LARGE INTESTINE
MICHAEL W. ROSS R. REID HANSON, JR.
The equine large intestine consists of the following
segments (in aboral direction): the cecum, the large
colon, and the small colon (Fig. 36-1). Although these
segments form a continuum for the passage of digesta
from the ileum to the anus, the three portions are
considered to be separate structures, anatomically, func-
tionally, and surgically. The large intestine of the horse
is well developed and can be distinguished from that of
other domestic mammals by the large capacity and shape
of the cecum, and length of the small (descending)
colon.' The large intestine is sacculated for most of its
length and is approximately 7.5 to 8.0 m long.2
Cecum
The cecum is approximately 1m long, has a capacity
of 16 to 68 L , and occupies the right caudal abdominal
quadrant.' The cecum is comma shaped and is divided
into a base and body. The cecal base has a strong
mesenteric attachment to the dorsal body wall and
extends craniad to the level of the fourteenth or fifteenth
rib.2 The cecal base curves ventrally into the cecal body,
which ends in a cul-de-sac, the apex. The cecal body
has four longitudinal bands (teniae), the dorsal, lateral,
ventral, and medial bands, causing deep sacculations in
the body. The ventral band joins the medial near the
apex. The ileocecal fold runs from the antimesenteric
border of the ileum to the dorsal cecal band. The ileum
enters the medial, ventral aspect of the cecal base and
terminates in the ileocecal orifice. The cecal base is
divided into cranial and caudal portions by a transverse
fold, arising from the floor of the cecal base, just craniad
to the ileocecal junction. The cranial cecal base, or
cupula, is voluminous, forms a sigmoid structure, and
ends in the cecocolic orifice, which is located caudal in
the cupula. A well-developed cecocolic ligament (fold)
runs from the lateral cecal band to the lateral free band
of the right ventral colon. Because of its dense dorsal
mesenteric attachment, the cecocolic ligament and il-
eocecal fold, the cecum is immobile without concomitant
mobility of adjacent organs.
The cecal blood supply is derived from the cecal
artery, a branch of the ileocolic artery. The medial and
lateral cecal arteries (and veins) course in a loose
R. Reid Hanson, Jr. wrote the subsection on the Transverse and Small Colon
under the section on Anatomy and the section on Surgical Disorders.
mesenteric attachment along the medial and lateral cecal
bands, respectively. Because both cecal arteries are
derived from a single parent vessel without collateral
input, the cecum is particularly prone to thromboem-
bolic disease.
The caudal portion of the cecal base and body can
be felt on rectal examination. The ventral band is
prominent and is palpable per rectum. The cecal body
can be exteriorized through a ventral midline incision;
however, because of the presence of the dorsal attach-
ment, the base and ileocecal junction can be seen but
not exteriorized.
Large Colon
The large colon, measuring between 3 and 4.5 m,
is composed of the right ventral colon (RVC), the left
ventral colon (LVC), the left dorsal colon (LDC), and
the right dorsal colon (RDC) and begins at the cecocolic
orifice and ends at the transverse colon. The large colon
forms a long U-shaped loop, which is attached to the
dorsal body wall at the R D C and RVC. This well-
developed, voluminous loop is mobile, predisposing the
bowel to anatomic displacements and physical obstruc-
tions. The diameter of the large colon varies, with
narrowing occurring at the pelvic flexure, formed be-
tween the LVC and the LDC. The R D C narrows before
entering the transverse colon. The narrow areas are
prone to obstruction by digesta or foreign material.
The RVC begins at the cecocolic orifice and courses
cranioventrally to the sternal flexure, which lies dorsal
to the xyphoid cartilage. The RVC is sacculated and has
four bands-medial and lateral mesocolic bands and
medial and lateral free bands (Fig. 36-2). The RVC is
continuous with the LVC at the sternal flexure. The
LVC is similar to the RVC in sacculations and bands,
and runs caudally to the pelvic inlet. The LVC joins the
LDC at the pelvic flexure. At the pelvic flexure, the
bands of the LVC fade, leaving the pelvic flexure
unsacculated and with a narrow lumen. A single meso-
colic band is found in the LDC. The LDC runs cranially
to the diaphragmatic flexure and joins the RDC. Three
bands are found in the moderately sacculated R D C as
it courses caudodorsally, to end in the transverse colon.
The RDC has an enormous diameter described as a
stomach-like dilatation.'
The ventral and dorsal segments of the colon are
attached by the intercolonic mesentery. The major blood
380 ALIMENTARY SYSTEM

Small colon Transverse colon

Left dorsal
colon
\

FIGURE 36-1. The equine large intestine. Note the

mesenteric attachments of the cecum are located at the
cecal base and right dorsal colon (Redrawn from Mc-
Ilwraith CW: Equine digestive system. In Jennings PB
(Ed): The Practice of Large Animal Surgery. Philadel-
phia, W. B. Saunders Company, 1984, p 628.)

~ p e of
x cecum

supply to the colonic loop running in the mesentery is

derived from the right colic artery, supplying the dorsal
colon, and the colic branch from the ileocolic artery,
supplying the ventral colon (Fig. 36-2).3 These vessels
join at the pelvic flexure. The large colon is much less
susceptible to thromboembolic disease because of this
anastomosis and an extensive plexus of communications,
the rete mirabile (within the intercolonic mesenterv). J , ,

which is peculiar t; the equine specie^.^

Rectal examination is useful in identifying portions
of the large colon in health and disease. The pelvic
flexure can be palpated in most normal horses, and the
ventral colon is easily recognized by the distinguishing
bands. The R D C can only be felt with extensive impac-
tion. With the exception of the initial 15 cm of the RVC
and the last 25 cm of the RDC, the entire large colon
can be exteriorized through a ventral midline surgical
~ ~~

incision.

Transversce and Small Colon

The transverse colon is a constricted portion of

large intestine passing from right to left, cranial to the
root of the mesentery. The transverse colon joins the
voluminous R D C and small colon (SC) and can be felt
at surgery but cannot be exteriorized through a ventral
midline incision. The SC, a caudal continuation of the
transverse colon on the left of the mesenteric root,
occupies the caudal left quadrant of the abdomen along
with the jejunum. The SC is approximately 4 m long
and has a diameter of approximately 6 to 8 cm. The
mesocolon, which suspends the SC from the dorsal body
wall, increases to a midsection width of 80 to 100 cm.
The SC is connected to the duodenum by the short
duodenocolic fold. The SC continues at the pelvic inlet
as the peritoneal rectum that enlarges to form the
ampulla recti. The SC has wide, muscular mesenteric
and antimesenteric bands and coarse sacculations.
FIGURE 36-2. Cross-sectional diagram of the equine large intestine,
showing longitudinal smooth muscle bands (teniae, dark sections),
intercolonic mesentery, and associated vessels. SC, small colon, and
associated mesocolon; RDC, right dorsal colon; RVC, right ventral
colon; LCA, lateral cecal artery; MCA, medial cecal artery; LVC,
left ventral colon; LDC, left dorsal colon; RCA, right colic artery, a
branch from the cranial mesenteric artery; CB, colic branch, from the
ileocolic artery. The ileum is shown with its dorsal mesenteric attach-
ment and the ileocecal fold, coursing from its antimesenteric band, to
the dorsal band of the cecum. The cecocolic ligament courses from
the lateral cecal band to the lateral free band of the RVC. (Redrawn
from Habel RE: Applied Veterinary Anatomy. Philadelphia, W. B.
Saunders Company, 1986, p 247.)
 LARGE INTESTINE 381

FIGURE 36-3. Lateral view of the small (descending)

colon. 1, arcuate artery; 2, marginal artery; 3, long
artery; 4, small branch supplying the mesenteric tenia;
5, secondary arcade; 6, small branch to mesocolon.
(Redrawn from Beard WL, Lohse CL, Robertson JT:
Vascular anatomy of the descending colon in the horse.
Vet Surg 18:130, 1989.)

The major arterial supply to the SC is from the
caudal mesenteric artery, which divides into two major
branches-the left colic artery and the cranial rectal
artery. The left colic artery supplies the oral 75% of the
small colon and branches into four to eight arcuate
arteries that divide again into marginal arteries (Fig.
36-3).5.6 The cranial rectal artery courses caudally in
the small colon mesentery to supply the aboral 25% of
the small colon with similar arcuate and marginal arte-
ries. The joining marginal arteries form one functional
artery 1 to 2 cm dorsal to the entire bowel surface,
which is obscured from view by mesocolic fat (Fig. 36-
4). Marginal arterial overlapping obviates the need for
preservation of the marginal artery when performing
resection and anastomosis.
The SC can be easily recognized on rectal exami-
nation by the presence of fecal balls and the thick
antimesenteric band. The oral 30 cm and aboral 30 cm
of the small colon cannot be exteriorized through a
ventral midline surgical incision.
The extrinsic innervation of the large intestine is
derived from the celiacomesenteric plexus, celiac and
cranial mesenteric ganglion, and pelvic plexus. The more
important intrinsic neurons form the enteric nervous
system and the myenteric plexus. Extrinsic denervation
does not interrupt the intrinsic myoelectric activity of
the equine
mates of the resorptive capacity of the large intestine of
a 160 kg pony approximate 30 Llday, a volume equal to
the extracellular fluid volume (ECF) of the animal.8
Fecal water averages less than 10% of ileal outflow (Fig.
36-5), and net fluid absorption may approximate 95%
of delivered fluid. Diseases interrupting fluid dynamics
could potentially cause life-threatening changes in ECF
and electrolyte balance. The greatest quantitative net
water absorption occurs in the cecum.
Solute transport in the large intestine appears com-
plex but contributes greatly to the transmucosal move-
ment of water. Although digesta osmolality is main-
tained at roughly isotonic levels from the cecum to the
SC, concentrations of cations and anions change consid-
erably. The Na' concentration decreases markedly, but
there is a concomitant increase in K+ and NH,- concen-
trations from the cecum to the SC.' Organic acids
increase in the cecum and ventral colon but then de-
crease in the dorsal and SC. There is a steady increase
in the phosphate concentration. Although osmotic
changes in organic acid (VFA) production may contrib-

