VOL 56 / NOVEMBER 2015
1177
R A P P O R T D E CA S
Figure 1. The pancreas and stomach of a 13-year-old Quarter horse. A — The pancreas was 30 cm long 3 20 cm wide 3 5 cm thick, very firm, and pale. B — The pancreas was composed of prominent, 1- to 2-cm lobules. C — The squamous portion of the gastric mucosa, surrounding the cardia (center of the image), contained many, small, coalescing to confluent, red, depressed foci, interpreted as erosions, ulcers, or both. The pylorus is visible at the top of the image and many mature larvae (bots) of Gasterophilus spp. are visible at the right of the image. D — The pale nodules are islands of surviving, squamous, gastric mucosa.
lay down during examination. The horse’s heart rate varied between 70 and 80 beats/min, the oral mucous membranes were hyperemic, and the capillary refill time was . 2 s. A large volume (19 L) of reflux was obtained following nasogastric intubation. The horse received many liters of intravenous fluid and various medications were administered in an attempt to alleviate the clinical signs, including: butorphanol, an opioid analgesic; detomidine, a sedative and analgesic; flunixin meglumine; and xylazine, a sedative, analgesic, and muscle relaxant. These medications and continued refluxing via a nasogastric tube provided temporary relief but, approximately 7 h after being admitted to the VMC, the horse became refractory. Rectal examinations at the time of admission and again 4 h later revealed an increasingly distended large colon of undetermined cause, although colonic displacement or torsion were differential diagnoses. Feces were never detected within the rectum. Transabdominal ultrasonographic examination revealed normal small intestinal appearance and motility. At 6:30 am, about 60 to 70 h after first becoming colicky, and about 10 h after being admitted to the VMC, the horse was euthanized because of an inability to control its pain and because the owners did not wish to pursue surgical exploration of the abdomen. The gelding was then submitted to Prairie Diagnostic Services, within the WCVM, for postmortem examination. A 1178
necropsy was performed about 6 h after the horse was euthanized. The large intestine, except the descending colon, was diffusely distended by gas and ingested fibrous plant material. The most aborad, approximately 2.5 m of the descending colon were nearly empty. A segment of orad colon, interpreted to be the transverse colon, was strongly adhered to a firm, 30 cm long 3 20 cm wide 3 5 cm thick mass, located in the dorsal abdomen, just cranial to the kidneys and slightly to the left of the sagittal midline. The mass was later identified as the pancreas, and was diffusely very firm, pale- or cream-colored, and composed of prominent 1 to 2 cm lobules (Figures 1A and 1B). There was no evidence of large colon displacement or torsion. The liver was in its normal location and appeared to be normal in size and shape, but had an abnormal dull or olive green hue and was firmer and tougher than normal. The squamous portion of the gastric mucosa, surrounding the cardia, contained many, small (a few millimeters to a few centimeters) coalescing to confluent, red, depressed foci, interpreted as erosions, ulcers, or both (Figures 1C and 1D). The cortices of both adrenal glands were diffusely 5- to 6-mm thick while the medullae were typically 3- to 4-mm thick, a change interpreted to represent diffuse adrenal cortical hyperplasia (Figure 2A). Histologically, the pancreas contained a moderately increased amount of interlobular fibrous tissue infiltrated with mild CVJ / VOL 56 / NOVEMBER 2015
CA S E R E P O R T
Figure 2. The histologic appearance of the adrenal glands, pancreas and liver of a 13-year-old Quarter horse. A — The cortex of the right and left adrenal gland was diffusely hyperplastic, i.e., more than twice the thickness of each medulla. Hematoxylin and eosin. B — There was a moderately increased amount of interlobular fibrous tissue within the pancreas. Masson’s Trichrome. C — The interlobular fibrous tissue (center of image) of the pancreas contained moderate numbers of inflammatory cells; mostly neutrophils. Hematoxylin and eosin. D — There was a moderate degree of periportal and perilobular fibrosis and associated bile duct hyperplasia within the liver. Masson’s Trichrome.
