Gastric and Esophageal Diverticulum Rupture in a Friesian Gelding
Lindsay A. Chase
Clinical Sciences Advisor: Dr. Kathleen R. Mullen
Basic Science Advisor: Dr. Elizabeth L. Buckles
Senior Seminar Paper
Cornell University College of Veterinary Medicine
5/7/2014
Key words: Horse, Friesian, Diverticulum, Rupture, Esophagus
Abstract:
A 17-year-old Friesian gelding presented to the Cornell University Large Animal
Hospital for a 1-day history of lethargy, inappetence and an 8-hour history of dyspnea and colic.
On presentation he was tachycardic and tachypneic. His mucus membranes were injected with a
toxic line and a prolonged capillary refill time. Borborygmi were absent on abdominal
auscultation. Nasogastric intubation was attempted but resistance was met at the area of the
cardia. Endoscopic exam revealed an impaction of feed material in the distal esophagus.
Ultrasound exam showed mixed echogenic peritoneal fluid. Peritoneal fluid analysis revealed a
septic peritonitis consistent with a rupture of the gastrointestinal system. Because of these
findings, euthanasia was elected and a necropsy examination was performed.
This case report will discuss the work up and treatment of this patient along with results
of the necropsy examination and current research in the area of Friesian horse inherited diseases.
History and Signalment:
A 17-year-old Friesian gelding presented to the Cornell University Large Animal
Emergency Service for a 1-day history of lethargy, inappetence and an approximately 8-hour
history of dyspnea and colic. The horse was seen by the referring veterinarian who found the
horse to be tachycardic (heart rate of 80 beats/minute, reference range (RR): 28-44), dyspneic,
and febrile (102.6oF, RR: 99-101.5) with muddy mucous membranes and a prolonged capillary
refill time. No borborygmi were heard on abdominal auscultation. Rectal palpation was normal
at this time. A nasogastric tube was passed and no gastric reflux was obtained. A mixture of
mineral oil and water was then given via the nasogastric tube, during which the horse displayed
signs of discomfort. The veterinarian administered flunixin meglumine, ceftiofur crystalline free
acid, and detomidine. The horse was then referred to Cornell for suspected colitis.
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Clinical Presentation and Diagnostics:
Upon presentation, the patient was admitted to the isolation facility due to his history of
fever and possible impending diarrhea. The horse was depressed, tachycardic (heart rate of 86
beats/minute, RR: 28-44) and tachypneic (respiratory rate of 52 breaths/minute, RR: 8-16). He
was over-conditioned with a body condition score of 7/9 (ideal is 4.5/9). A small amount of
malodorous nasal discharge was observed on physical exam. His mucous membranes were dark
pink with a toxic line and the capillary refill time was prolonged at 3 seconds. Borborygmi were
absent on abdominal auscultation in all quadrants. The rectal palpation was largely
unremarkable with thickened, but compressible, small intestine being the only finding. Thoracic
ultrasound showed no pleural fluid or evidence of pleuritis. Abdominal ultrasound revealed
thickened walls of the large colon and small intestine and a normal sized, non-distended
stomach. Nasogastric intubation was attempted but a large amount of resistance was met at the
area of the cardia.
In-house bloodwork revealed a packed cell volume of 62% (RR: 34%-46%) and total
solids by refractometer of 6.3 g/dL (RR: 5.2-7.8), indicative of dehydration with
hypoproteinemia. Complete blood count showed a mild lymphopenia (1.0 thou/uL, RR: 1.8-5.0)
and neutropenia (2.0 thou/uL, RR: 3.0-7.0). Blood chemistry values revealed a hypochloremic
metabolic alkalosis (pH 7.523, RR: 7.32-7.44; chloride 92 mEq/L, RR: 100-110; HCO3 31
mmol/L, RR: 25-30). The patient also had an ionized hypocalcemia (1.19 mg/dL, RR: 1.25-1.78)
and elevated creatinine (2.6 mg/dL, RR: 0.4-2.2). Additionally the horse was hyperlactatemic
(4.8 mmol/L, RR: 0.3-1.5), suggestive of dehydration and/or anaerobic metabolism due to
hypoperfusion.
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Differential Diagnoses:
Our patient’s main presenting complaint was colic or abdominal pain. Equine colic can
be caused by a myriad of different reasons. It is prudent to remember that colic can have a
gastrointestinal cause or a non-gastrointestinal cause. Gastrointestinal causes can include
proximal disease (gastric ulcers, gastric impaction, gastric rupture, choke, and esophageal
rupture) small intestinal disease - both strangulating (lipomas, mesenteric rents, and entrapment
in hernias) and non-strangulating (enteritis, inflammatory bowel disease, and impactions), and
large intestinal disease (displacements, volvulus, impactions, colitis, and enteroliths). Nongastrointestinal causes can include liver disease (hepatitis, cholangiohepatitis, choliliths, abscess
and neoplasia), genitourinary disease (uterine artery rupture, urinary calculi, and cystitis),
musculoskeletal disease (rhabdomyolysis and laminitis) and other disease processes
(pleuropneumonia, and neuropathies). Because of the horse’s signalment, inability to pass a
nasogastric tube, and signs of endotoxic shock, our top differential was esophageal disease
(megaesophagus or diverticulum) or gastric impaction. Other differentials included enterocolitis.