The two important physiologic functions of the large

intestine include (1) storage and absorption of fluid and
(2) retention of digesta for microbial digestion. These
functions have extreme importance in fluid and electro-
lyte balance and nutritional considerations. Complex
mechanisms are required to regulate digesta transit, to
provide optimal conditions for transport of electrolytes
and fluid, and to allow microbial fermentation of di-
gesta.'
5
FIGURE 36-4. Cross sectlon of the small colon with vascular anatomy
Fluid Absorption shown. 1, marginal artery; 2, secondary arcade; 3, long artery; 4,
branch supplying tenia; 5, anastomosis across antimesenteric surface.
The most important function of the large intestine (Redrawn from Beard WL, Lohse CL, Robertson JT: Vascular
is likely the absorption of large volumes of fluid. Esti- anatomy of the descending colon in the horse. Vet Surg 18:130, 1989.)
382 ALIMENTARY SYSTEM
PONY MAN
* tion of particulate digesta for microbial digestion (Fig.
1.5
FIGURE 36-5. Net water movement through the large intestine of a
70-kg man and 160-kg pony. Both species absorb approximately 90%
of ileal outflow, but in the pony, this represents approximately 30
Llday. The volume is roughly equivalent to the animal's extracellular
fluid volume. Note the cecum of the pony has greatest net water
absorption. (Redrawn from Argenzio RA, Lowe JE, Pickard DW, et
al: Digesta passage and water exchange in equine large intestine. Am
J Physiol 22631035, 1974.)
ute to net water movement, it appears likely that Na+
transport is the single most important f a ~ t o r . ~
A net decrease in cecal HCO,- is likely caused by
buffering of organic acids. This buffering reaction
(NaHCO, + HAC + NaAC + H,O + CO,
[AC:acetate] may aid in absorption of VFA, Na+ and
C0,+.7 An important function of the colon involves
acid-base balance. Horses with simple colonic obstruc-
tions may develop metabolic alkalosis, because of dis-
ruption of colonic buffering ~ a p a c i t y A
. ~ reduction in
VFA production in horses with colonic diseases may
decrease the normal Cl-:HCO,- exchange mechanism,
and lead to a relative decrease in HCO,- se~retion.~. lo
Microbial Digesti
A major physiologic function of the large intestine
is retention of fluid and digesta to facilitate important
microbial digestion. Like colonic fluid dynamics, micro-
bial digestion is regulated by the rate of passage of
digesta through the large intestine. Experimentally, fluid
(polyethylene glycol) and particulate markers leave the
cecum quickly and are passed to the ventral and dorsal
colon (Fig. 36-6).8 Marked retention of particulate
markers occurs in the ventral and dorsal colons, which
are considered the major sites of digesta retention.
Marker concentrations are similar in the RVC and LVC,
and therefore, the ventral colon is considered a single
compartment. Similar marker concentrations in the
LDC and R D C are found, and thus, a single dorsal
colonic compartment exists. The ventral-dorsal colonic
junction, the pelvic flexure, represents a major barrier
to the outflow of markers. The dorsal colon preferen-
tially retains larger markers. Transit of fluid and partic-
ulate markers occurs rapidly through the SC.
Experimentally, no retrograde transit of carbon
occurs from the ventral colon to the cecum or from the
dorsal colon to the ventral colon." Neither polyethylene
glycol nor particulate markers are passed in retrograde
fashion from cecum to ileum, or from dorsal to ventral
colon.10 From these results, it appears likely that the
ileocecal junction, cecocolic junction, pelvic flexure, and
transverse colon are responsible for the retention of
digesta and compartmentalization of the large intestine.
Mean transit time in the cecum is approximately 5
hours, whereas mean transit time for the large colon is
50 hours. Fifty percent transit of liquid markers to feces
occurs 24 hours after oral administration, but 50%
transit of particulate markers, 2 cm in length, takes
greater than 10 days, demonstrating considerable reten-
3 6 6 ) . This prolonged retention appears to be greater
than that in the ruminant fore stomach^.^^
Motility
The motor events of the large intestine are complex
and are incompletely understood. Both propulsion (the
aboral movement of digesta) and retropulsion (the oral
movement of digesta) exist in the cecum and the large
colon.
Digesta enters the cecum from the ileocecal junc-
tion, propelled by the migrating action potential com-
plex-a prominent, rapidly progressive electrical event
of the ileum.I3 Researchers have identified several mo-
tility patterns of the normal cecum through endoscopy
or visually through cannulas,I4.Is cinefluoro~copy,'~ and
indwelling intraluminal monometry, and by monitoring
myoelectric activity.I7.l8 Coordinated series of spike
bursts occur in the cecal base, which propel digesta to
the cecal apex (Fig. 36-7). Several series of spike bursts
within the cecal body appear to contribute to nonpro-
gressive, haustra-to-haustra mixing events. A progres-
sive motility pattern has been identified, which is initi-
ated at the cecal apex, propagated to the cecal body,
through the caudal and cranial portions of the cecal
base, and into the RVC. This pattern occurs once every
3 minutes in the fed pony, is associated with a loud
distinctive "rush" of digesta heard on auscultation, and
is likely responsible for the transit of digesta from the
cecum to the RVC. An electric pacemaker area located
within the ventral 10 to 15 cm of the cecal apex appears
to initiate this progressive motility pattern.I3. l8 Several
retropulsive patterns, generated from the cranial or
caudal cecal base, appear to be coupled with this pro-
gressive pattern.
In the RVC, the aboral, progressive pattern gen-
I LARGE INTESTINE
FIGURE 36-6. Retention of liquid and
particulate markers by the cecum, ven-
tral colon segments, and dorsal colon
segments (including small colon), and
fecal excretion of markers. Liquid
markers are passed rapidly from the
cecum, and 50% excretion occurred
within 3 days after administration. Re-
tention of particulate markers increased
as marker size increased. Less than
50% excretion of 2-cm markers oc-
curred in 10 days. Note relatively
greater retention of larger markers in
the dorsal colon. (From Argenzio RA,
Lowe JE, Pickard DW: Digesta passage
and water exchange in equine large
intestine. Am J Physiol 226:1035,
1974.)
erated at the cecal apex is rapidly propagated and
appears to be the dominant motility pattern. Both
propulsion and retropulsion exist in the RVC, indepen-
dent of the progressive pattern. Progressive motor
events of the RVC likely continue around the sternal
flexure to the LVC and end near the pelvic flexure.
The motor events of the pelvic flexure, LVC, and
LDC have been studied e~tensively.~. 14. l9 Coordinated
oral, aboral, and bidirectional pressure peaks exist,
originating from the pelvic flexure area, which demon-
strates that a colonic pacemaker region may exist here
(Fig. 36-8).19 Further study by in vitro electromyography
demonstrated the existence of an electric pacemaker
and direct electric coupling of longitudinal and circular
smooth muscle.4-I9 The electric pacemaker initiates pro-
pulsion and retropulsion, impeding the transit of digesta.
Retropulsive spike bursts are likely propagated through
the LVC to the RVC, and propulsive spike bursts may
continue around the dorsal colons to the transverse
colon.
In vivo electromyography of the cecum and large
colon has demonstrated the existence of long spike
bursts (LSB) which are longer than 5 seconds and short
spike bursts (SSB) which are shorter than 5 s e c ~ n d s . ' ~ , of
In the colon, LSB are associated with progressive and
simultaneous mechanical activity, whereas SSB result in
local mixing events. In the cecum, SSB commonly occur
during the progressive motility pattern and the terms
383
SSB and LSB may not be useful to describe cecal motor
events. Because of the large size and obvious reservoir
nature of the RDC, strong retropulsion likely exists in
this area, but the motility of the RDC, transverse colon,
and SC has not been characterized.
Motility of the cecum and large colon is markedly
affected by various pharmacologic agents and physio-
logic changes. Administration of xylazine, an a-2 adre-
nergic agonist, reduces cecal progressive motilityU and
mechanical activity24 for 30 minutes. Butorphanol, a
synthetic narcotic agonistlantagonist, reduces cecal pro-
gressive motility. The combination of xylazine and bu-
torphanol further delays return of progressive motility.
The anticholinesterase neostigmine increases cecal pro-
gressive motility for approximately 30 minutes.
In the large colon, narcotic agonists increase the
resting tone of intestinal muscle, whereas in limited
studies of narcotic antagonists, an increase in propulsive
motility is seen.25Xylazine and atropine sulfate reduce
motility of the pelvic flexure, whereas neostigmine in-
creases progressive motility.21 The acaricide Amitraz
causes dissociation of the coordinated pressure peaks of
the LVC and LDC. Paralysis of visceral afferent nerves
~ ~the pelvic flexure by the use of local anesthetics
decreases coordinated pressure peaks.19 Feeding and
electrical stimulation of extrinsic nerve supply increase
intraluminal pressure peaks. Colonic cooling decreases
conduction velocity and amplitude of pressure peaks.4
384 ALIMENTARY SYSTEM
FIGURE 36-7. Myoelectric activity of the cecum and right ventral
colon (RVC) in a pony. Time progresses from left to right. The
approximate location of the electrodes correspond to the numbers in
the anatomic insert. Two progressive motility patterns (b, b') initiate
at the cecal apex, the pacemaker region, and progress to sequentially
involve the cecal body, base, and continue into the RVC. Retrograde
motility patterns (a, a') progress from the cecal base to the apex,
before the progressive pattern, forming a repetitive pattern known as
the cecal myoelectric complex. A local haustra-to-haustra pattern (c),
likely involving mixing events in the cecal body, is present. (From
Ross MW, Rutkowski JA, Cullen KK: Myoelectric activity of the
cecum and right ventral colon in female ponies. Am J Vet Res 50:374,
1989.)
Experimental Strongylus vulgaris infestation results in
severe evidence of thromboembolism but fails to consis-
tently alter colonic m ~ t i l i t y . ~Substance
,'~ P-like immu-
noreactivity of enteric neurons is found in submucosal
ganglia, although its relationship to motility is un-
known.26
Simple obstruction (nonstrangulating), character-
ized by complete or near-complete occlusion of the
intestinal lumen, and strangulation obstruction, charac-
terized by vascular compromise of the involved intestine,
occur frequently in the large intestine. Horses with
obstruction of the large intestine represent between 37%
to 46% of horses admitted for evaluation of colic or for
surgical treatment.27-29The type and severity of obstruc-
tion dictate whether medical or surgical management is
instituted. Large intestinal obstruction differs from small
intestinal obstruction because of the aboral position of
the large intestine, the large size of the colonic segments,
and different physiologic functions and by-products.
Simple Obstruction
Simple obstruction of the large intestine is common
and is caused by impaction with feedstuffs, fibrous
foreign material, enteroliths, and fecaliths. Simple ob-
struction also occurs with nonstrangulating displacement
of the large colon, although displacement may progress
to strangulation obstruction. Functional obstruction,
known as spasmodic colic, is a form of simple obstruc-
tion.
Pathophysiologic changes with simple obstruction
vary with severity and duration of the lesion. Partial
obstruction, such as cecal impaction, or intermittent
enterolith obstruction of the RDC, causes mild patho-
physiologic changes. Complete simple obstruction can
progress rapidly, however, causing severe clinical signs
and irreversible pathophysiologic changes.
Abnormal motility, causing ileus or, for example,
impaction of the ventral colon, leads to the gradual
accumulation of gas from microbial digestion. The large
size of the ventral colon allows great quantities of gas
to accumulate, causing abdominal distention and colic.
Accumulation of digesta and fluid contribute to disten-
tion. Intestinal distention can decrease intestinal blood
flow, but in cats, intraluminal pressure increases from
34 to 54 cm H 2 0 are needed for this to occur.30 In
equine natural small intestine obstructions, intraluminal
pressure changes of only 4.5 to 21 cm of H,O are
found.31 Pressure changes in large intestinal diseases
may be higher and may contribute to vascular derange-
ments. Increases in intraluminal pressure could increase
mural pressure, causing collapse of venules, increased
capillary hydrostatic pressure, and interstitial edema. In
the small intestine, mural edema does not develop after
4 hours of luminal distention." In ponies with experi-
mentally produced pelvic flexure impaction, there is an
increase in blood flow to intestinal segments with ob-
s t r ~ c t i o n In
. ~ ~horses operated on with simple obstruc-
tions, mural edema occurs, although it is not known
whether edema is related to distention or other hemo-
dynamic changes. Initial increases in intestinal blood
flow may contribute to mural congestion and cause
edema.
Simple obstruction alters normal fluid and solute
absorption. The colon may become secretory, contrib-
uting to luminal distention and clinical dehydration.
Abnormal fluid dynamics with net fluid and electrolyte
loss into the lumen may contribute to disturbances of
motility and further propagate the obstructive process.
In simple obstruction, septic or endotoxic shock is
unusual and does not occur until late when necrosis of
the intestinal segment occurs. Depletion of plasma vol-

