EQUINE VETERINARY EDUCATION
Equine vet. Educ. (2011) 23 (6) 281-285
doi: 10.1111/j.2042-3292.2010.00178.x
Case Report eve_178
A case of a colocolic intussusception in a horse
V. Albanese*, B. Credille, A. Ellis†, L. Baldwin, P. O. E. Mueller and A. Woolums
Departments of Large Animal Medicine and †Pathology, University of Georgia, College of Veterinary
Medicine, Georgia, USA.
Keywords: horse; large colon; impaction; intussusception; necropsy
Summary
The purpose of this report is to describe the clinical course
and pathological findings in a horse admitted to the
emergency service of the University of Georgia Large
Animal Teaching Hospital for evaluation of colic, fever
and diarrhoea of several days’ duration. A presumptive
historical diagnosis of colitis was made initially, but, due
to the lack of faecal output during the first 12 h of
hospitalisation and subsequent examination findings, an
impaction of the ascending colon was suspected. Initial
therapy consisted of rehydration with oral fluids and
management of the abdominal pain with analgesic
therapy. The horse did not respond to medical therapy and
because of signs of persistent abdominal pain and
financial constraints, the owner elected euthanasia after
several days of supportive care. At necropsy, the horse
was diagnosed with a colocolic intussusception.
Introduction
Intussusceptions are an uncommon cause of colic in
the mature horse. Caecocolic and caecocaecal
intussusceptions are the most commonly encountered
intussusceptions affecting the large intestine in mature
horses, but only accounted for 1.3% of horses operated on
for an acute abdomen (Gaughan and Hackett 1990).
Colocolic intussusceptions have been described rarely in
the veterinary literature. This case report describes the
clinical course and pathological findings in a 5-year-old
Tennessee Walking Horse gelding.
Case history
A 5-year-old Tennessee Walking Horse gelding presented
to the University of Georgia Large Animal Teaching Hospital
for evaluation of diarrhoea and pyrexia of approximately 3
*Corresponding author email demialba@tin.italifornia
Present address: Chino Valley Equine Hospital, 2945 English Place, Chino
Hills, California. 91709, USA.
281
281..285
days’ duration. One week before admission, the horse was
treated for a presumed large colon impaction. He
subsequently passed foul smelling, blood tinged faeces
and was started on a 3 day course of trimethoprim/
sulphadiazine (25 mg/kg bwt, q. 12 h, per os). Soon after
this therapy was initiated, the horse developed diarrhoea
that lasted 24 h. Faecal consistency then became more
formed but not normal, and defaecations became less
frequent. No previous history of colic was reported by the
owner and no recent changes had been made to the
gelding’s diet, which consisted of Bermuda grass hay and
a complete pelleted feed. The horse had no history of
recent travel and his dental prophylaxis was up to date,
with the last dental evaluation performed 3 months before
admission.
Clinical findings
On presentation, the gelding was quiet, alert and
responsive with a body condition score of 7/9 (Henneke
et al. 1983). His rectal temperature was 38.5°C, his heart
rate was 60 beats/min and respiratory rate 24 breaths/min.
The gelding’s mucous membranes were pink and moist
with a capillary refill time of 2 s. Cardiothoracic
auscultation was unremarkable, and peripheral pulses
were strong and synchronous with the heart beat.
Borborygmi were increased in the left hemiabdomen.
Initial examination of the abdomen per rectum was
unremarkable.
Initial laboratory tests revealed a mild hypocalcaemia
(total serum calcium 2.4 mmol/l, reference range [rr]
2.7–3.2 mmol/l; ionised calcium 1.33 mmol/l, rr
1.61–1.85 mmol/l) and mildly elevated creatinine kinase
(465 u/l, rr 87–339 u/l). Packed cell volume and total solids
measured 35% (rr 26–42%) and 52 g/l (rr 54–75 g/l),
respectively.
An ultrasonographic examination of the abdomen was
recommended and offered but declined by the owner. An
abdominocentesis was not collected.
Due to the history of diarrhoea and fever, faecal
samples were submitted for testing for Clostridium difficile
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cytotoxin by ELISA, as well as for Salmonella enterica by
PCR over 3 consecutive days; all reports returned as
negative.
Treatment and outcome
During the first 12 h following admission, the patient was
maintained on intravenous balanced electrolyte fluids
(Normosol-R)1 at a rate of 3 ml/kg bwt/h. The patient
remained quiet and alert with no signs of abdominal pain;
however, during the initial 24 h period of hospitalisation the
horse passed a small amount of formed faeces on only
one occasion.