to moderate numbers of inflammatory cells that included mostly neutrophils, with fewer lymphocytes and plasma cells (Figures 2B and 2C). The architecture of the pancreatic parenchyma was also abnormal. While a few recognizable acini were present, most exocrine pancreatic cells were haphazardly arranged and composed of irregular and attenuated exocrine cells. Some exocrine cells appeared to be missing, leaving behind a space that was partially filled with fine strands of fibrous tissue. None of the remaining exocrine cells had a normal appearance, i.e., they lacked basophilia with apical eosinophilia. Islets were present in normal numbers, but also appeared to be missing a moderate proportion of cells. The liver also contained a moderate degree of fibrosis around the periportal and perilobular areas that nearly surrounded the lobule in some locations, suggestive of biliary fibrosis (Figure 2D). Associated with the fibrosis was a moderate degree of bile duct hyperplasia. Within each hepatic lobule were small CVJ / VOL 56 / NOVEMBER 2015
globules or “lakes” of homogeneous, orange to golden, extracellular material, interpreted to be bile, and to represent bile stasis. Bacterial cultures were performed on the pancreas, liver, and contents of the duodenum and moderate to large numbers of Streptococcus zooepidemicus and Escherichia coli were isolated from the duodenum and liver, while moderate to large numbers of S. zooepidemicus, E. coli, and an Enterococcus species were isolated from the pancreas.
Discussion There appears to be a limited body of literature concerning pancreatitis in the horse and much of this literature describes acute pancreatitis. Descriptions of chronic pancreatitis in the horse appear in popular textbooks on veterinary pathology (4,5), although only 1 of these textbooks describes interstitial pancreatitis (4). These descriptions suggest that chronic pancreatitis in the horse has not, typically, been associated with clinically 1179
R A P P O R T D E CA S
apparent disease. A common cause of chronic pancreatitis in the horse, and other domestic animals, is believed to be the ascension of intestinal contents, including bacteria, through the pancreatic duct (3–5). In the horse, the pancreatic duct and bile duct merge prior to connecting with the duodenum as the major duodenal papilla (6). Although circumstantial, the presence of periportal, or biliary, hepatic fibrosis and bile duct hyperplasia, as well as the isolation of the same bacteria from the pancreas, liver, and duodenum provides evidence that intestinal contents, including bacteria, likely entered both the pancreatic duct and bile duct via the major duodenal papilla. In the horse described here, the chronic active interstitial pancreatitis was associated with a relatively large area of adhesion to the transverse colon. The postmortem findings suggest that this adhesion was the origin of the obstruction and the clinical signs of colic. Specifically, the approximately 2.5 m of descending colon aborad to the site of adhesion to the pancreas were nearly empty while the remainder of the large intestine, orad to the pancreas, was markedly distended with fibrous ingesta and gas. In overviews of intestinal obstruction in humans (7) and horses (8,9), it has been common to categorize the causes as either mechanical or functional. Mechanical causes include any luminal or extraluminal lesion that physically narrows or occludes the intestine. Functional obstruction, also referred to as pseudo-obstruction, adynamic ileus or, simply, ileus, are terms used to describe the impairment of the aborad transit of intestinal contents in the absence of a grossly detectably abnormality (9). Therefore, adhesions of the intestines are categorized as mechanical obstructions (7,8). When these adhesions result in the entrapment of loops of intestine, the pathophysiology of the obstruction is obvious. However, in the absence of an appreciable physical or mechanical cause of the blockage, as in this horse, the pathophysiology of the obstruction is less clear. In this horse, it is possible that the firm texture of the pancreas that nearly surrounded the transverse colon (see the tip of the pancreas at the left of Figure 1A) caused a physical narrowing of the lumen. However, it is also interesting to speculate that the presence of inflammation within the pancreas, which was directly apposed to the transverse colon, might have interfered with normal functioning and contributed to a functional obstruction (10). Although secondary in nature, the changes noted in the stomach and both adrenal glands of this horse are worthy of comment. Histologically, the non-glandular stomach con-