FIGURE 36-8. Motor events of the
left ventral and left dorsal colon seg-
ments and pelvic flexure. Number of
motility tracing channels corresponds
to the portion of the intraluminal
catheters located in anatomic insert.
Note the coordinated bidirectional
pressure peaks, starting between loci
3-4, corresponding to both propul-
sion (4 + 6 ) and retropulsion (3 +
1). A wandering pacemaker area ex-
ists that initiates the bidirectional and
unidirectional peaks and is responsi-
ble for controlling coordinated motil-
ity events in the area of the equine
large intestine. (From Sellers AF,
Lowe JE, Brondum J: Motor events
in equine large colon. Am J Physiol
237:E457. 1979.)
ume and reduction of cardiac output causing
clinical signs of dehydration, elevation of the heart rate,
and poor peripheral perfusion. These changes generally
occur late in most horses with simple obstruction, and
many of the systemic changes may be related to pain
rather than to the hemodynamics of fluid loss.
Acid-base disturbances occur but are generally not
severe. The classic metabolic disturbance of horses with
colic, namely metabolic acidosis, is uncommon in horses
with simple obstruction, unless ischemia and necrosis of
the obstructed segment occurs. Necrosis of the small or
large colon can occur with severe impactions. Horses
with cecal perforation secondary to simple obstructions
develop cardiovascular collapse and metabolic acidosis.
In horses with spasmodic colic (gaseous distention of
the large colon) or impaction of the large colon, mild
metabolic alkalosis may occur, secondary to alterations
of VFA production and normal Cl-:HCO,- exchange
mechanism (see the section on Physiology). Severe
gaseous distention of the large colon may compress the
duodenum, causing partial or complete obstruction. This
results in retention of gastric and upper gastrointestinal
secretions, and may lead to further metabolic alkalosis
because of sequestration of gastric hydrochloric acid.
Generally, acid-base disturbances are mild.
The hallmark pathophysiologic changes of horses
with simple obstruction, namely, gas distention and
secondary distention of intestinal segments orad to the
obstruction, abdominal distention, pain, progressive de-
hydration, slow cardiovascular collapse, and mild acid-
base disturbances, progress with the severity of the
lesion. Because of the aboral location of the large
intestine relative to the small intestine, cardiovascular
changes are generally slower to develop. Within the
large intestine, horses with small colon obstruction de-
velop signs more slowly than horses with large colon
LARGE INTESTINE 385
obstructions. Therefore, clinical signs may take 24 to 48
hours to develop.
Abdominal auscultation of horses with simple ob-
struction often reveals an increase in borborygmi early
in the disease process, followed by a progressive de-
crease. In ponies, experimental simple obstruction of
the small intestine produces similar initial increases in
electric activity in the oral segment, followed by a
progressive decrease later in the obstructive process.35
Strangulation Obstruction
Strangulation obstruction occurs most commonly
due to volvulus (torsion) of the large colon (VLC) but
can affect the cecum and SC as well. Two forms of
strangulation obstruction exist. Hemorrhagic strangula-
tion obstruction occurs when luminal obstruction is
accompanied by venous o c c l ~ s i o n .In ~ ~this common
form, there is a rapid onset of mural edema; thick, dark
purple serosa; and purple-black mucosa. The second
form, ischemic strangulation obstruction, involves lu-
minal compromise plus venous and arterial occlusion.36
In ischemic strangulation obstruction, more mild edema
develops, and the bowel serosa becomes gray or blue-
gray.
In horses with VLC, hemorrhagic strangulation
obstruction is most common but can rapidly progress to
complete ischemic o b s t r ~ c t i o nTherefore,
.~~ a combina-
tion of pathophysiologic mechanisms is generally
present. The prognosis in horses with this severe form
of disease is poor.
Initial venous occlusion causes severe edema of the
bowel wall and stagnation of blood flow. Vascular oc-
clusion and low-flow states cause mucosal damage. Al-
though mucosal changes have not been studied exten-
386 ALIMENTARY SYSTEM
sively, changes may be similar to those seen in small
intestinal o c c l ~ s i o n .In
~ ~ the small intestinal villi, a
countercurrent exchange mechanism exists owing to the
hairpin-like vascular a r r a n g e ~ n e n t .During
~~ low-flow
vascular states, oxygen and other nutrients may "short-
circuit7' the villus tip, leaving the tip relatively anoxic
compared with the villus base.36 During venous occlu-
sion, this mechanism would explain the initial and most
severe changes seen at the villus tip.36 In the colon, the
mucosal architecture is different, but because of the
close proximity of arterioles and draining venules, a
countercurrent exchange mechanism may exist to ex-
plain mucosal damage."38
If both venous and arterial occlusion exist, or initial
venous occlusion progresses to arterial occlusion, more
severe histologic changes result. In horses with ischemic
occlusion or hemorrhagic occlusion, the histologic
changes may be similar. The equine colonic mucosa may
be approximately 25% more resistant to ischemia than
the equine small intestinal m u ~ o s a . ~Histologic ~.~~
changes of hemorrhage and edema in the mucosa and
submucosa, the degree of superficial and crypt cell
damage, and a measurement that reflects mucosal pres-
sure are used to grade large colon d a ~ n a g e . ~With ~,~'
increasing mucosal edema, there is an increase in inter-
stitial-to-crypt ratio, a measurement of the width occu-
pied by the interstitium relative to crypt Increas-
ing interstitial-to-crypt ratio, an increase in the percent
of superficial colonic mucosal cell sloughing, and an
increase in crypt cell damage correspond to more severe
colonic damage.36
Fluid and electrolyte loss accompany progressive
mucosal damage. In hemorrhagic occlusion, initial fluid
loss and cardiovascular collapse accompany bowel
edema and mucosa damage, causing clinical signs of
hypovolemic shock. In horses with advanced hemor-
rhagic occlusion or with ischemic occlusion, extensive
mucosal damage is accompanied by disruption of the
mucosal barrier. Transmural necrosis occurs, allowing
absorption of endotoxin and, later, enteric bacteria
access to the peritoneal cavity and then to the systemic
c i r ~ u l a t i o n .The
~ ~ hepatic reticuloendothelial system,
which is normally able to absorb endotoxin efficiently,
becomes ischemic with cardiovascular deterioration, and
further endotoxin distribution occurs.40 Endotoxin
causes further deterioration in the hemodynamic, he-
matologic, and blood chemical systems, including hy-
potension, increased packed cell volume, leukopenia,
metabolic acidosis, disseminated intravascular coagula-
tion (DIC), and disruption of glucose metab~lism.~'
From both a pathophysiologic and clinical stand-
point, the most important consideration in treatment
and prognosis is early medical and surgical intervention
to limit loss of bowel integrity. Progressive bowel dete-
rioration causes clinical signs of cardiovascular collapse,
tachycardia, poor peripheral perfusion, increased capil-
lary refill time, and poor peripheral pulse. Dehydration
is accompanied by an increase in packed cell volume
(PCV), but with further loss of bowel integrity, loss of
plasma protein total (TTP) occurs. Elevation of PCV
may not be accompanied by an increase in plasma
protein, and the increase in PCV/TTP ratio is generally
a poor prognostic sign.
The pathophysiologic mechanism leading to mu-
cosal damage during hemorrhagic or ischemic insults is
clear, but recently, additional damage caused by return
of blood flow, or reperfusion injury, has come to light.
After surgical correction of strangulation obstruction,
further damage may occur. Lipid peroxidation and pro-
tein denaturation leading to enzyme activation and al-
teration of membrane integrity occur, secondary to an
increase in superoxide (0,) radicals, hydroxyl radical
(,OH), single oxygen, and hydrogen p e r o ~ i d e . ~ ~ . ~ ~
Normal scavenging systems, including ascorbate, gluta-
thione peroxidase, catalase, and superoxide dismutase
may be depleted, allowing the build-up of damaging
free radicals.36 During the ischemic period, neutrophils
build up and may increase the severity of the reperfusion
i n j ~ r y . ~In
~ ,clinical
"~ situations, serosal color and gross
vascular supply may improve after a strangulated seg-
ment is untwisted. However, mucosal and submucosal
damage continues, leading to ileus, peritonitis, cardio-
vascular collapse, and death within 1 to 3 days. For an
in-depth discussion on this subject, please review Chap-
ter 33.
Cecum
Cecal Impaction
ETIOLOGY
The most important disease of the cecum is cecal
impaction (CI), which represents approximately 5% of
all intestinal impaction^.^. 45- Cecal impaction generally
involves fibrous feedstuffs, but impaction with sand can
occur. Although classic cases of CI include older horses
with poor dentition and fed poor quality feedstuffs,
recent reports indicate that younger horses, particularly
horses hospitalized for other nonrelated disorders, are
at r i ~ k . " ~ The
, ~ ' pathogenesis of CI likely involves a
primary cecal motility dysfunction. Observations at sur-
gery or necropsy reveal a large, digesta-filled cecum and
a relatively empty RVC (Fig. 36-9). Because only a
single motor event is common to the cecum and RVC,
interruption of this progressive motility pattern leads to
cecal filling (see the section on Physiology). Propulsion
in the RVC continues, and this segment empties. Al-
tered cecal blood flow secondary to parasite damage,
dietary changes, or other clinical conditions may inter-
rupt or slow the cecal pacemaker. Transit of small
volumes of digesta and gas continue, because oil appears
in the feces and gas accumulation of the cecal base is
unusual. Initially, digesta is normal in character but may
become dry, resembling the expected "impacted di-
gesta."
HISTORY AND CLINICAL SIGNS
Typically, horses with CI are intermittently an-
orexic, depressed, and show signs of mild abdominal
pain, such as looking at the flanks, rolling, and pawing.
Frequently, the horses have experienced a management

FIGURE 36-9. The cecum and large colon. ( A ) , Cecum and
large colon from a normal horse, showing, the normal
relative size of the organs. (B), Cecum and large colon from
a horse with cecal impaction and subsequent perforation.
Note the large, digesta filled cecum and relatively empty
large colon. A motility dysfunction exists that causes cecal
filling but allows colonic emptying. This lesion is found in
horses with cecal impaction or cecal perforation secondary
to cecal outflow dysfunction.
change or are being treated for unrelated gastrointestinal
or musculoskeletal disorders. Vital parameters and lab-
oratory values are usually within normal limits.
Rectal examination is diagnostic, but in rare in-
stances, the enlarged cecum cannot be felt. The clinician
must differentiate the cecum from other organs such as
the RDC or a displacement of the ventral colon. A firm,
near-hard viscus is often felt, with a single, distinct band
(ventral cecal tenia). The cecum is attached to the dorsal
body wall, and the examiner cannot pass a hand dorsal
to the impacted mass. Because the colon is usually
empty, it is difficult to feel the pelvic flexure. Fecal
production is reduced, and feces range from dry to
"cow-flop" in nature. Intermittent diarrhea can occur.
Cecal progressive borborygmi are reduced.
TREATMENT
SELECTION.Disagreement exists over the most
appropriate treatment of horses with CI. Medical man-
agement has been ad~ocated.~~-'OMost authors acknowl-
LARGE INTESTINE 387
edge the limitations of medical management, although
one author reports good success.50 Because the chance
of cecal perforation exists with continued cecal filling,
other authors have recommended surgical management,
particularly in horses unresponsive to medical therapy.
Earlier surgical techniques included manual massage,
sometimes accom~aniedbv water infusion of the im-
pacted digesta, evacuation of cecal contents by enter-
otomy (typhlotomy), and partial to complete typhlec-
t ~ m y .47,~ 49,~ 51-53
. Results with enterotomy and
evacuation of cecal contents, or infusion and massage,
were variable, which sparked development of newer
surgical techniques.'16 These techniques were developed
to address the pathogenesis of CI, namely the develop-
ment of a primary cecal motility dysfunction, which is
slow to return after surgery.
Currently, management of horses with CI depends
largely on the result of rectal examination and physical
examination of the patient. If the cecum is small or
moderate in size and the patient's vital parameters are
normal, initial medical management is recommended.
388 ALIMENTARY SYSTEM

Surgery is recommended if the cecum is extremely large,

or the digesta is near hard in consistency, in horses with
CI refractory to medical management, or in horses with
recurrent CI.54
NONSURGICAL MANAGEMENT. Successful medi-
cal management requires both oral and intravenous fluid
therapy, and withholding feed until the cecum returns
to normal size, based on rectal examination. Neostig-
mine (0.0125 to 0.025 mglkg) may increase cecal pro-
gressive motility, and has been used with limited success;
however, one should be extremely careful because cecal
perforation is a potential sequela. Until it is clinically
justified, use of the drug should be restricted to horses
with recurrent impaction or when economic constraints
restrict surgical intervention. Stimulation of cecal motil-
ity by walking and grazing may represent a beneficial
adjunctive treatment, although the volume of grass
ingested must be closely regulated. Because fasting
causes cessation of cecal progressive motility, it may be
important to stimulate motility in this manner.13
SURGICALMANAGEMENT.Recently, several sur-
gical techniques have been developed to prevent recur-
rence of clinical signs and are used in conjunction with
surgical techniques such as infusion, massage, or simple
evacuati~n.~~-~' FIGURE 36-10. The cecum and origin of the right ventral colon. The
Typhlotomy. Typhlotomy may be used alone or dotted areas show the location of the cecocolic anastomosis, a surgical
procedure useful for horses with cecal impaction. The anastomosis is
in combination with cecocolic, jejunocolic, or ileocolic performed between the lateral (A) and dorsal (B) cecal bands, and
anastomoses. Typhlotomy is performed midway be- the lateral (C) and medial (D) free bands of the RVC. The cecocolic
tween the ventral and lateral cecal bands, after appro- ligament (E) runs between the lateral cecal band and lateral free band
priate draping has been performed to prevent peritoneal of the RVC. (Redrawn from Ross MW, Tate LP, Donawick WJ, et
contamination. Peritoneal contamination is generally al: Cecocolic anastomosis for the surgical management of cecal im-
paction in horses. Vet Surg 15:85, 1986.)
more common with typhlotomy incisions than with col-
otomy incisions, because only the apex and body of the
cecum can be exteriorized. The surgeon must remember
that the cecal base is divided and the cupula (cranial prevent cecal filling, and the complete ileocolic anasto-
base) is generally large and digesta filled and needs to mosis with ileal transection was s ~ p e r i o r . ~However,
'
be emptied. the incomplete jejunocolic anastomosis was successful
Cecocolic Anastomosis. Cecocolic anastomosis, a in preventing recurrence of CI in one horse.s6
technique developed to avert the possible postoperative In summary, if surgery is required in horses with
complications of recurrent CI and perforation, provides CI, typhlotomy and manual evacuation should be fol-
an alternative route of digesta transit from the cecum lowed by some form of bypass procedure. Complete
to the RVC (Fig. 36-10).55 Generally, the technique is ileocolic anastomosis offers advantages over other pro-
combined with typhlotomy and evacuation of cecal con- cedures and has been effective clinically. Incomplete
tents. The anastomosis, a combination of hand-sewn ileocolic or jejunocolic anastomoses, or cecocolic anas-
seromuscular layer closures and use of the GIA-stapling tomoses remain viable surgical alternative.
instrument (U.S. Surgical, Norwalk, CT), is performed
between the lateral and dorsal cecal bands, and the -
Cecal Perforation
lateral free and lateral mesocolic bands of the RVC. In
the original report, 12 of 14 horses (86%) survived 2 PATHOGENESIS
months or longer and 10 horses (71%) survived longer
than 1 year. Four horses had intermittent colic related Cecal perforation (CP), although not considered a
to gas distention of the cecum or large colon, but none surgical disease, is a relatively recently characterized,
developed recurrent cecal impaction. important cecal disease. Because of the close association
Jejunocolic and Ileocolic Anastomoses. Jejuno- of CP to CI, equine surgeons should be familiar with
colic'6 or ileocolic anastomosess7represent more recently the pathogenesis of the disease. The pathogenesis of
developed surgical techniques designed to completely or CP, a uniformly fatal disease, appears to involve two
incompletely bypass the cecum, thus rerouting digesta different pathways: (1) CP may be primarily idiopathic
from the aboral small intestine to the colon. Typhlotomy in origin in broodmares near parturition, in which no
with cecal evacuation can be performed. Jejunocolic or obvious cecal motility dysfunction exists; and (2) more
ileocolic anastomoses can be performed in a side-to-side commonly, CP is secondary to a primary cecal motility
fashion, using combined hand-sewn seromuscular layer dysfunction, which although undetected, leads to cecal
closures and use of the GIA-stapling instrument. The filling and, later, to perforation.
incomplete side-to-side ileocolic anastomosis did not IDIOPATHIC DISEASE. Cecal perforation and