Given the history of oral administration of
trimethoprim-sulphadiazine, antibiotic-associated colitis
was considered as a possible cause of the horse’s clinical
signs and empirical therapy was initiated with a course of
metronidazole (30 mg/kg bwt q. 8 h per rectum), flunixin
meglumine (1.1 mg/kg bwt q. 12 h i.v.) (Banamine)2 and
i.v. balanced electrolyte fluid therapy at maintenance
rate (3 ml/kg bwt/h) (Normosol-R). Food was offered, but
the patient remained relatively inappetent with continued
decreased faecal output.
Examination of the abdomen per rectum performed
36 h following admission identified a moderately gas
distended colon along with a solid mass in the centre
of the abdomen, barely palpable at the examiner’s
fingertips. The mass was suspected to be a large colon
impaction. Upon withdrawal of the examiner’s arm, the
rectal sleeve was covered with dark brown, tarry, foul
smelling faeces and streaks of dark blood. Transabdominal
ultrasound examination of the abdomen was again
recommended to which the owner consented. The
ultrasound evaluation revealed no abnormalities. The
patient was subsequently held without feed and enteral
fluid therapy with a combination of magnesium sulphate
(0.5 g/kg bwt once by nasogastric tube) and balanced
electrolytes (5 l of tap water containing Na 141.35 mmol/l,
K 4.02 mmol/l, Cl 104.91 mmol/l and HCO3 40.46 mmol/l,
administered by nasogastric tube q. 4 h) was initiated.
Forty-eight hours following admission, the horse started
demonstrating signs of abdominal pain and moderate
gross bilateral abdominal distention with an elevated heart
rate (56–60 beats/min). No net reflux was obtained at that
time by siphonage through a nasogastric tube. On
examination of the abdomen per rectum, taut colonic
bands were palpated coursing transversely across the
abdomen and the large colon was markedly distended
with gas. Enteral therapy was discontinued. Exploratory
surgery was offered but declined by the owners. As a result,
the patient was maintained on no food, intravenous
balanced electrolyte fluids (Normosol-R) at 5 ml/kg bwt/h
along with flunixin meglumine (1.1 mg/kg bwt q. 12 h, i.v.)
(Banamine), Sucralfate (20 mg/kg bwt q. 8 h per os)
(Teva-Sucralfate)3 was also administered to decrease pain
from gastritis or gastric ulcers associated with prolonged
fasting. The horse remained persistently tachycardic,
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Colocolic intussusception in a horse
despite resolution of his signs of abdominal pain and
abdominal distension.
Sixty hours after admission, examination of the
abdomen per rectum revealed substantially less gas
distended colon as well as a firm, indentable, mass
approximately 30 cm in diameter in the centre of the
abdomen, barely palpable by the examiner’s fingertips.
This was presumed to be the same structure that was
palpated 24 h previously. A leucogram and serum
biochemical profile were submitted; the leucogram was
within normal limits but abnormalities in the serum
biochemical profile included hyperfibrinogenaemia of
5.0 g/l (rr 1.0–4.0 g/l), hypoproteinaemia (serum total
protein 46 g/l, rr 49–70 g/l) due to hypoalbuminaemia
(17 g/l, rr 18–30 g/l); and hypocalcaemia (2.5 mmol/l, rr
2.7–3.2 mmol/l), presumably due to the hypoproteinaemia.
Serum SDH was elevated at 81 u/l (rr 1–8 u/l). Triglycerides
were not directly measured but lipaemia was
macroscopically noted at the time of blood sampling and
was attributed to the horse’s anorexia and negative
energy balance. Dextrose was added to the intravenous
fluids at a final concentration of 2.5% in order to
reduce further fat mobilisation, and KCl (10 mmol/l) was
added to prevent hypokalaemia secondary to prolonged
anorexia.
Considering the reduction in colonic distension and
absence of abdominal pain, a second attempt at enteral
fluid therapy was initiated 66 h following admission and
continued for an additional 30 h. The patient remained
relatively quiet although persistently tachycardic. The
following morning, the horse again displayed marked
abdominal distension followed by persistent, severe
signs of colic unresponsive to continued analgesic
administration. In addition, 9 l of net reflux were obtained
by siphonage through a nasogastric tube.
At that time, surgery was again offered to the owners,
but declined. Analgesic management of the patient
included multiple administrations of detomidine
(Dormosedan)4 5–10 mg boluses both i.v. and i.m. to
effect, in combination with butorphanol (Torbugesic)5
5–10 mg boluses both i.v. and i.m., to effect.
Trocharisation of the large colon to relieve the pain
associated with the distention of the colon itself was
recommended and offered but declined by the owners.
As a result of the worsening condition and unresponsive
signs of colic, the horse was subjected to euthanasia
108 h after admission.