1180
tained multiple, often coalescing to confluent, areas of erosion and underlying inflammation, particularly around the cardia. There are several known risk factors for gastric erosion and ulceration in horses (11,12), a few of which were present in this horse, including anorexia, the administration of a non-steroidal anti-inflammatory drug, reflux of duodenal contents and, very likely, stress. Further evidence that this horse had experienced stress was the presence of diffuse cortical hyperplasia of both adrenal glands. While intuitive, changes to the adrenal cortices in association with stress have been demonstrated in laboratory animals (13,14). CVJ
References 1. Johnson PJ, Wiedmeyer CE, Messer NT. Conditions of the equine pancreas. Equine Vet Educ 2009;21:26–29. 2. Newman SJ. Equine pancreatic disease: A review and characterization of the lesions of four cases (2005–2014). J Vet Diagn Invest 2015; 27:92–96. 3. Yamout SZ, Nieto JE, Anderson J, De Cock HE, Vapniarsky N, Aleman M. Pathological evidence of pancreatitis in 43 horses (1986–2011). Equine Vet J 2012;43:45–50. 4. Charles JA. Pancreas. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. 5th ed. Vol 2. Toronto, Ontario: Saunders Elsevier, 2007:389–424. 5. Cullen JM, Brown DL. Hepatobiliary system and exocrine pancreas. In: Zachary JF, McGavin MD, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, Missouri: Elsevier Mosby, 2012:405–457. 6. Nickel R, Schummer A, Seiferle E. The Viscera of the Domestic Mammals. 2nd ed. New York, New York: Springer-Verlag, 1979:99–122; 180–203. 7. Liu C, Crawford JM. The gastrointestinal tract. In: Kurar V, Abbas AK, Fausto N, eds. Robbins and Cotran Pathologic Basis of Disease. 7th ed. Philadelphia, Pennsylvania: Saunders Elsevier, 2005:797–875. 8. Fubini SL. Abdominal adhesions. In: Mair T, Divers T, Ducharme N, eds. Manual of Equine Gastroenterology. Philadelphia, Pennsylvania: Saunders, 2002:209–211. 9. Rakestraw P. Ileus. In: Mair T, Divers T, Ducharme N, eds. Manual of Equine Gastroenterology. Philadelphia, Pennsylvania: Saunders, 2002:211–215. 10. Koenig J, Cote N. Equine gastrointestinal motility — Ileus and pharmacological modification. Can Vet J 2006;47:551–559. 11. Brown CC, Baker DC, Barker IK. Alimentary system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. 5th ed. Vol 2. Toronto, Ontario: Saunders Elsevier, 2007:1–296. 12. Videla R, Andrews FM. New perspectives in equine gastric ulcer syndrome. Vet Clin North Am Equine Pract 2009;25:283–301. 13. Kapitonova MY, Kuznetsov SL, Khlebnikov VV, Zagrebin VL, Morozova ZCh, Degtyar YV. Immunohistochemical characteristic of the hypophysis in normal conditions and chronic stress. Neurosci Behave Physiol 2010;40:97–102. 14. Ulrich-Lai YM, Figueiredo HF, Ostrander MM, Choi DC, Engeland WC, Herman JP. Chronic stress induces adrenal hyperplasia and hypertrophy in a subregion-specific manner. Am J Physiol Endocrinol Metab 2006;291:E965–E973.
CVJ / VOL 56 / NOVEMBER 2015
“C
olic” is a nonspecific term used to refer to abdominal pain and represents a common, but potentially serious medical condition in horses. Pancreatic disease, including pancreatitis, is thought to be rare in horses (1–3) and a previous study of pancreatitis in horses, diagnosed postmortem, described 3 types based on chronicity of the disease: acute, active chronic, and chronic (3). The evidence of pancreatitis used in that study included lesions associated with autodigestion, including necrosis of the pancreatic parenchyma and associated fat, replacement fibrosis, and varying degrees of inflammation. An apparently even less common form of pancreatitis, in horses and other mammals, is chronic interstitial pancreatitis in which fibrous tissue expands the interlobular stroma and subdivides many of the lobules (4). The purpose of this article is twofold: to describe and illustrate previously unrecognized or unreported lesions in the pancreas of a horse diagnosed with chronic active interstitial pancreatitis; and to advise equine veterinary practitioners and veterinary pathologists that, in contrast to current opinion, complications associated with chronic pancreatitis may have clinical significance in horses, such as the intestinal obstruction and signs of colic reported here.