Treatment:
In order to address the dehydration, a 1 L intravenous bolus of hypertonic saline was
administered followed by a 20 L isotonic fluid bolus. An antiendotoxic dose of flunixin was
given at 0.25 mg/kg and cryotherapy was initiated on his forelimbs to help prevent laminitis from
endotoxemia. The patient was also started on a lidocaine constant rate infusion (CRI) to help
with pain control and as a promotility agent. A hetastarch CRI was a started to increase his
colloid oncotic pressure. He was offered water and drank 3 L, after which he became
uncomfortable, severely tachycardic (120 beats/minute, RR: 28-44) and tachypneic. None of the
water was observed to spontaneously reflux. At this time the intravenous fluids were stopped
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and an electrocardiogram (ECG) was run to help rule out cardiac disease which is a common
finding in Friesians. The ECG showed wide QRS complexes consistent with electrolyte
derangements with no other abnormalities. After this result, the intravenous fluids were
restarted. Cardiac troponin was found to be elevated at 0.69 ug/L (RR: 0-0.06), consistent with
myocardial damage secondary to endotoxemia or primary myocardial insult.
After the intravenous fluid boluses were finished the patient was maintained on a CRI of
isotonic fluids with electrolyte supplementation and he was re-assessed. No clinical
improvement was seen and upper gastrointestinal endoscopy revealed an impaction of feed
material in the distal esophagus. Repeat thoracic and abdominal ultrasounds were then performed
which now showed pleural effusion and copious amounts of mixed echogenic peritoneal fluid.
Abdominocentesis and peritoneal fluid analysis revealed a septic peritonitis with a mixed
extracellular and intracellular bacterial population consistent with a rupture of the
gastrointestinal system. No feed material was found in the sample. Because of these findings
and the grave prognosis associated with gastrointestinal rupture in horses, euthanasia was elected
and a necropsy examination was performed.
Necropsy Exam:
The abdomen contained approximately 60 L of clear to slightly opaque thin fluid mixed
with strands of fibrin. Stands of fibrin were also loosely adhered to the serosal surfaces of the
viscera. No feed material was grossly observed in the fluid. A segment of the esophagus just
caudal to the diaphragm was expanded by a large thin walled dilatation (pulsion diverticulum)
that was impacted with large amounts of feed material. There was an 8 cm long full thickness
rupture in the wall of this diverticulum and the tissue along the edges of the tear was necrotic.
Additionally the muscularis of the wall of the distal third of the esophagus was severely
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thickened, measuring 1.7 cm thick (normal reported thickness being 0.5 cm +/- 0.1 cm1).
Examination of the stomach revealed a 10 cm long, 5-8 cm wide separation of the tunica
muscularis along the lesser curvature. This lesion entrapped approximately 60 mL of feed.
Within the center of this tear was a 5.5 full thickness rent in the gastric wall. The diaphragm was
adhered to the gastric defects by organizing fibrin and necrotic tissue. Within the wall of the
pylorus was an area of marked edema between the mucosal and serosal layers.
Histopathology was largely unremarkable aside from the marked smooth muscle
hypertrophy of the distal esophagus and the necrosis and fibrinosuppurative exudate associated
with the gastric and esophageal tears. An esosinophilic enteritis was also observed in the small
intestine but did not appear to be related to the gastric or esophageal lesions. There was no
morphologic evidence of any condition that would have predisposed to either the gastric or
esophageal lesions.
Discussion:
The Friesian breed has a long history; it was developed in Friesland province of the
Netherlands starting in the 1500’s.2 In 1879 the studbook was founded and in 1928 it was
recorded that 8 stallions bred 358 mares.2 The breed also had a reduction in the number of
breeding stallions after World War II and then became very popular in the 1980’s.1,3 All of these
examples illustrate the unfortunate inbreeding that has occurred in the Friesian breed.