Post mortem findings
A complete necropsy examination identified an extensive
colocolic intussusception involving the left and right dorsal
colons, the intussusceptum being the left dorsal colon and
the intussuscipiens being the right dorsal colon (Fig 1). The
intussusceptum was friable with marked oedema and
haemorrhage and multifocal, fibrinonecrotic plaques
were present along the mucosal surface. The lumen of the
V. Albanese et al.
Fig 1: Post mortem: An extensive colocolic intussusception is
shown: the intussusceptum is the left dorsal colon (thin arrow) and
the intussuscipiens is the right dorsal colon (thick arrow).
right dorsal colon contained multifocal proliferations
composed of long, accordion-like folds of otherwise
normal mucosa that partially obstructed the lumen. Firm
material with a dark red to black, 2–5 mm rim surrounding
dried feed material was impacted within these mucosal
folds. Histological examination of these aggregates
demonstrated necrotic mucosa surrounding clumps of
plant material and large numbers of bacteria. Proximal to
the lesion, the pelvic flexure and proximal left dorsal colon
were markedly distended with ingesta.
Discussion
Intussusceptions occur when intestine ‘telescopes’ into an
adjacent segment of intestine. The recipient section of
bowel is termed the ‘intussuscipiens’ and the invaginated
bowel the ‘intussusceptum’.
In horses, caecocaecal and caecocolic
intussusceptions are the most common forms of
intussusception of the large intestine, although they are
both relatively rare compared to all forms of colic.
Caecocolic intussusceptions usually occur in young horses,
and their aetiology is largely unknown. Motility disorders
are thought to play a role, and other potential risk
factors include dietary changes, caecal wall abscesses,
Salmonellosis, tapeworm (Anoplocephala perfoliata)
infestation, cyathostominosis, Eimeria leuckarti, Strongylus
vulgaris arteritis, organophosphates and administration of
parasympathomimetic drugs (Rakestraw and Hardy
2006).
Clinical signs are extremely variable depending on how
compromised or obstructed the affected portion is,
ranging from intermittent mild to moderate signs of
abdominal pain, soft faeces or diarrhoea, and fever in
chronic cases to severe pain requiring immediate surgical
intervention (Edwards 1986; Gaughan and Hackett 1990;
Dart et al. 1997; Martin et al. 1999; Edwards 2002).
283
Caecocaecal intussusceptions are more likely to be
nonstrangulating, incomplete obstructions producing mild
pain, developing into a more chronic disease form (Martin
et al. 1999). Caecocolic intussusceptions typically develop
ischaemic necrosis of the distal end of the intussusceptum,
including the apex of the caecum and part of the body
(Robertson 1990). Diagnosis is usually difficult, although
ultrasonography may be helpful in establishing a diagnosis
(McGladdery 1996; Martin et al. 1999; Boussauw et al.
2001). Frequently, the compromised intussusceptum is
sequestered within the intussuscipiens, rendering
peritoneal fluid analysis an insensitive indicator of
pathology (Boussauw et al. 2001). With time and
progression of the disease, peritoneal fluid changes may
be seen (Gaughan and Hackett 1990; Ward and Fubini
1994; Martin et al. 1999). Often, the diagnosis is made at
surgery after the horse fails to respond to medical therapy
(Gaughan and Hackett 1990; Ward and Fubini 1994; Dart
et al. 1997; Martin et al. 1999).
Intussusception of the large colon is rarely encountered
in the horse (Meagher and Stirk 1974; Robertson and Tate
1982; Dyson and Orsini 1983; Wilson et al. 1983) with the
most recent case report in 1983. All affected horses in
the aforementioned reports were young, with the segment
involved being the pelvic flexure and the left colon
(Meagher and Stirk 1974; Robertson and Tate 1982; Dyson
and Orsini 1983; Wilson et al. 1983). Predisposing factors
potentially leading to a large colon intussusception are as
for the other types of large intestine intussusceptions,
changes in diet, impaction of the colon, and mesenteric
arteritis in association with Strongylus vulgaris migration
(Robertson and Tate 1982), although none of these factors
were identified in the present case.