Case description On the advice of a referring veterinary practitioner, the owners of a 13-year-old, 530 kg, castrated male (gelding), Quarter horse presented the animal to the Veterinary Medical Centre (VMC)
(Traduit par Isabelle Vallières)
of the Western College of Veterinary Medicine (WCVM) for assistance because the gelding had been intermittently colicky for 3 d. The horse had also stopped eating, drinking, and passing feces, and had refluxed many liters of red to brown fluid, mixed with feed material, from the stomach when a nasogastric tube was placed. Blood work prior to referral supported the clinical diagnosis of dehydration [hematocrit (HCT) = 55.7%; reference interval (RI): 32.0 to 50.0% and blood urea nitrogen (BUN) = 14.3 mmol/L; RI: 2.5 to 8.9 mmol/L], and also revealed markedly elevated gamma glutamyl transferase activity (171 U/L; RI: 5 to 24 U/L) indicative of cholestasis, biliary hyperplasia, or both; and markedly elevated aspartate aminotransferase activity (1562 U/L; RI: 175 to 340 U/L) suggestive of hepatocellular injury, in light of a moderate elevation in creatine kinase activity (850 U/L; RI: 120 to 470 U/L). Treatment had consisted of the administration of butylscopolamine, an abdominal specific antispasmotic, intravenous fluids, and immediately prior to referral, flunixin meglumine, a non-steroidal antiinflammatory drug with analgesic and antipyretic properties. The owners had cared for the horse since birth and they reported that he had no previous episodes of colic or other known disease, no prior abdominal surgery, and was not currently receiving any medications. On admission to the VMC after regular business hours, the horse exhibited clinical signs of moderately severe colic, which included looking at its abdomen, pawing, and attempting to
Department of Large Animal Clinical Sciences (Lohmann) and Department of Veterinary Pathology (Allen), Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4. Address all correspondence to Dr. Andrew Allen; [email protected] Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office ([email protected]) for additional copies or permission to use this material elsewhere. CVJ / VOL 56 / NOVEMBER 2015
1177
R A P P O R T D E CA S
Figure 1. The pancreas and stomach of a 13-year-old Quarter horse. A — The pancreas was 30 cm long 3 20 cm wide 3 5 cm thick, very firm, and pale. B — The pancreas was composed of prominent, 1- to 2-cm lobules. C — The squamous portion of the gastric mucosa, surrounding the cardia (center of the image), contained many, small, coalescing to confluent, red, depressed foci, interpreted as erosions, ulcers, or both. The pylorus is visible at the top of the image and many mature larvae (bots) of Gasterophilus spp. are visible at the right of the image. D — The pale nodules are islands of surviving, squamous, gastric mucosa.
lay down during examination. The horse’s heart rate varied between 70 and 80 beats/min, the oral mucous membranes were hyperemic, and the capillary refill time was . 2 s. A large volume (19 L) of reflux was obtained following nasogastric intubation. The horse received many liters of intravenous fluid and various medications were administered in an attempt to alleviate the clinical signs, including: butorphanol, an opioid analgesic; detomidine, a sedative and analgesic; flunixin meglumine; and xylazine, a sedative, analgesic, and muscle relaxant. These medications and continued refluxing via a nasogastric tube provided temporary relief but, approximately 7 h after being admitted to the VMC, the horse became refractory. Rectal examinations at the time of admission and again 4 h later revealed an increasingly distended large colon of undetermined cause, although colonic displacement or torsion were differential diagnoses. Feces were never detected within the rectum. Transabdominal ultrasonographic examination revealed normal small intestinal appearance and motility. At 6:30 am, about 60 to 70 h after first becoming colicky, and about 10 h after being admitted to the VMC, the horse was euthanized because of an inability to control its pain and because the owners did not wish to pursue surgical exploration of the abdomen. The gelding was then submitted to Prairie Diagnostic Services, within the WCVM, for postmortem examination. A 1178
necropsy was performed about 6 h after the horse was euthanized. The large intestine, except the descending colon, was diffusely distended by gas and ingested fibrous plant material. The most aborad, approximately 2.5 m of the descending colon were nearly empty. A segment of orad colon, interpreted to be the transverse colon, was strongly adhered to a firm, 30 cm long 3 20 cm wide 3 5 cm thick mass, located in the dorsal abdomen, just cranial to the kidneys and slightly to the left of the sagittal midline. The mass was later identified as the pancreas, and was diffusely very firm, pale- or cream-colored, and composed of prominent 1 to 2 cm lobules (Figures 1A and 1B). There was no evidence of large colon displacement or torsion. The liver was in its normal location and appeared to be normal in size and shape, but had an abnormal dull or olive green hue and was firmer and tougher than normal. The squamous portion of the gastric mucosa, surrounding the cardia, contained many, small (a few millimeters to a few centimeters) coalescing to confluent, red, depressed foci, interpreted as erosions, ulcers, or both (Figures 1C and 1D). The cortices of both adrenal glands were diffusely 5- to 6-mm thick while the medullae were typically 3- to 4-mm thick, a change interpreted to represent diffuse adrenal cortical hyperplasia (Figure 2A). Histologically, the pancreas contained a moderately increased amount of interlobular fibrous tissue infiltrated with mild CVJ / VOL 56 / NOVEMBER 2015
CA S E R E P O R T
Figure 2. The histologic appearance of the adrenal glands, pancreas and liver of a 13-year-old Quarter horse. A — The cortex of the right and left adrenal gland was diffusely hyperplastic, i.e., more than twice the thickness of each medulla. Hematoxylin and eosin. B — There was a moderately increased amount of interlobular fibrous tissue within the pancreas. Masson’s Trichrome. C — The interlobular fibrous tissue (center of image) of the pancreas contained moderate numbers of inflammatory cells; mostly neutrophils. Hematoxylin and eosin. D — There was a moderate degree of periportal and perilobular fibrosis and associated bile duct hyperplasia within the liver. Masson’s Trichrome.