death occurred in 11 horses within 24 hours after
parturiti~n58-62 and during gestation in one mare.63 In
this form of CP, gas accumulation may lead to perfora-
tion. The cecum and colon are normal in size, and no
accumulation of digesta is found. In women undergoing
obstetric procedures, signs of intestinal obstruction and
late CP may occur. Cecal perforation in horses may be
similar to this form of intestinal pseudo-obstruction
(Ogilvie's syndrome) in humans.
M o n ~ mDYSFUNCTION. The most common
form of CP appears to be related to a dysfunction of
cecal motility, leading to filling (impaction) and subse-
quent perforation. At necropsy examination, the cecum
appears large and digesta filled, and the colon is rela-
tively empty (see Fig. 36-9), similar to that seen in
horses with CI. In a recent study, 22 horses (6 weeks to
13 years of age) had signs of CP.61 All horses had a
single site of perforation (Fig. 36-11). The majority of
these horses were hospitalized, receiving treatment with
nonsteroidal anti-inflammatory drugs (NSAIDs). Early
signs of the disease may be masked by the analgesic
properties of NSAIDs, allowing horses actually affected
with CI to progress to CP. Horses hospitalized with
other disorders and treated with NSAIDs also appear
to be at risk to develop CP. Subtle signs of gastrointes-
tinal disease, such as partial anorexia, a reduction in
fecal output, a change in fecal quality, or decreased
borborygmi, should be carefully investigated. A rectal
examination is indicated, but the clinician must remem-
ber that because of colonic emptying, the enlarged
cecum can assume a more cranial location and may not
be palpable.
Clinical signs after CP include those seen with
severe endotoxin shock or gram-negative sepsis. Al-
though complete typhlectomy and peritoneal lavage
remain theoretical treatment alternatives, euthanasia is
most appropriate.
MEDIAL LATERAL
FIGURE 36-1 I . Diagram of the medial and lateral aspects of the
cecum, showing the reported sites of cecal perforation in 17 horses.
A single site was identified in each horse. a, dorsal base, 3 horses; b,
dorsomedial base, 2 horses; c, ventromedial base, 1 horse; d, ventral
body, 6 horses; e , lateral body, 3 horses; f, distal lateral body, 2
horses. The interrupted line indicates the anatomic division between
the cecal base and body. The cecum may perforate more frequently
along bands, but no location appears particularly at risk. (From Ross
I MW, Martin BB, Donawick WJ: Cecal perforation in the horse. J
Am Vet Med Assoc 187:249, 1985.)
1
LARGE INTESTINE 389
Cecocecal and Cecocolic lntunusception
HISTORY AND CLINICAL SIGNS
Intussusception of the cecal body into the base or
a continuation of the invagination into the RVC is
uncommon but requires surgical i n t e r ~ e n t i o n The
.~~~
disease is not breed, age, or sex specific. The etiology
is unclear, but various authors have suggested the in-
volvement of the tapeworm Anoplocephala perfoliata.
Tapeworms may cause abnormal motility of the cecum
if they are present in high number^.^' Tapeworms were
present in only 3 of 10 horses with intussu~ception.~~ A
recent report questions the importance of tapeworms,
because intussusception occurred in horses not infested
with tapeworms with a frequency of two times that of
infested horses.68 Abnormal motility caused by an or-
ganophosphate was proposed as a cause of intussuscep-
tion.(j9
Three distinct forms of the disease exist, based on
clinical examination and duration of the clinical signs.
In the acute form, horses have severe abdominal pain
and require immediate attention. Changes in vital pa-
rameters and laboratory values are generally more se-
vere in this form, and the acute onset may reflect a
greater degree of vascular and neural compromise of
the intussusceptum. In the subacute form, horses are
generally depressed and have intermittent abdominal
pain and reduced fecal output. In the chronic form,
horses exhibit weight loss, pyrexia, and mild, intermit-
tent abdominal pain. When the invaginated portion
becomes devitalized, there is an exacerbation of clin-
ical signs, cardiovascular deterioration, acidosis, and
changes in peritoneal fluid values.
The clinical signs vary, depending on the time of
examination relative to the onset of the disease. Rectal
examination is most helpful in establishing the diagnosis.
Four of eight horses with intussusception had an en-
larged viscus felt on rectal examination, and in some
horses, the cecum was not palpable at
TREATMENT
Surgical management is mandatory for a successful
outcome, and in some horses, exploratory surgery is
necessary to confirm the diagnosis. At surgery, the cecal
apex is not found or a mass may be identified in the
cecal base or the origin of the RVC. Manual reduction
is often possible. The involved cecum is generally edem-
atous, devitalized, and requires resection. Following
double ligation of the medial and lateral cecal vessels,
the devitalized portion is resected, followed by a double
inverting closure of the cecal body. As much as 50% to
60% of the cecum can be removed through a ventral
midline approach.
In horses with cecocolic intussusception in which
extramural manual reduction is not possible, an enter-
otomy of the RVC is necessary. The 15- to 20-cm long
colotomy incision, made between the medial and lateral
free bands of the RVC, is followed by intraluminal
resection and closure of the edematous cecal apex.
Double ligation of the cecal vessels is required. After
resection and closure, eversion of the cecum through
390 ALIMENTARY SYSTEM
the cecocolic orifice is usually possible. Once the colot-
omy incision is closed, an additional closure of the cecal
body is performed. Manual reduction of the intussus-
ceptum from within the lumen of the RVC can precede
resection in some horses.
The prognosis is considered favorable, if all of the
necrotic cecum can be removed. The pacemaker area,
necessary for generation of normal cecal motility, wan-
ders over a 40 cm area near the apex in ponies.''
Therefore, nearly the entire cecal body can be removed.
Cecal Infarction
Thromboembolic disease of the cecal arteries is rare
but can occur following damage from S. vulgaris migra-
tion. The arterial supply of the entire cecum arises from
the single cecal artery, a precarious vascular arrange-
ment. The medial and lateral cecal arteries are located
180 degrees apart and lack extensive communications,
further predisposing the cecum to vascular insult.
The disease can occur in a horse of any age but is
more common in horses younger than 1 year of age.
Clinical signs can vary from those associated with acute,
severe abdominal pain and cardiovascular collapse, re-
quiring immediate surgical intervention to low-grade
abdominal pain, diarrhea, and peritonitis. Peritoneal
fluid changes reflect ischemic necrosis.
Surgical therapy consisting of partial typhlectomy
may be successful, if the entire necrotic portion can be
removed. Complete typhlectomy after 18th rib resection
in left lateral recumbency is also a consideration. Pro-
gressive infarction after surgical removal can occur. The
prognosis in these horses is grave.
Cecal Torsion
As a primary disease entity, cecal torsion is rare
but can occur under unusual situations, such as with
adhesion or entrapment of the cecum. Normally, the
cecum is relatively immobile and can move only with
concomitant movement of the RVC and ileum. Re-
cently, cecal torsion was described as a consequence of
hypoplasia of the cecocolic ligament.'O The cecum may
be displaced or twisted in horses with volvulus of the
large colon. When this occurs, the axis of rotation
involves the dorsal mesenteric attachment of the cecum.
The lesions in these horses are often severe, and the
prognosis depends on the degree of vascular compro-
mise. If a true cecal torsion is present, partial or com-
plete typhlectomy may be necessary.
Miscellaneous Conditions of the Cecum
Adhesion of the cecum to the ventral body wall is
unusual, except after ventral midline exploratory inci-
sions. Clinicians have suspected cecal adhesion in horses
with mild, intermittent colic. Rectal examination may
reveal chronic cecal malposition. Cecal-cutaneous fistula
is rare but was reported after application of an umbilical
hernia clamp.'l Congenital abnormalities are rare, but
the author has observed a single horse with colic due to
absence of the dorsal mesenteric attachment of the
cecum and subsequent large colon displacement.
Large Colon
The large colon is particularly prone to simple and
strangulation obstruction because of certain physiologic
functions. Retention of digesta and water absorption,
complex motility patterns, the relative lack of mesenteric
attachment, and changes in lumen diameter predispose
the large colon to disease. Many forms of simple obstruc-
tion respond favorably to medical management but may
progress to or be confused with lesions requiring surgical
intervention.
Impaction of the Ventral Large Colon
ETIOLOGY
Impaction of the ventral colon is one of the most
common and important diseases of the equine colon.
Commonly referred to as pelvic flexure impaction, this
form of simple, intraluminal obstruction involves the
accumulation of digesta in the LVC initially, with sub-
sequent filling of the sternal flexure and RVC. The
pathogenesis likely involves interruption or dysfunction
of the pelvic flexure pacemaker region. Impactions are
unlikely to develop through simple ingestion of dry or
coarse feedstuffs. A decrease in propulsive motility or
an increase in retropulsive motility could cause the
accumulation of digesta. In horses with colonic impac-
tion, the digesta appears to be retained just orad t o the
pelvic flexure, involving a long segment of the ventral
colon, and does not simply involve the pelvic flexure
alone. The digesta is generally firm and contains fibrous
feed material, although sand accumulation can cause a
similar lesion. In horses with sand im~actionof this
area, a shorter segment of colon is involved and the
actual pelvic flexure can be obstructed. Factors such as
poor feed quality, poor dentition, reduced water intake,
and parasite damage could cause impaction. Change in
management conditions such as a stable change, a move
from pasture to barn housing, shipping, and systemic
diseases may also predispose the large colon to impac-
tions.
HISTORY AND CLINICAL FINDINGS
Typically, horses with impaction of the ventral
colon exhibit a gradual onset of clinical signs. Often,
horses are partially or completely anorexic, and there is
a gradual decrease in fecal production. Signs of low-
grade abdominal pain, such as rolling, pawing, stretch-
ing, and looking at the flanks, are present initially but
may progress to signs of severe abdominal pain with
increasing large colon distention. Initial vital parameters
are normal, but during painful episodes, heart and
respiratory rates can be moderately elevated. Initially,
auscultation may reveal an increase in borborygmi, but
with disease progression, intestinal sounds are often
reduced or absent. It could be shown experimentally

that loud longer borborygmi are associated with colic
and simultaneous increases in intraluminal pressure of
40 mm Hg.33
Horses treated early with oral fluid and electrolytes,
restriction in oral feed intake, and analgesics to control
abdominal pain generally respond favorably. However,
many horses are refractory to early or inadequate treat-
ment, and clinical signs progress. Signs may progress
for 5 to 7 days. Gradual filling of the LVC and RVC
with digesta and subsequent gas distention of the ventral
colon and cecum occurs with complete obstruction. A
gradual increase in abdominal distention is accompanied
by increased signs of abdominal pain and an elevation
in heart and respiratory rates. Auscultation reveals
tympanitic sounds, and simultaneous auscultation and
percussion reveal a high-pitched "ping" over the cecum.
Clinicopathologic changes are generally minimal, but
there may be a mild increase in PCV and total protein
levels, indicating mild dehydration. Peritoneal fluid
changes occur only with advanced impaction and sub-
sequent devitalization of the colon. Late in the disease,
progressive distention of the RVC and cecum may cause
duodenal compression and passive build-up of gastric
fluid, but this is unusual.
During rectal examination, the firm, enlarged ter-
minal LVC can be readily palpated. Often, the left colon
segments are rotated 90 to 180 degrees in horses with
impaction of the ventral colon. The LVC can be iden-
tified by the distinct free and mesocolic bands. Rectal
examination is useful in monitoring progress of the
impaction. The initial soft, doughy mass may progress
to a firm, near-hard, digesta-filled ventral colon. Cecal
gas distention can be readily palpated. Occasionally, the
LVC and pelvic flexure are pushed caudally into the
pelvic canal. Rectal examination reveals the firm, im-
pacted viscus close to the anus. Obstruction in these
horses is complicated by additional extraluminal restric-
tion of the pelvic canal, resembling a pelvic hernia.72
TREATMENT
NONSURGICALMANAGEMENT. Horses with im-
paction of the ventral colon should respond favorably
to medical management. Withholding feed and admin-
FIGURE 36-12. Drawing of the equine cecum and large
colon of a horse with impaction of the ventral large
colon during colotomy and evacuation. The ventral colon
segments are enlarged with firm digesta, whereas the
dorsal colon segments are small and relatively empty.
The enterotomy is performed between free bands in the
terminal left ventral colon and a soft rubber tube is used
to provide warm water lavage of the impacted colon.
The same technique can be used for impaction of the
colon at other sites. (Redrawn from Foerner JJ: Diseases
of the large intestine, differential diagnosis, and surgical
management. Vet Clin North Am Equine Pract 4:130,
1987.)
LARGE INTESTINE 391
istering oral and intravenous fluids and analgesic therapy
are usually successful. Feed should be withheld until the
colic subsides, manure production has returned, and the
impaction has resolved, based on rectal examination
findings. During resolution of the impaction, semi-
formed and sometimes fluid feces can be passed. Occa-
sionally, clinicians report mild colic associated with the
return of normal motility and resolution of the impac-
tion.
The pathogenesis o f impactions may, in part, in-
volve dehydration of the impacted digesta. Transit of
dry digesta may be further impeded. Aggressive oral
fluid therapy (8 L water and electrolytes given via
nasogastric tube, three to four times each day), com-
bined with intravenous fluid therapy (1 to 2 Llhr),
hydrates the digesta, returns the patient to a more
normal systemic hydration status, and may improve local
conditions of the bowel wall that are necessary for
normal motility.
Abdominal pain is controlled by judicious use of
flunixin meglumine in most horses. In some horses,
however, xylazine administration is needed and effective
for more potent analgesia, but xylazine inhibits progres-
sive motility of the colon for a minimum of 30 minutes
after admini~tration.~~ The clinician must avoid giving
multiple doses of xylazine or narcotic analgesics, because
motility dysfunctions may be prolonged.
SURGICALMANAGEMENT. Surgical management
is necessary in horses with impaction causing severe
abdominal distention, in horses with severe abdominal
pain, or in horses with progressive cardiovascular dete-
rioration or changes in peritoneal fluid values. Ventral
midline exploratory celiotomy reveals various degrees
of digesta filling of the ventral colon and a small LDC
(Fig. 36-12). Edema of the intercolonic mesentery and
mild thickening of the bowel wall are commonly en-
countered. Extreme care must be taken not t o rupture
the distended ventral colon during manipulation. To
prevent this fatal sequela, the surgeon should use the
arms for bowel handling (see Fig. 33-19), and use large
abdominal incisions (up to 45 to 50 cm in some horses).
Occasionally, infusion of sterile saline solution and mas-
sage of the digesta result in a successful outcome.
Enterotomy combined with evacuation of the accumu-
lated digesta is most successful but must be performed
Origin of
small colon
392 ALIMENTARY SYSTEM
with adequate preparation to avoid excessive contami-
nation. The enterotomy should be performed in the
terminal LVC between bands. The pelvic flexure and
origin of the LDC should be avoided. Evacuation is
aided by using a hose and large volumes of water. An
assistant, prepared and gowned for aseptic surgery, is
necessary to aid during manipulation of digesta in the
RVC.
The prognosis after surgery is good to excellent.
Occasionally, a motility dysfunction persists and impac-
tion recurs. Medical management is instituted.
Impaction of the Right Dorsal Colon
ETIOLOGY
The RDC preferentially retains larger digesta par-
ticles and has a large reservoir function for microbial
digestion. Strong retropulsion must exist. Marked nar-
rowing of the lumen diameter occurs as the RDC enters
the transverse colon. Because of these factors, the RDC
is prone to impaction. Impactions of the right dorsal
colon are not as common as those of the ventral colon
but generally consist of very firm digesta or sand. Horses
with this disease may respond slowly to medical therapy
and are at risk for recurrence of the problem. Impaction
of the RDC may be more common in mares before
parturition, which suggests that a motility problem may
be a factor. An enlarged firm RDC is often found in
horses with nonstrangulating displacements or volvulus
of the large colon. The pathogenesis may involve a
primary motility dysfunction of the RDC, digesta and
gas accumulation, rotation with eventual displacement,
or volvulus.
HISTORY AND CLINICAL FINDINGS
Horses with impaction of the RDC show signs
similar to that seen in horses with impactions of the
cecum or ventral colon. Because of the aboral position
of the impaction, signs are slow to progress. Intermittent
fecal passage indicates that a partial obstruction may
exist. In horses with advanced disease, secondary duo-
denal obstruction due to enlargement of the RDC may
cause gastric distention.
Rectal examination is most helpful. In the normal
horse, the RDC is not palpable. In horses with impac-
tion, the RDC shifts caudally and may be palpated as a
firm viscus without obvious bands. Occasionally, a me-
socolic band with an associated vessel is felt. The ex-
aminer can usually pass the hand dorsal to the firm
viscus, a useful technique to help differentiate impaction
of the RDC from that of the cecum. In these horses,
the clinician is most likely palpating the oral portion of
the RDC.
TREATMENT
NONSURGICAL MANAGEMENT. Aggressive medi-
cal management as described for horses with impaction
of the ventral colon can be successful, but horses may
be refractory to treatment. Prolonged impaction of the
RDC may lead to perforation.
SURGICALMANAGEMENT. Surgical management
generally involves softening the impacted material with
infusion of saline or water. This process can be per-
formed through a needle and tubing apparatus or with
the aid of a nonsterile assistant passing a hose from the
anus. This procedure has been termed a "high-enema."
However, if a large volume of digesta or sand is present,
enterotomy may be necessary. Enterotomy in the LVC,
combined with the use of the intraluminal tube, is the
safest method to avoid possible peritoneal soiling. A ;
sterilely prepared assistant to help with manipulation
and evacuation of the material is necessary. Removal of
impacted sand by this method is difficult because the I
sand tends to settle in this area. I
Recurrent impaction or obstruction of the RDC
may be caused by functional obstruction. In a recent 1
case of recurrent colic, a contracted, corrugated RDC
was detected during emergency celiotomy." A func-
1
tional obstruction of the RDC, postulated to be related
to irritable bowel syndrome in humans, was suspected.
A side-to-side colocolostomy between the RDC and SC
was successful in alleviating clinical signs.
Fibrous Foreign Body Obstruction
I
Obstruction of the RDC, transverse colon, and oral
SC can occur with nondigestible material. Bailing twine,
rubber fencing, nylon material, socks, or other nondi-
gestible material cause obstruction. Typically, a hard
concretion of fecal material forms around these sub-
stances. Rubber fencing material causes a classic form
of the disease after horses ingest strands of the polyester
and nylon fiber. In one notable outbreak, 28 horses had
colic after ingesting the material.74 In one study, 10 of
207 horses with colic had fibrous foreign body impaction.
Affected horses were 3 years of age or younger and had
mild colic signs.75In the original description, 2 to 5 years
were needed for obstruction to occur after ingestion of
the material.74
Signs are similar to those seen with impactions,
including the ability to pass mineral oil around the
offending material, but surgical management is manda-
tory. The site of obstruction is nearly always the terminal
RDC or the transverse or oral SC, sites that are not
directly accessible. One or more enterotomies located
orally or aborally to the lesion may be needed. Enter-
otomy in the dorsal colon, followed by manual retrieval,
is most useful. Retrograde flushing or other forms of
hydropulsion are ineffective because the concretions are
tenacious.
In horses with long-standing obstruction, the bowel
wall may be devitalized, rendering a grave prognosis. If
the bowel wall is healthy and the offending material can
be removed, the prognosis is good. In one report, 5 of
10 horses
Enterolith Obstruction
ETIOLOGY
Enteroliths, which are large concretions formed
primarily of ammonium magnesium phosphate, can ob-
struct the terminal RDC, transverse colon, or SC. The