Colocolic intussusceptions are often characterised by
mild abdominal discomfort with continued passage of soft
faeces (Robertson 1990). More severe signs of colic
develop when the obstruction becomes complete and
results in gas distention. Mild tachycardia is a feature
(Sullins 1990). The cases of colocolic intussusception
previously described were characterised by mild
abdominal discomfort of several hours to several days
duration with or without soft faeces (Meagher and Stirk
1974; Robertson and Tate 1982; Dyson and Orsini 1983;
Wilson et al. 1983). Laboratory findings were inconsistent in
the 3 cited reports, although in one case peritoneal fluid
was abnormal (Dyson and Orsini 1983) and in another
severe hyperfibrinogenaemia, hyperlactataemia and
a toxic left shift were recorded (Wilson et al. 1983). In
the case of this report, hypoproteinaemia was the
most remarkable finding. Hypoproteinaemia due to
hypoalbuminaemia commonly occurs in gastrointestinal
diseases because of loss of plasma proteins through an
inflamed or necrotic intestinal mucosa. In horses,
inflammatory diseases involving the large colon, such as
colitis and infiltrative inflammatory bowel diseases also
result in hypoproteinaemia. Clinical findings of colocolic
intussusception may also include a palpable mass
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upon abdominal examination per rectum. In our case
a mass was present and palpable in the centre of the
caudal abdomen. Ultrasonography may also be useful
if the affected portion is close enough to the abdominal
or rectal wall to allow imaging. In this case
ultrasonographic examination of the abdomen performed
transabdominally was unrewarding. Transrectal
ultrasonography was not included in our diagnostic
work-up.
Previously reported cases of colocolic intussusception
were all successfully managed surgically, 2 by manual
reduction and 2 by resection and anastomosis. In our case,
the lesion was nonreducible at necropsy examination;
however, it might have been possible to reduce it at
surgery earlier in the course of disease. Based on the
necropsy findings, the affected portion of ascending
colon could probably have been exteriorised and
a resection and anastomosis performed. Prognostic
recommendations for colocolic intussusceptions are
difficult to make given the few reported cases, however,
the prognosis would probably be similar to that for
caecocolic intussusceptions and relate to the amount of
intussuscepted bowel, the ability to reduce the lesion
without opening the intestinal lumen, control of potential
contamination at surgery, and the amount and viability of
the remainder of the intestine (Edwards 1986; Gaughan
and Hackett 1990; Martin et al. 1999; Edwards 2002;
Rakestraw and Hardy 2006).
A thickened portion of the colonic wall was observed
at necropsy of this case; whether that initiated the
intussusception or whether it was secondary to the
intussusception is not clear. However, the absence of
histopathological abnormalities in the sampled area
makes the second hypothesis seem more likely. None of
the previously mentioned risk factors for intussusception
were identified in the present case.
Intussusception occurs infrequently in human adults
(1% of all cases of intestinal obstruction and 5% of all cases
of intussusception) (Haas et al. 2003; Barussaud et al. 2006).
A demonstrable aetiology is found in 70–90% of cases of
adult intussusception, and approximately 40% of them are
caused by primary or secondary malignant neoplasm
(Reijnen et al. 1989; Eisen et al. 1999). Adult intussusception
occurs more frequently in the small (50–88%) than in the
large bowel (12–50%) (Azar and Berger 1997; Begos et al.
1997; Eisen et al. 1999; Warshauer and Lee 1999; Haas et al.
2003; Barussaud et al. 2006).
The most common clinical sign of intestinal
intussusception is abdominal pain that can be acute,
subacute or chronic. The pathogenesis of intussusception
in human adults is thought to be altered bowel peristalsis at
an intraluminal lesion, most often neoplasia, which is then a
lead point for the intussusceptum (Huang et al. 2000;
Chang et al. 2007; Wang et al. 2007). Diagnosing
intussusception in human adults is challenging due to
the varied presenting symptoms and time course.
Adult intussusceptions are detected by plain abdominal
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Colocolic intussusception in a horse
film, barium studies, abdominal ultrasound, abdominal
computed tomography (CT), angiography,
radionucleotide studies and magnetic resonance
imaging, with CT being the most sensitive reported
diagnostic test (Eisen et al. 1999; Barussaud et al. 2006;
Zubaidi et al. 2006; Chang et al. 2007; Wang et al. 2007;
Yamada et al. 2007). Of these various modalities used in
man, abdominal ultrasound is the only practically
available modality for use in mature horses.
Conclusions
Colocolic intussusceptions in horses, although rare, do
occur and should be considered as a differential in cases
of simple obstruction of the large intestine nonresponsive to
medical therapy, especially if presence of an abdominal
mass is suspected. Their aetiology is largely unknown
although abnormal motility may be a factor. The
association between colocolic intussusceptions and
colonic masses, which has been identified in man, has not
been established in horses.
Manufacturers’ addresses
1Abbott Animal Health, Abbott Park, Illinois, USA.
2Intervet,Schering-Plough Animal Health Corporation, Kenilworth, New
Jersey, USA.
3Teva pharmaceuticals, North Wales, Pennsylvania, USA.
4Pfizer Animal Health, New York, New York, USA.
5Fort Dodge, New York, New York, USA.
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