to moderate numbers of inflammatory cells that included mostly neutrophils, with fewer lymphocytes and plasma cells (Figures 2B and 2C). The architecture of the pancreatic parenchyma was also abnormal. While a few recognizable acini were present, most exocrine pancreatic cells were haphazardly arranged and composed of irregular and attenuated exocrine cells. Some exocrine cells appeared to be missing, leaving behind a space that was partially filled with fine strands of fibrous tissue. None of the remaining exocrine cells had a normal appearance, i.e., they lacked basophilia with apical eosinophilia. Islets were present in normal numbers, but also appeared to be missing a moderate proportion of cells. The liver also contained a moderate degree of fibrosis around the periportal and perilobular areas that nearly surrounded the lobule in some locations, suggestive of biliary fibrosis (Figure 2D). Associated with the fibrosis was a moderate degree of bile duct hyperplasia. Within each hepatic lobule were small CVJ / VOL 56 / NOVEMBER 2015
globules or “lakes” of homogeneous, orange to golden, extracellular material, interpreted to be bile, and to represent bile stasis. Bacterial cultures were performed on the pancreas, liver, and contents of the duodenum and moderate to large numbers of Streptococcus zooepidemicus and Escherichia coli were isolated from the duodenum and liver, while moderate to large numbers of S. zooepidemicus, E. coli, and an Enterococcus species were isolated from the pancreas.
Discussion There appears to be a limited body of literature concerning pancreatitis in the horse and much of this literature describes acute pancreatitis. Descriptions of chronic pancreatitis in the horse appear in popular textbooks on veterinary pathology (4,5), although only 1 of these textbooks describes interstitial pancreatitis (4). These descriptions suggest that chronic pancreatitis in the horse has not, typically, been associated with clinically 1179
R A P P O R T D E CA S
apparent disease. A common cause of chronic pancreatitis in the horse, and other domestic animals, is believed to be the ascension of intestinal contents, including bacteria, through the pancreatic duct (3–5). In the horse, the pancreatic duct and bile duct merge prior to connecting with the duodenum as the major duodenal papilla (6). Although circumstantial, the presence of periportal, or biliary, hepatic fibrosis and bile duct hyperplasia, as well as the isolation of the same bacteria from the pancreas, liver, and duodenum provides evidence that intestinal contents, including bacteria, likely entered both the pancreatic duct and bile duct via the major duodenal papilla. In the horse described here, the chronic active interstitial pancreatitis was associated with a relatively large area of adhesion to the transverse colon. The postmortem findings suggest that this adhesion was the origin of the obstruction and the clinical signs of colic. Specifically, the approximately 2.5 m of descending colon aborad to the site of adhesion to the pancreas were nearly empty while the remainder of the large intestine, orad to the pancreas, was markedly distended with fibrous ingesta and gas. In overviews of intestinal obstruction in humans (7) and horses (8,9), it has been common to categorize the causes as either mechanical or functional. Mechanical causes include any luminal or extraluminal lesion that physically narrows or occludes the intestine. Functional obstruction, also referred to as pseudo-obstruction, adynamic ileus or, simply, ileus, are terms used to describe the impairment of the aborad transit of intestinal contents in the absence of a grossly detectably abnormality (9). Therefore, adhesions of the intestines are categorized as mechanical obstructions (7,8). When these adhesions result in the entrapment of