mineral is deposited in concentric layers around a nidus
of foreign material, such as small pieces of wood or
chert or a small ~ t o n e . Ammonia
~ ~ . ~ ~ is continually
produced in the large colon, and phosphates are found
in abundance in horse feeds. The limiting factor in
enterolith formation may be the level of magnesium in
ingested feed or water.76 Enteroliths are formed in two
basic shapes, spheres or tetrahedra. Clusters can occur,
and multiple enteroliths are common. Enteroliths gen-
erally are not found in horses younger than 5 years of
age and are most common in horses 5 to 10 years of
age.78
CLINICAL SIGNS
Clinical signs are typical of horses with impaction
colic with one exception. Horses with enteroliths fail to
pass any feces when complete obstruction occurs. Fail-
ure to pass manure for up to 24 hours may alert the
clinician to this form of colic. Typically, signs are inter-
mittent for several days, and then when complete ob-
struction occurs, they progress to become acute. Gas
and fecal distention of the colon oral to the lesion cause
abdominal distention. Vital parameters and laboratory
data are within normal limits unless the bowel wall
becomes devitalized. With complete obstruction, severe
abdominal distention, pain, and cardiovascular collapse
occur. Rectal examination is most helpful, but the
enterolith is seldom palpated.
I TREATMENT
Surgical management is necessary; unfortunately,
the enterolith lodges in areas that are inaccessible.
Therefore, the surgeon must make judicious use of
hydropulsion or manual extraction. A technique of
retrograde flushing of obstructions in the transverse
colon by introducing a tube into the SC has been
described.79 However, the surgeon must be careful be-
cause high pressures can cause a rupture of compromised
or normal bowel. Intraluminal retrieval, with the sur-
geon's hand introduced through an enterotomy site in
the RDC near the diaphragmatic flexure, is useful when
enteroliths lodge in the transverse colon or RDC. Trans-
mural manipulation and massage to "milk" the entero-
lith into the R D C or aborally into a more accessible
portion of the SC is useful. Rupture of the bowel can
occur with manipulation, especially in the SC.
The prognosis is reported to be fair. A 47% success
rate was reported in one with the best results
achieved when the enterolith was removed before the
bowel became devitalized. After removal of the entero-
lith, especially one in the shape of a tetrahedron, the
entire large bowel should be palpated for the presence
of additional enteroliths.
Sand Impaction of the Large Colon
ETIOLOGY
I study, the mortality rate was 30%.83 The long-term
Sand impaction of the large colon occurs most
I commonly at the pelvic flexure and terminal RDC.
LARGE INTESTINE 393
Horses stabled in a sandy environment and fed from the
ground appear at risk. Clinicians often associate this
form of colic with specific geographic areas. Ingested
sand may cause foreign body enteritis or sediment over
time to. cause impaction. Offending sand is generally
fine beach sand or clay, but gravel can occasionally be
found.
CLINICAL SIGNS -
In a recent study, sand colic was diagnosed in 48
horses, none of which were younger than 1 year of
age." Clinical signs range from mild to severe pain and
normal to deteriorating cardiovascular status. Rectal
examination reveals cecal and large colon gas distention.
An impaction could be felt in only seven of 48 horses."
Sand can be present in feces without causing colic. In
many horses, surgical exploration is undertaken because
of abdominal pain, large colon distention, and deterio-
rating cardiovascular signs, without an accurate preop-
erative diagnosis. Abdominoparacentesis should be per-
formed carefully, because the heavily laden sand-
impacted colon can be lacerated inadvertently. In three
of six horses with inadvertent enterocentesis, sand was
found in the fluid, which was diagnostic for the disease.*
Abdominoparacentesis should not be performed in
horses that obviously require surgical intervention or in
horses in which the procedure may be of low diagnostic
value. Auscultation of horses with sand impaction may
reveal sounds compatible with sand b o r b ~ r y g m i . ~ ' . ~ ~
Horses with true sand impaction of the large colon
rarely respond to medical management.
TREATMENT
Sand impaction is often a surgical diagnosis and
may be difficult to treat. Coordinated efforts are needed
between the surgeon and the assistant surgeon, and both
intraluminal and transmural manipulation are needed.
Judicious, copious intraluminal lavage combined with
egress tubing in some horses is needed.80 Because sand
can settle in more than one viscus, multiple enterotomies
may be needed. Twenty-six of 48 horses had multiple
sites of sand i m p a ~ t i o n Single
. ~ ~ impactions were seen
most commonly at the pelvic flexure (14 horses), but
when multiple impactions were present, the RDC was
more frequently involved (15 horses). Sand impaction
of the pelvic flexure may act as a pendulum, predisposing
the horse to volvulus of the colon. Cranial dis~lacement
of the pelvic flexure and nonstrangulating and strangu-
lating colonic displacements were seen in 16 of 48 horses
with sand i m p a ~ t i o n . ~ ~another
.In study, 10 of 40 horses
had volvulus or displacement of the colon.*
COMPLICATIONS
Complications after surgery include recurrence of
the disease, peritonitis, diarrhea, and incisional prob-
lems. The prognosis is guarded to poor for horses with
true sand impaction requiring s~rgery,'~ and in one
survival rate was 60% in a recent clinical study, which
indicated a relatively high mortality rate compared with
394 ALIMENTARY SYSTEM
other impactions of the large i n t e ~ t i n e Forty-four
.~~ of
48 horses with sand impaction were discharged from the
hospital, and follow up on 38 horses revealed a relatively
low mortality rate (8.3%).80 Clinicians may differ with
respect to how they arrive at the diagnosis of sand
impaction or to the importance they place on the surgical
finding of small amounts of sand when other lesions are
present.
Minimizing exposure to sand may be important in
preventing recurrence. The weekly dosing of the natural
fiber laxative psyllium hydrophobic mucilloid is useful
in removing small amounts of sand from the large colon.
Tympanites of the Large Colon and Cecum
CLINICAL SIGNS
Primary gas distention of the cecum and large colon
occur but are generally short lived and respond to
medical management. Occasionally, however, a more
severe form of tympanites occurs. Clinical signs vary,
depending on the degree of abdominal distention. Rectal
examination reveals gas distention of the cecum char-
acterized by taut bands. The bowel may shift and assume
a transverse position in the caudal abdomen. The left
ventral and dorsal colon segments may rotate 90 de-
grees. This anatomic abnormality is confusing, leading
one to suspect a surgical lesion. Generally, no edema
of the bowel wall is felt. Atropine can cause a particu-
larly severe form of tympanites and should be used with
~ a u t i o n . ~Glycopyrrolate,
" an antimuscarinic drug used
for treatment of horses with increased respiratory secre-
tions or bronchoconstriction, can also cause large intes-
tinal stasis, tympanites, and colic.
TREATMENT
Medical management should be undertaken. The
horse's response to treatment may be diagnostic. If
auscultation and rectal palpation confirm cecal disten-
tion, cecal trocarization is both therapeutic and diag-
nostic. If the horse responds to treatment, primary
tympanites is the diagnosis; whereas if distention recurs,
tympanites may be secondary to another lesion. Cecal
trocarization in the right paralumbar fossa is not without
risk, and the peritoneal fluid nucleated cell count may
rise dramatically (up to 100,00O/pL) after the proce-
d ~ r e . 'Bowel
~ laceration and subsequent peritonitis can
occur; therefore, the procedure should be used judi-
ciously and sparingly.
Surgical management may be necessary to alleviate
colonic distention or may be undertaken because of the
confusing nature of the clinical signs. At surgery, the
cecum and colon are usually in the normal anatomic
position and needle decompression is performed. Sur-
geons often suspect colonic displacement has occurred
but has corrected itself once the horse is rolled into
dorsal recumbency. The prognosis is good, but recur-
rence is possible if an underlying problem exists.
Nonstrangulating Colonic Obstruction
ETIOLOGY
Because of the length of the bowel and the lack of
extensive mesenteric attachments, the gas-distended
large colon can twist or become malpositioned, dis-
placed, or incarcerated (entrapped). In a clinical study,
32 of 232 horses (14%) undergoing surgery for colic had
nonstrangulating displacements of the large colon.85Sev-
eral forms of large colon displacement are recognized
that cause similar clinical signs. In conditions such as
impaction and tympanites of the large colon, there can
be a 90-degree rotation of the colon without anatomic
obstruction. However, 180- to 270-degree rotations of
the colon cause anatomic obstruction of the flow of
digesta and varying degrees of venous stasis. Some forms
of nonstrangulating displacements may progress to stran-
gulating lesions and may simply represent early forms
of strangulation obstruction.
CLINICAL SIGNS
Each form of displacement has specific character-
istics, but the history and clinical signs are similar.
Horses exhibit signs of displacement for 12 to 24 hours
before becoming more acutely painful. Generally, low-
grade signs of abdominal pain occur that are similar to
those seen in horses with impactions. Horses generally
respond to symptomatic treatment only to become pain-
ful-once again within several hours. Heart and respira-
tory rates are elevated during painful episodes but are
usually normal, until late in the course of the condition.
The preoperative heart rate was reported in one study
to be elevated to a mean of 64 beats per minute in
horses with displacement^.^^ Progressive abdominal dis-
tention usually causes increased abdominal pain. Occa-
sionally, up to 2 to 3 gallons of gastric fluid are obtained
by nasogastric intubation, presumably owing to duo-
denal compression by the distended large colon. Tension
of the duodenocolic ligament has also been incriminated.
Gastric reflux may be more of a problem in horses with
left dorsal displacement of the lkft colon segments. In
most horses, gastric distention is not present.
Rectal examination is most helpful in establishing a
diagnosis and distinguishing this form of colic from
tympanites or impaction. Gaseous~distentionof the large
colon and cecum with the associated tight bands is
characteristic. Preoperative diagnosis of left dorsal dis-
placement and right displacement of the left colon
portions is possible, but there are no pathognomonic
findings on rectal palpation. Most important, the clini-
cian should note large colon distention, displacement,
and mild edema of the bowel wall and make the correct
decision for surgical intervention. The diagnosis is con-
firmed at surgery.
TREATMENT
Surgical correction of the anatomic displacement is
mandatory. The pelvic flexure should be located first,
and the remainder of the colon can then be identified.
If the pelvic flexure cannot be found, the cecocolic
 L A R G E INTESTINE 395