Additionally the breed has been heavily selected for its high head carriage and hyperflexive and
hyperextensive, high action gait.3 Genetic studies have shown a low level of variation in protein
and microsatellite markers indicating a low level of heterozygosity.4 Aortic rupture,
aortopulmonary fistulation, megaesophagus, dwarfism, hydrocephalus, chronic proliferating
lymphangitis, insect bite hypersensitivity, tendon ligament laxity and retained placenta all occur
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at a higher rate in this breed compared to others, leading researches to investigate a heritable
basis for these diseases.1,3
In a retrospective study published in late last year, all of the equine necropsy submissions
over a 6-year period were examined at Michigan State University Diagnostic Center for
Population and Animal Health to characterize the prevalence, clinical signs, and pathology of
esophageal disease in a necropsy population of Friesian horses and to compare and contrast these
findings with those observed in other breeds.1 Eight hundred fifty-two horses were submitted, 42
of which had recorded esophageal lesions, 10 of those being severe enough to be the cause of
death or the reason for euthanasia.1 Thirty-five percent (6/17) of Friesian horses submitted were
found to have severe lesions compared to 0.5% (4/835) of other breeds.1 This was a significantly
higher rate of severe esophageal disease occurrence in the Friesian breed. This study also
showed that caudal esophageal muscular hypertrophy occurred at a significantly higher rate in
Friesians at 35.3% compared to 2.3% in all other breeds.1 The equine esophagus is composed of
striated muscle in the cranial 2/3 and smooth muscle in the distal 1/3.1 In both our patient and in
this study the esophageal muscular hypertrophy only occurred in the smooth muscle of the distal
1/3 of the esophagus.1 This type of esophageal hypertrophy is usually an incidental idiopathic
finding in older horses but in this study it was associated with esophageal disease in Friesians,
specifically megaesophagus.5,1 Because of the higher incidence of esophageal disease within the
Friesian breed there is likely an underlying genetic cause.
Our patient was not found to have megaesophagus but severe esophageal disease was
present. Two types of esophageal diverticula exist. Traction, which forms after an esophageal
injury and has a shallow body and a wide opening.6 Therefore traction diverticula are not prone
to feed impaction and peristalsis can be transmitted normally past the structure.6 Pulsion
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diverticula, like our patient possessed, are caused by an out-pouching of the mucosa through a
defect in the wall of the esophagus.6 This type of diverticula consists of a flask-like body and a
narrow opening, therefore prone to feed impaction and rupture, which occurred in this case.6
Pulsion esophageal diverticula do occur in the horse but much more commonly in the cervical
portion of the esophagus.6 Horses that possess this type of lesion commonly present with a
history of dysphagia, weight loss, recurrent choke and swelling of the ventral neck.6 Our patient
had two different sites of gastrointestinal wall defects with no gross or histopathologic cause
determined. These two defects could also be manifestations of a genetic disorder of the Friesian
breed.
One hypothesis for explaining the high incidence of diseases in the Friesian breed is a
link between the conformational selection of a high head carriage, hyperelastic, hyperflexive gait
and a systemic collagen abnormalitiy.3 In a recent study examining the hisopathologic
characteristics of the aorta of Friesian horses with aortic rupture specific changes were found.7
These changes included disorganization and fragmentation of the elastic laminae, aberrant
collagen morphology, smooth muscle hypertrophy and necrosis.7 These findings support the
hypothesis of a genetic collagen or elastin defect predisposing Friesian horses to aortic rupture.7
Another study examined the tendon properties of the stay apparatus in dwarf Friesians, nondwarf Friesians and control ponies.8 It was shown that the tendons of dwarf Friesians were more
elastic (less stiff) compared to that of reported stiffness in Thoroughbred tendons and the nondwarf Friesians had intermediate properties between the two, indicating a breed specific
difference.8
Continued breed specific research is currently being performed by Dr. William Back at
the Utrecht University on hydrocephalus, dwarfism, megaesophagus and aortic rupture in
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conjunction with the Friesian Horse Association of North America and the Fenway Foundation
for Friesian Horses.9 If the gene(s) associated with these conditions can be identified, there is
hope that the prevalence of these diseases in the Friesian breed can be significantly reduced
through selective breeding.
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References
1. Komine M, Langohr IM, Kiupel M. Megaesophagus in Friesian Horses Associated With
Muscular Hypertrophy of the Caudal Esophagus. Vet Pathol. 2013;
2. Kasperek L. Friesian Timeline; 2014; Available from: http://www.fhana.com/timeline/
(Accessed April 2014).
3. Boerma S, Back W, Sloet van Oldruitenborgh-Oosterbaan MM. The Friesian horse breed:
A clinical challenge to the equine veterinarian?. Equine Veterinary Education.
2012;24(2):66-71.
4. Luís C, Juras R, Oom MM, Cothran EG. Genetic diversity and relationships of
Portuguese and other horse breeds based on protein and microsatellite loci variation.
Anim Genet. 2007;38(1):20-7.
5. Benders NA, Veldhuis kroeze EJ, Van der kolk JH. Idiopathic muscular hypertrophy of
the oesophagus in the horse: a retrospective study of 31 cases. Equine Vet J.
2004;36(1):46-50.
6. Yamout SZ, Magdesian KG, Tokarz DA, Le jeune SS. Intrathoracic pulsion diverticulum
in a horse. Can Vet J. 2012;53(4):408-11.
7. Ploeg M, Saey V, Delesalle C, et al. Thoracic Aortic Rupture and Aortopulmonary
Fistulation in the Friesian Horse: Histomorphologic Characterization. Vet Pathol. 2014;
8. Gussekloo SW, Lankester J, Kersten W, Back W. Effect of differences in tendon
properties on functionality of the passive stay apparatus in horses. Am J Vet Res.
2011;72(4):474-83.
9. Horse Health; 2014; Available from: http://www.fhana.com/horsehealth/ (Accessed April
2014).
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