loops of intestine, the pathophysiology of the obstruction is obvious. However, in the absence of an appreciable physical or mechanical cause of the blockage, as in this horse, the pathophysiology of the obstruction is less clear. In this horse, it is possible that the firm texture of the pancreas that nearly surrounded the transverse colon (see the tip of the pancreas at the left of Figure 1A) caused a physical narrowing of the lumen. However, it is also interesting to speculate that the presence of inflammation within the pancreas, which was directly apposed to the transverse colon, might have interfered with normal functioning and contributed to a functional obstruction (10). Although secondary in nature, the changes noted in the stomach and both adrenal glands of this horse are worthy of comment. Histologically, the non-glandular stomach con-
1180
tained multiple, often coalescing to confluent, areas of erosion and underlying inflammation, particularly around the cardia. There are several known risk factors for gastric erosion and ulceration in horses (11,12), a few of which were present in this horse, including anorexia, the administration of a non-steroidal anti-inflammatory drug, reflux of duodenal contents and, very likely, stress. Further evidence that this horse had experienced stress was the presence of diffuse cortical hyperplasia of both adrenal glands. While intuitive, changes to the adrenal cortices in association with stress have been demonstrated in laboratory animals (13,14). CVJ
References 1. Johnson PJ, Wiedmeyer CE, Messer NT. Conditions of the equine pancreas. Equine Vet Educ 2009;21:26–29. 2. Newman SJ. Equine pancreatic disease: A review and characterization of the lesions of four cases (2005–2014). J Vet Diagn Invest 2015; 27:92–96. 3. Yamout SZ, Nieto JE, Anderson J, De Cock HE, Vapniarsky N, Aleman M. Pathological evidence of pancreatitis in 43 horses (1986–2011). Equine Vet J 2012;43:45–50. 4. Charles JA. Pancreas. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. 5th ed. Vol 2. Toronto, Ontario: Saunders Elsevier, 2007:389–424. 5. Cullen JM, Brown DL. Hepatobiliary system and exocrine pancreas. In: Zachary JF, McGavin MD, eds. Pathologic Basis of Veterinary Disease. 5th ed. St. Louis, Missouri: Elsevier Mosby, 2012:405–457. 6. Nickel R, Schummer A, Seiferle E. The Viscera of the Domestic Mammals. 2nd ed. New York, New York: Springer-Verlag, 1979:99–122; 180–203. 7. Liu C, Crawford JM. The gastrointestinal tract. In: Kurar V, Abbas AK, Fausto N, eds. Robbins and Cotran Pathologic Basis of Disease. 7th ed. Philadelphia, Pennsylvania: Saunders Elsevier, 2005:797–875. 8. Fubini SL. Abdominal adhesions. In: Mair T, Divers T, Ducharme N, eds. Manual of Equine Gastroenterology. Philadelphia, Pennsylvania: Saunders, 2002:209–211. 9. Rakestraw P. Ileus. In: Mair T, Divers T, Ducharme N, eds. Manual of Equine Gastroenterology. Philadelphia, Pennsylvania: Saunders, 2002:211–215. 10. Koenig J, Cote N. Equine gastrointestinal motility — Ileus and pharmacological modification. Can Vet J 2006;47:551–559. 11. Brown CC, Baker DC, Barker IK. Alimentary system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. 5th ed. Vol 2. Toronto, Ontario: Saunders Elsevier, 2007:1–296. 12. Videla R, Andrews FM. New perspectives in equine gastric ulcer syndrome. Vet Clin North Am Equine Pract 2009;25:283–301. 13. Kapitonova MY, Kuznetsov SL, Khlebnikov VV, Zagrebin VL, Morozova ZCh, Degtyar YV. Immunohistochemical characteristic of the hypophysis in normal conditions and chronic stress. Neurosci Behave Physiol 2010;40:97–102. 14. Ulrich-Lai YM, Figueiredo HF, Ostrander MM, Choi DC, Engeland WC, Herman JP. Chronic stress induces adrenal hyperplasia and hypertrophy in a subregion-specific manner. Am J Physiol Endocrinol Metab 2006;291:E965–E973.
CVJ / VOL 56 / NOVEMBER 2015