ligament is found and the surgeon follows the ventral

colon to the pelvic flexure. The LVC and LDC are
exteriorized, rotated, and placed back into the abdomen
in the correct anatomic position. Generally, needle
decompression of gas-distended cecum and large colon
is adequate, but occasionally, an enterotomy is needed
to relieve the accumulation of digesta. The enterotomy
should be performed in the terminal LVC. Enterotomy
is generally not necessary, because once the displace-
ment is corrected, horses quickly regain normal intes-
tinal motility. The prognosis of horses with nonstran-
gulating displacements is good, and the condition is
considered one of the most favorable forms of all
surgical problems. The long-term survival rate was 71%
in horses with displacement^.^ The survival rate com-
pares most favorably with that of horses requiring small
intestinal resection and a n a s t o m o ~ i s In . ~ a study of 140
horses, the overall survival rate of small intestinal resec-
tion and anastomosis was 22%, although only 11% of
horses survived more than 3 years after resection and
ana~tomosis.~
Nonsurgical correction of left dorsal displacement
has been described (see the section on Left Dorsal
D i s p l a ~ e m e n t ) .Right
~ ~ , ~ ~dorsal and left dorsal displace-
ment can recur, requiring additional surgery and possi-
ble colopexy.
NONSTRANGULATING VOLVULUSOF THE LARGE
COLON. Rotation of the colon between 90 to 270
degrees causes physical obstruction of the colon, inter-
rupts digesta transit, and causes gas distention and colic.
Nonstrangulating volvulus is one recognized form of
displacement of the large colon and is classified as a
simple obstruction (Fig. 36-13). Edema and hyperemia
of the bowel wall is common, and therefore, partial
venous obstruction occurs. Rotation of the colonic axis
usually occurs in a clockwise direction when viewed
from a caudal position, as if the examiner were perform-
ing a rectal examination. This rotation is also seen in
horses with strangulating volvulus of the large colon.
Obstruction occurs at the sternal and diaphragmatic
flexures, although a report describes involvement of the
cecum in some h ~ r s e s Needle .~ decompression is nec-
essary in the ventral and dorsal colon segments and the
cecum. The surgeon must identify the lesion, exteriorize FIGURE 36-13. Nonstrangulating displacement of the large colon as
the colon, and reposition it correctly. viewed from the ventral aspect at exploratory surgery. (A), 180-degree
volvulus of the large colon, located at the sternal and diaphragmatic
RIGHT DISPLACEMENT OF THE L E F ~COLON. flexures. (B), Right displacement of the left colon segments. Without
Frequently called right dorsal displacement, this form further rotation or volvulus, this form of displacement may cause
of nonstrangulating obstruction may be related to a chronic, intermittent wlic before complete luminal occlusion occurs.
motility dysfunction of the RDC. Commonly, the RDC (Redrawn from Hackett RP: Non-strangulating colonic displacement
is digesta filled, predisposing the horse to gas distention in horses. J Am Vet Med Assoc 182:235, 1983.)
and rotation. Rectal examination reveals a tight band
associated with the LVC, traversing across the caudal
abdomen and coursing lateral to the cecum. In some and progressive abdominal distention become obvious.
horses, the cecum is pushed forward and is not palpable. Medical management including withholding feed, anal-
Usually, the ventral cecal band is tight due to cecal gas gesic administration, and occasional trocarization of the
distention. Right displacement of the left colon portions gas-distended colon can help resolve the clinical signs.
can be a chronic condition and can initially be present However, when the horse is returned to full feed, colic
without colic signs. Without concurrent volvulus or recurs.
severe gas and digesta accumulation, a malposition of This form of displacement can cause chronic inter-
the left colon segments in a U-shaped fashion to the mittent colic. The more typical form involves progressive
right impedes but does not stop the transit of digesta large colon distention, secondary abdominal distention,
(Fig. 36-13A). With further rotation or with filling of and an increase in abdominal pain, which requires
the RDC, a simple obstruction occurs. Signs of colic surgical intervention. Various forms of the displacement
396 ALIMENTARY SYSTEM
are described to include flexion and torsion of the colon
portions.89 In the most common form, the pelvic flexure
rotates cranially to the right and finally sits tranversely
in the abdomen, thus completing a counterclockwise
rotation (when viewed from the ventral aspect at the
time of surgery). Clockwise rotation can occur but is
less common.
LEFTDORSAL DISPLACEMENT OF THE LARGECO-
LON. Left dorsal displacement of the large colon, fre-
quently called renosplenic (nephrosplenic) ligament en-
trapment, is a well-recognized form of nonstrangulating
d i s p l a ~ e m e n t .87'~ ~ , 90- 91 The etiology is unknown, but
one possibility includes concomitant splenic contraction
and gas distention of the LVC and LDC. With dorsal
displacement of the colon and subsequent refilling .of
the spleen, the colon is t r a ~ p e d . 'Regardless
~
the lesion involves an entrapment of the LDC and LVC
of etiology,
over the dense, fibrous suspensory ligament between the
kidney and spleen. Occasionally, concurrent impaction
or volvulus of the colon is present (Fig. 36-14). This
form of displacement can be seen in younger horses,
whereas other forms of displacement are unusual in this
age category.
FIGURE 36-14. Left dorsal displacement of the colon, over the
renosplenic ligament. (A), Surgeon's view of left dorsal displacement.
Occasionally, the digesta in the entrapped portion of the colon is firm,
requiring enterotomy, or a volvulus of the colon occurs in the
entrapped portion. (Redrawn from Hackett RP: Non-strangulating
colonic displacement in horses. J Am Vet Med Assoc 182:235, 1983.)
(B), With concomitant gas distention of the left colon segments and
a medial shift of the spleen, the colon segments become incarcerated
dorsal to the renosplenic ligament. LDC, left dorsal colon; LVC, left
ventral colon. (Redrawn from McIlwraith CW: Equine digestive
system. In Jennings PB (Ed): The Practice of Large Animal Surgery.
Philadelphia, W. B. Saunders Company, 1984, p 638.)
In left dorsal displacement of the large colon,
clinical signs may vary from mild to severe, presumably
relating to the amount of tension on the renosplenic
ligament or the amount of involved intestine. The level
of colic is usually compatible with other forms of non-
strangulating displacement, but occasionally, horses are
violent. The classic signs found on rectal examination
that are associated with this form of displacement in-
clude (1) gas-filled LVC and LDC coursing craniodor-
sally over the renosplenic ligament; (2) a ventral and
medial shift in splenic position; and (3) a tight, gas-
distended cecum. However, there are no pathognomonic
signs. With simple tympanites of the large colon, the
left ventral and dorsal colon segments can assume
dorsal position in the abdomen, mimicking left dor
displacement of the large colon. Other large col
displacements can mimic left dorsal displacement of 1
~
large colon as well. The lesion may be suspected more
frequently than it actually occurs.
Other more subtle clinical findings may lead one to
suspect left dorsal displacement. In this form of displace-
ment, horses can have a rather surprising amount of I
gastric distention, requiring nasogastric intubation. Rel-
ative to the amount of pain and distention, the heart 1
rate is lower than expected. The PCV may be normal
or slightly low, despite mild or moderate clinical dehy-
dration. Splanchnic or splenic sequestration of red blood
cell volume may explain this clinical finding. Abdomi-
nocentesis may yield bloody fluid from splenic puncture
because of the ventral positioning of the spleen. Occa-
sionally, horses with left dorsal displacement of the large
colon suffer from intermittent pain, and a more chronic
form of colic results.
Two forms of correction have been advocated.
Surgical exploration, decompression, and repositioning
of the colon provide the most direct means of diagnosis
and anatomic repositioning, without risking other com-
plications reported with nonsurgical management.% At
surgery, the LVC and LDC are found dorsal to and
entrapped by the renosplenic ligament. The lesion is
unequivocal when found and is easily corrected. To free
the colon, the surgeon needs to carefully push the spleen
medially, while with both hands and arms, gently rock-
ing the colon free, bringing the structure first dorsally
around the spleen, and then laterally and ventrally. This
maneuver is more easily accomplished if the surgeon is
standing on the horse's right side during ventral midline
exploratory. Both hands are cupped around the colon,
after the arms are used to push the spleen to the right
(toward the surgeon).
A method of nonsurgical correction of left dorsal
displacement of the large colon has been d e ~ c r i b e d . ~ . ' ~
After inducing general anesthesia, the horse is posi-
tioned in right lateral recumbency. While providing a
gentle "rocking" motion (shaking) of the abdomen, the
horse's limbs are gradually hoisted to a vertical position
and then the horse is rolled into left lateral recumbency.
After completion of the rolling procedure, the spleen is
once again against the lateral body wall, now lateral to
the LVC and LDC. Occasionally, manipulation by rectal
palpation is needed to free the entrapped colon. In a
recent clinical study, 5 of 27 horses required rectal
manipulation combined with rolling.% Maintenance of
R the dorsal recumbent position for a few minutes may
facilitate the correction of the problem. Published com-
plications of the procedure include recurrence, inability
to free the colon by the technique, cecal torsion, or
large colon torsion.
Recurrence of left dorsal displacement of the large
colon and other displacements or volvulus of-the large
colon have prompted surgeons to consider stabilizing
the colon by c o l ~ p e x y . ~92' ,In two of nine horses, recur-
rence of left dorsal displacement of the large colon was
found, requiring a second celiotomy. Other reported
complications are adhesion formation after surgery in
one horse and subsequent large colon necrosis in an-
other. A technique to obliterate the renosplenic space
was reported to be successful in preventing left dorsal
displacement of the large colon in eight horse^.^',^^
Currently, surgical correction and colopexy should be
undertaken if the condition recurs. Colopexy, however,
results in a permanent adhesion of the large colon and
may have long-term complications (see the section on
Colopexy).
CRANIALDISPLACEMENT OF THE PELVICFLEX-
URE. At exploratory surgery, the pelvic flexure may
be located in the cranial abdomen. A cranial position
of the pelvic flexure may not be a true lesion and may
occur secondary to rolling or placing the horse in dorsal
recumbency. If accompanied by a lesion of another
intestinal segment, without large colon gas distention or
impaction, the cranial displacement of the pelvic flexure
may be incidental. However, in some horses, cranial
displacement of the pelvic flexure with concomitant
impaction or gas distention of the large colon, colic, and
no other lesions found at exploratory surgery appears
to be a true lesion. In one study, eight horses had the
c o n d i t i ~ n Gas
. ~ ~ distention and associated impaction of
various colonic segments was common. The prognosis
is considered good.
OTHERTYPESOF DISPLACEMENT. The colon can
rotate or displace into various positions, some of which
are described, while others seem atypical. Tympanites
can be associated with rotation of the colon. However,
if large colon distention and an odd form of displacement
are found at surgery, a thorough exploration should be
performed to rule out other forms of obstruction. Intra-
luminal obstruction of the terminal RDC or transverse
FIGURE 36-15. The cecum and large colon of a horse
with volvulus of the large colon at the level of the
cecocolic ligament. Volvulus at this level is the most
common form of the disease. Note that clockwise rota-
tion of the bowel (as viewed from the caudal aspect of
the horse) is most common. Once the horse is in dorsal
recumbency, the surgeon untwists the colon in a clock-
wise direction as well. RDC, right dorsal colon; RVC,
right ventral colon.
L A R G E INTESTINE 397
colon can cause gas distention and rotation of the colon.
Unless these areas are carefully palpated, lesions can be
easily missed.
Adhesions, Abscc and Neoplasia
Nonstrangulating, simple obstruction of the large
colon can occur with adhesions, abscessation, or neo-
plastic diseases. Mural abscessation and neoplasia are
extremely rare. Omental adhesions to various portions
of the large colon can occur after surgical incision,
traumatic perforation, or ulceration. Adhesions of the
large colon to the body wall can cause partial obstruction
and displacement. At surgery, adhesions should be
carefully disrupted to avoid penetration of the bowel
lumen. If chronic scarring is present, intestinal resection
or bypass may be needed. For more information on this
subject please review Chapter 33.
Strangulation Obstruction of the Large Colon
VOLVULUS OF THE LARGE COLON (VLC)
PATHOGENESIS. Volvulus of the large colon
(sometimes including the cecum) causes one of the most
acute, devastating forms of colic. By far, the most
common form of the disease causes acute cardiovascular
deterioration, severe abdominal pain, gross abdominal
distention, and death within 4 to 24 hours unless the
horse is operated on in a timely fashion. Initially, the
pathogenesis involves venous occlusion and hemorrhagic
strangulation obstruction, but later, progressive arterial
occlusion causes ischemic changes. The colon rotates in
clockwise fashion as viewed from behind, looking for-
ward along the axis formed by the RVC and RDC (Fig.
36-15). The volvulus is generally 360 degrees, but sur-
geons have reported rotations of up to 720 degrees. The
classic form of the disease involves a twist at the level
of the cecocolic ligament, but the axis of rotation can
be at the cecal base. Occasionally, VLC occurs at the
sternal and diaphragmatic flexures, but this condition is
unusual.
Broodmares, late in gestation or after parturition,
appear at risk of developing VLC. Other forms of
nonstrangulating displacements may also occur in brood-
398 ALIMENTARY SYSTEM
mares. In a recent study of 122 horses with VLC, 73
horses were females and 42% had foaled or were preg-
nant.94The disease is not restricted to broodmares, but
changes in digestion or visceral positioning during preg-
nancy may predispose mares to the disease. The enlarg-
ing uterus may induce a shift in the position of the large
colon or cause partial obstruction of the RDC. Digesta,
gas distention, and secondary rotation of the colon lead
to strangulation. A change in intestinal motility may
occur during pregnancy. Large colon motility dysfunc-
tion occurs in women during pregnancy, but the condi-
tion is not known to exist in horses. The history may
indicate a previous management change such as change
in housing or in the type o r quality of feedstuffs pro-
vided.
CLINICAL FINDINGS.The clinical signs generally
reflect the duration of the volvulus. Severe, unrelenting
pain is the most common clinical sign, and based on this
factor alone, a decision for surgical intervention is often
made. Horses sweat profusely and often display skin
wounds. Abdominal distention is common and often
severe, causing respiratory compromise. The heart rate
is elevated between 60 and 80 beats per minute but is
lower than expected for the degree of abdominal pain
present. Horses with VLC and high heart rates (greater
than 65 to 70 beats per minute) accompanied by severe
dehydration (PCV >60%) have a very poor prognosis,
because these parameters reflect severe changes in car-
diovascular status. In a recent study, there were signifi-
cant differences between survivors and nonsurvivors
(values were lower in survivors) in heart rate, respiratory
rate, capillary refill time, and PCV.94 In this study, the
mean duration of clinical signs was 19 hours (range, 2
to 156 hours). Occasionally, horses may have a more
chronic clinical course. Early nonstrangulating lesions
may progress to strangulation obstruction.
Rectal examination usually reveals large colon dis-
tention and tight bands coursing transversely in the
caudal abdomen. An important finding is edema of the
colonic wall, which reflects severe venous congestion.
Occasionally, rectal examination reveals an empty cau-
dal abdominal quadrant. The empty abdomen leads to
a springy or bouncy feeling of the rectum, resembling
the finding of pneumoperitoneum. In these horses, pain
is severe and the colon has shifted forward, causing
severe compression of the cranial abdominal viscera. In
rare instances, rectal examination reveals edema of the
colon without colonic gas distention. Severe unrelenting
pain is the most consistent sign leading to surgical
intervention, regardless of the findings on rectal exami-
nation.
Examination before surgery may be pre-empted by
unrelenting abdominal pain. Laboratory data generally
reflect dehydration, with protein loss into the bowel wall
and lumen. Mild metabolic acidosis may become severe
in advanced disease. Peritoneal fluid can range from
normal to serosanguinous in color. Serosanguinous fluid
is common and generally is considered a poor prognostic
sign. Mean protein levels and nucleated cell counts are
usually slightly elevated, but generally, the clinical
course is too short to have consistent elevations in these
parameters.
TREATMENT. Early surgical intervention is man-
datory for a successful outcome. Even if surgery is
undertaken as early as 3 to 4 hours after the onset of
signs, there is no guarantee of a successful result.
Aggressive intravenous fluid therapy is needed before
surgery, if possible, to restore blood volume. Reperfu-
sion injury may cause significant bowel damage after
surgical correction, and some consideration should be
given to the administration of free radical scavengers.
A practical choice would be dimethyl sulfoxide (DMSO)
(1 gmlkg IV), but recent evidence suggests it is not
effective in preventing injury from either hemorrhagic
or ischemic strangulation o b s t r ~ c t i o n Broad-spectrum
.~~
intravenous antibiotics, flunixin meglumine, and corti-
costeroids are beneficial and should be given before
surgery.
In horses with VLC, induction and early mainte-
nance of general anesthesia are critical and are compli-
cated by the extreme large colon distention and poor
metabolic state of the patient. Abdominal distention
prevents adequate ventilation and predisposes the horse
to ventilation-perfusion mismatches. Blood gas values
typically show hypercapnia and inadequate oxygenation.
Rapid release of endotoxin and stagnated venous blood
after untwisting the colon may cause a hypotensive crisis,
leading to fatal cardiac arrhythmias. Hypotension is
common, and maintenance of anesthesia can be difficult.
Early decompression of the bowel generally helps in
improving ventilation, but oxygenation and peripheral
perfusion still may be inadequate. Judicious use of
preoperative cecal trocarization may help early in the
anesthetic management. Efficient and timely surgical
intervention, minimizing surgery time, and aggressive
management of hypotension maximize survival after
surgery.
Large ventral midline incisions (up to 40 to 50 cm)
are beneficial and allow easier manipulation of the
distended colon. Early gaseous decompression and un-
twisting of the colon should be performed before ma-
nipulation. The surgeon needs to be gentle in handling
the colon, because rupture, particularly of the RDC,
occurs frequently. As much of the colon as possible
should be exteriorized and held by an assistant. The
surgeon then untwists the colon 360 degrees in a clock-
wise direction as viewed from the ventral midline ap-
proach with the horse in dorsal recumbency. A thick,
edematous colonic wall; hemorrhagic, congested inter-
colonic mesentery; and various shades of serosal discol-
oration (from dark purple to greenish gray) are seen.
After untwisting the colon, there is generally some
improvement in serosal color, unless complete ischemia
or end-stage hemorrhagic strangulation obstruction ex-
ists. Generally, a period of 10 to 15 minutes should be
given to assess bowel viability. Absence of a pulse in
colonic vessels, failure of the colon to return to its
normal serosal color, necrotic odor, and black mucosal
color are grave signs, and horses with these signs should
be euthanized. Surface oximetry, if available, may help
in predicting possibility of survival in horses with colonic
strangulation obstruction.% Although clinical evaluation
of horses with experimental colonic strangulation ob-
struction would have led to a prediction of poor survival,
a return of serosal surface oxygen tension of greater
than 50% of baseline correctly predicted survival in a

I high percentage of horses. Recently, microscopic eval-
"ation of frozen sections of colonic wall have been
useful in determining colonic viability with the aid of
clinical assessment of p e r f ~ s i o n . ~ ~
Horses with loss of glandular epithelium are un-
likely to survive. Resection of the involved colon re-
mains a possibility, particularly if the volvulus occurs at
the diaphragmatic flexure. However, successful resec-
tion in horses with true VLC at the cecocolic ligament
or at the base of the cecum is difficult because the
surgeon usually cannot remove all of the necrotic colon.
A resection of 95% of the colon, as reported, may not
be possible,98 because in clinical cases, a minimum of 25
to 30 cm of R D C and RVC are left intact. Although
close to 95% of the length of the large colon may be
removed in normal horses, removal at this level may
leave 15 to 25% of the absorptive surface area severely
affected by mucosal damage. Substantial damage to the
RDC and associated endotoxemia reduce the survival
j rate in such horses even with the use of resection.
Because of the severity of the lesion, up to 50% of
the horses operated on for VLC may be euthanized at
~I the time of surgery. Decompression, untwisting, and
repositioning of the colon are required. If the colon is
filled with digesta, making manipulation difficult, enter-
otomy and evacuation may be needed. Evacuation of
the potentially dangerous toxins that may be absorbed
after surgery may be desired, but the procedure is not
1 mandatory. The R D C is usually large, and evacuation
of this segment is difficult. A colopexy should be con-
sidered if VLC recurs.
Aggressive management with intravenous fluids,
antimicrobial agents, and anti-inflammatory agents is
~ needed after surgery. Because of the high numbers of
anaerobic organisms, metronidazole (15 mglkg, PO,
QID) may help in horses with peritonitis or contami-
nation from enterotomy sites. Endotoxin absorption
from damaged mucosa can complicate recovery. Im-
munotherapy with J-5 antisera, producing passive im-
munity with antibodies directed against a core polysac-
charide of gram-negative bacteria, has shown promising
early results.99.loo Plasma administration to supplement
protein loss from compromised bowel may help. Early
after surgery, hemorrhagic diarrhea, fever, and leuko-
penia are common in horses with moderate to severe
colonic compromise. Continued fecal passage is a good
prognostic sign, but horses that develop ileus, large
colon distention, and abdominal pain after surgery have
a very poor prognosis. Reoperation, decompression,
and large colon resection or euthanasia may be neces-
sary.
PROGNOSIS. The reported survival rate of horses
with VLC ranges from 12% to 34.7%.36,94However,
because differences exist with lesion definition and se-
verity grading, survival rates may differ. Actual survival
rates for horses with VLC of 360 degrees are likely in
the 10% to 20% range.
INTUSSUSCEPTION OF THE LARGE COLON
Intussusception of the colon is rare but has been
r e p ~ r t e d . l ~ ' -The
' ~ ~ short, strong intercolonic mesentery
LARGE INTESTINE 399
should inhibit the development of intussusception, but
abnormal motility, impaction, and parasite lesions may
predispose the horse to the disease. Intussusception has
been reported at the pelvic flexure, the LVC, and the
LDC. These segments may be predisposed to the dis-
ease. Intussusception is less likely in the right colon
segments, because the RDC and the RVC have dorsal
mesenteric attachments and the cecocolic ligament at-
taches to the RVC.' Intussusception may cause initial
simple obstruction, but venous obstruction, mural swell-
ing, and arterial occlusion lead to strangulation obstruc-
tion. Clinical signs and laboratory parameters reflect the
duration of the obstruction.
Surgical intervention is mandatory. Manual reduc-
tion was successful in one horse,lo2 but usually resection
and anastomosis are necessary. Both side-to-side o r end-
to-end anastomoses are successful, but end-to-end pro-
cedures are difficult because of the disparity in size of
the colonic segments. The prognosis is guarded to good,
depending on the timing of surgery, the degree of
ischemia, and the surgical technique performed.
LARGE COLON INFARCTION
Thromboembolism of the colonic vessels is rare,
but can occur secondary to migration of S. vulgaris
larvae. The arterial supply of the colon arises from two
separate branches, forms a loop at the pelvic flexure,
and has extensive communications between the vessels.
The vascular supply of the colon is relatively protected
compared with the cecum.
With extensive thromboembolic disease, infarction
can occur, causing clinical signs associated with stran-
gulation obstruction. Horses usually suffer from acute
pain but can show depression with chronic pain. Resec-
tion and anastomosis are successful if the ischemic
segment is short. Generally, the LDC and the LVC are
involved, and end-to-end o r side-to-side anastomoses
can be performed after resection. In one horse, end-to-
end colocolostomy was successful after infarction of the
LDC.'" Continued thromboembolic disease after sur-
gery limits the prognosis.
Large Colon Resection
Partial resection of the large colon can be per-
formed successfully using both hand-sewn and autosu-
ture techniq~es.'~.'" Much debate remains, however,
regarding what is called 95%, or near-complete, resec-
tion of the large c o l ~ n . ' ~ ~Lesions
-'~ aboral to the
cecocolic ligament can be exteriorized from a ventral
midline incision, and resection is possible. In a recent
study, 36 of 122 horses had lesions amenable to resection
from an anatomic ~ t a n d p o i n t Although
.~~ the most com-
mon site for VLC is the level of the cecocolic ligament,
the damage extends into the terminal R D C and the oral
portion of the RVC. Resection, even at the cecocolic
ligament, leaves necrotic bowel in situ, and endotoxin
absorption and death are likely. Because the wall is
thicker and compromised in horses with VLC, surgical
techniques used in horses with experimental resection
may fail.
400 ALIMENTARY SYSTEM
Little doubt exists that extensive large colon resec-
tion can be performed successfully in normal horses.
Resection at the level of the cecocolic ligament may
remove all but 5% to 10% of the length of the large
colon but may leave 15% to 20% of the absorptive
surface area. Five of 10 normal horses survived 18
months after resection at the cecocolic ligament.lo6
After attaching stay sutures, a side-to-side anasto-
mosis is performed between the RDC and the RVC at
the level of the cecocolic ligament, using the GIA
autosuture instrument. After completing the anastomo-
sis and ligating the dorsal and ventral colic arteries, the
large colon is transected using the TA-90 stapling instru-
ment (U.S. Surgical, Norwalk, CT) across both the
RDC and the RLC. This creates a side-to-side anasto-
mosis and two blind colonic ends. In three horses, death
was due to leakage from the staple lines. Modification
in application of the TA-90 autosuture device may avert
this and other complications such as adhesions to staple
lines. Hand-sewn inverting suture lines offer a distinct
advantage over the use of stapling equipment. Because
failure occurs with use of stapling equipment in normal
horses, it is likely to occur in horses with thick, edem-
atous large colon after volvulus. Additional information
on surgical techniques is found in Chapter 33.
In horses with a large colon resection at the ceco-
colic ligament, digestion of dietary crude protein, cel-
lulose, and phosphorus is decreased.lo8Fecal water out-
put is increased 55%, and total fecal output is increased
45%. Horses lose weight after surgery but generally are
able to regain weight within 6 months. In these horses,
there is a shorter transit time of particulate digesta, and
a decreased overall retention time because of the overall
decrease in intestinal length and capacity.lo7 In horses
with less extensive resection (60%), there is a decrease
in digestion of crude protein, fiber, nitrogen-free extract,
and phosphorus as we11.lW However, horses maintain
body weight and develop adaptive digestion ability by 6
months after surgery.
Further studies to evaluate digestion in horses with
extensive large colon resection indicate that grass hay
or alfalfa pellets did not provide adequate digestible
energy.llO.lllAlfalfa hay, with a shorter fermentation
lag time, is recommended, because transit and fermen-
tation time are reduced in these horses.
In summary, horses with a 60% reduction of the
length of the colon experience adaptive changes; how-
ever, in those with extensive resection (up to 95%),
although adaptive changes occur, feeding alfalfa hay is
recommended. Because of the increased fecal water
output, water consumption after surgery is increased.
Prognosis after large colon resection depends largely on
the length of resected segment. In horses with less than
50% removed, the survival rate was 81%, but in horses
with more than 50% of the colon resected, the survival
rate was only 53%.l1° Survival may correlate more
closely to the severity of the lesion than to the length
of the resected colon.
More clinical experience with extensive large colon
resection is needed to assess survival after resection in
horses in which discolored or damaged tissue is left in
situ. In a recent report, hand-sewn techniques resulted
in survival of 12 of 18 horses undergoing extensive
resectionfi2 Resection was performed at the level of the
cecocolic ligament in most horses.l12 Survival decreased
as the amount of devitalized tissue left in situ in-
creased.lI2 Large colon resection remains a viable alter-
native to untwisting, enterotomy, and repositioning, but
case selection is important. Hand-sewn techniques
should be considered because edematous, thickened
colon may not be suitable tissue for the application of
currently available stapling equipment.
Colopexy
Recurrence of nonstrangulating displacement, or
I
VLC, has led to the development of techniques for
disease prevention. Techniques involving suturing the
dorsal and ventral colon segments together fail to pre-
vent experimentally induced volvulus and induced
weight loss, and should not be used.". 113 A technique
of suturing the lateral free band of the LVC to the left
body wall, approximately 6 cm to the left of midline, is
the currently recommended te~hnique.l'~-"~ A nonab-
sorbable suture, such as #2 polypropylene or nylon is
preferred, because adhesions caused by absorbable ma-
terial tend to mature and lyse over time.
Colopexy of the LVC may cause weight loss ini-
tially, but the horse regains the weight without compli-
cation^."^ Trials to assess digesta passage after colopexv
revealed digesta was retained on day 4, and variatil
in the rate of digesta passage within horses decrea
after surgery.Il5 Therefore, after colopexy, stabilizat
of the large colon may increase transit time initially, out
no long-term complications such as impaction of the
large colon were encountered.
Colopexy appears to be safe but has received only
limited clinical evaluation. The effect of colopexy on
racing animals is unknown currently, but the technique
has been used successfully in brood mare^."^ Special care
must be taken not to penetrate the bowel lumen because
leakage and peritonitis may develop. The technique
should not be used if colon viability is q~estionab1e.l'~
Anecdotal reports of colon rupture near or at the site
of the fixation are worrisome. The technique should be
reserved for horses with recurrent disease and used only
after adequate client education has been made available.
Transverse and Small Colon
Diseases of the small colon (SC), combined with
those of the rectum, cause colic in 2.9% to 17.7% of
Obstruction of the SC is caused most fre-
quently by impactions or fecaliths.
The diagnosis of small colon disease may be difficult
when it is based only on clinical examination. Horses
with SC obstruction usually exhibit mild colic and pro-
gressive abdominal distention. Failure to pass feces can
be an important part of the history, leading the clinician
to suspect a lesion of the small or transverse colon.
Dehydration is not marked and vital signs are within
normal range. Volvulus or vascular accidents involving
the small colon have an abrupt onset and more rapid
deterioration in vital parameters.

Atresia Coli
I
I Atresia coli, a rare condition in foals, is seen more
commonly in Thoroughbreds and develops as a result of
an autosomal recessive inheritance. lZ4Vascular accidents
I intravenous fluid administration, and analgesic treat-
during fetal development resulting in disruption of blood
supply to the intestine can also produce atresia.lE-ln
I
I The lethal white foal syndrome of Paint horses is a
different disease. The allele responsible for the all-white
I color is associated with a deficiency of ganglion cells in
i the colon myenteric plexus, resulting in thin muscular
walls and s t e n o s i ~ . ' ~ ~
Foals with atresia coli often have elevated vital
parameters. A digital rectal examination reveals an
absence of feces. Contrast radiography is of limited
diagnostic value unless the atresia is in the transverse
colon or located aborally.lE
Exploratory celiotomy reveals atresia of the colonic
segment. Surgical correction is possible if it is performed
early. Concurrent findings include atresia ani, renal
hypoplasia, or renal a p 1 a ~ i a . lDisparity
~~ in the size of
aboral and oral bowel diameter requires careful approx-
imation, using end-to-end or end-to-oblique anastomotic
techniques. The side-to-side technique is of value but
may predispose the horse to blind loop syndrome.
Resection of the severely dilated oral portion is recom-
mended to obtain a normal vascularized and functional
intestine.lZ5 Complications arising from surgical correc-
tion include ileus of the dilated oral portion, peritonitis
I , resulting from leakage of the anastomosis, chronic in-
I continence, and diverticulitis.
Impaction of the Small Colon
I
ETIOLOGY
Simple obstructions of the SC are usually caused
by feed impactions or fecaliths but can also be due to
enteroliths, foreign bodies, phytobezoars, trichobezoars,
and p h y t o c o n g l ~ b a t e s . ~118,~ -129-133
~ ~ ~ Small colon impac-
tion is the most common form of simple obstruction.
Ponies appear to be predisposed to SC impaction.27Cold
weather, limited roughage diets, and lack of water may
predispose horses to the development of impactions. A
primary motility problem or vascular insult may lead to
the accumulation of digesta.
CLINICAL SIGNS
Horses with impactions of the SC have vague signs
of anorexia, dullness, and mild abdominal pain. Horses
may exhibit tenesmus if the impaction is near the rec-
tum. In more chronic impactions, a rapid deterioration
in condition may indicate necrosis of the affected bowel
or the development of gaseous distention of the large
colon. The diagnosis may be difficult to arrive at before
surgery. Single or multiple loops of SC with firm, near-
hard digesta can be felt on rectal examination. Although
the clinical signs and history may suggest a small colon
obstruction, confirmation on rectal examination often is
not possible.
LARGE INTESTINE 401
TREATMENT
NONSURGICAL MANAGEMENT. Medical manage-
ment is successful in horses with mild impactions. Ag-
gressive oral fluid therapy, sometimes accompanied by
ment are generally successful. Judicious use of enemas
in the standing horse have been advocated but are not
recommended unless the impaction is near the rectum
and adequate patient restraint is provided. Rectal or
small colon tearing is a potentially devastating compli-
cation.
SURGICALMANAGEMENT. If surgical manage-
ment is required, a combination of massage and a
procedure known as a high enema are generally suc-
cessful. A soft rubber hose attached to a garden hose is
gently inserted per rectum by a nonsterile assistant. The
surgeon aids in tube passage by transmural manipula-
tion. Warm water is infused to soften the digesta.
Distention and irrigation are continued until the material
is flushed from the rectum. This procedure is traumatic
to the bowel and occasionally predisposes the horse to
colonic rupture. In horses with more advanced disease,
necrosis of the colon can occur secondary to impaction,
which requires resection and anastomosis. The prognosis
after surgery is guarded. Recurrence of the impaction,
ileus, and adhesion formation are possible sequelae.
Fecaliths. Fecaliths, sometimes 15 to 20 cm in
diameter and length, are composed of inspissated fibrous
fecal material that is believed to form as a result of
improper fecal ball formation.l18 Fecaliths may develop
because of the diet composition and the resistance to
flow of digesta through the intestinal tract. Fecalith
obstruction of the small colon causes slow, progressive,
intermittent colic.
Phytoconglobates and Bezoars. Phytoconglobates
are concretions of undigested food fragments and for-
eign particulate matter formed into balls.'" Bezoars are
a combination of magnesium ammonium phosphate with
a plant fiber (phytobezoars) or animal hair (tricho-
bezoars). Trichobezoars and phytoconglobates are
rare."6. 120 Bezoars have a smooth glistening surface but
are light colored, unlike the darkly colored enteroliths.
Small colon obstruction with phytoconglobates and be-
zoars can cause colic similar to impactions or foreign
body obstruction.
Foreign Body Obstruction. Yearling and weanling
horses are prone to ingest foreign materials such as
twine, rope, clothing, rubberized fencing materials, and
tire threads. Twenty-eight horses with SC obstruction
were reported from one farm alone due to the ingestion
of nylon tires.74 In 10 horses, ingestion of strips of
conveyer belt caused foreign body o b s t r ~ c t i o n .The
~~
pitted, uneven surface of the obstructing mass, which is
surrounded by firm concretions of digesta, lodges against
the mucosa. The mass can reach 1 m in length and
weigh up to 7 kg.7SRupture of the SC can occur easily
during surgical manipulation. Horses with foreign body
obstruction show no clinical signs when the material
passes through the small intestine owing to the higher
fluid-to-solid ratio. Horses with foreign body obstruction
exhibit acute colic if obstruction is complete. The ob-
struction can be preceded by signs of intermittent colic
402 ALIMENTARY SYSTEM
if the obstruction is incomplete, or if the material
periodically returns to the RDC.'18
Surgical removal is mandatory. Colotomy in the
RDC is necessary to retrieve the foreign body from the
inaccessible area of the large colon. Intraluminal lubri-
cants can be useful in relieving the obstruction but may
contaminate peritoneal surfaces.
Enteroliths. Enteroliths are mineral concretions
composed primarily of magnesium ammonium phos-
phate salts, which are usually deposited concentrically
around a foreign material such as a stone or metal. In
a retrospective study, 24 of 30 horses had enteroliths
lodged within the small colon, 17 of which were lodged
in the oral portion of the organ.n The problem is seen
more commonly in horses from 5 to 10 years of age.77.
'35 The rate of enterolith formation is unknown, but the
age of one large concretion (12 x 9 cm) with a nidus of
a deciduous tooth was estimated to be 4 years.'36 En-
teroliths are not found in horses younger than 3 years
of age. In these horses, colonic obstruction occurs more
frequently by foreign materials.
Small enteroliths can be passed in the feces,
whereas others may cause obstruction for short periods
of time and then fall back into the RDC.79 When
obstruction becomes complete, abdominal pain is per-
sistent, tympany increases, and the patient's condition
deteriorates. The intestinal wall surrounding the entero-
lith may undergo pressure necrosis, and if the condition
is prolonged, the wall may perforate, leading to fatal
peritonitis. A surgical approach similar to that described
for foreign body removal is required for enterolith
removal from the transverse or oral portions of the SC.
Retrograde infusion of water through the rectum may
loosen enteroliths that cannot be readily manipulated
by hand.79
Retained Meconium. Retained meconium in foals
is considered a surgical disorder only when medical
therapy fails. Foals often exhibit tenesmus, intermittent
colic, and large colon tympany shortly after birth. A
fecal mass can be palpated craniad to the pelvic rim on
digital rectal examination.
The initial goals of therapy are to provide analgesia,
to protect the foal from self-mutilation, and to relieve
obstruction. Administration of warm, soapy water, by
gravity flow enema through a well-lubricated soft flexible
rubber tube is required. The addition of mineral oil or
glycerin but not dioctyl sodium sulfosuccinate may assist
passage of large firm meconium impaction^."^ Enemas
may have to be repeated. Maintenance oral fluid therapy
and exercise may stimulate bowel activity. If surgery is
undertaken, aborally directed massage of the meconium
in conjunction with an enema should be carried out
before a colotomy is performed.123
Vascular Lesions
The SC is rarely the site of primary vascular lesions
that cause colic. The caudal mesenteric artery, which
provides most of the blood supply to the SC, is rarely
the site of occlusive verminous arteritis. Vascular lesions
seen in the SC are intramural hematomas, mesocolic
rupture with segmental infarction, and submucosal
edema.120. 121.130.138-140
INTRAMURAL HEMATOMAS
Hematomas of the SC are rare.138.139 The etiology
is unknown, but rectal or other trauma is p0ssib1e.l~~
Intraluminal hematomas not attached to the mucosa can
easily be manipulated in the rectum and withdrawn
without entering the bowel. Submucosal hematomas
require resection and anastomosis.
MESOCOLIC RUPTURE
Rupture of the mesocolon with subsequent ischemic
1
necrosis of the SC is a rare complication of parturition
in the mare.116."'. 120. 140, 142 The parturient mare is
predisposed to type I11 or IV rectal prolapse, resulting
from pelvic ligament laxity, increased abdominal pres-
sure, forceful expulsive efforts, and uterine size.129Ex-
cessive tension can cause loss of vascular integrity of the
mesocolon. Eventration of the small intestine or small
colon can occur if the bladder, uterus, vagina, or rectum
prolapses or ruptures.'43 Mesenteric tears result in seg-
mental ischemic necrosis of the colon and later rupture.
Severe injuries of the mesocolon and the SC may result
in primary rupture and fatal peritonitis as well.140
The time from parturition to onset of abdominal
pain (0 to 24 hours) is variable, and colic may be
confused with the mild pain associated with uterine
contraction.'" Mares fail to pass feces and develop
impaction in the SC. Rectal palpation may not be
diagnostic. Abdominocentesis usually reveals a marked
increase in nucleated cell count and rote in levels. but
abdominal hemorrhage may be the' primary finding.
Exploratory celiotomy is recommended. Resection of
de~italized~colon and end-to-end anastomosis should be
attempted but is often not possible owing t o the location
of the lesion. Colostomy may be needed if the lesion is
located aborally.
Strangulation Obstruction
Strangulation obstruction of the SC is rare and can
be caused by enlarged ovaries or-testicular teratomas in
foals and in mature animals."'. '45. 146. 14' Volvulus, her-
niation, intussusception, prolapse, and neoplastic dis-
ease can cause strangulation obstruction. The initial
clinical signs are mild, but the horse's condition deteri-
orates rapidly unless surgical intervention is undertaken.
VOLVULUS, HERNIATION, AND INTUSSUSCEPTION
Small colon volvulus is rare and is usually associated
with abnormalities and malpositioning of other organs
or is due to complications secondary to intra-abdominal
adhesions or a b s c e ~ s e s . ~
Secondary
'~ impaction can oc-
cur oral to the affected segment. Resection of the
diseased segment may be necessary.
Internal or external herniation of the S C can cause
strangulation obstruction. The SC can become strangu-
lated in umbilical or inguinal hernias and tears in the
 L A R G E INTESTINE 403

motic breakdown and leakage as compared with other

FIGURE 36-16. Small colon intussusception in a Standardbred brood-
mare. Notice the dark discolored small colon orad to the intussuscep-
tion (entering layer). (From Ross MW, Stephens PR, Reimer JM:
Small colon intus~usce~tion in a broodmare: J Am Vet Med Assoc
192:372, 1988.)
intestinal segments. 15Z-155 The passage of solid fecal balls
through a relatively narrow lumen; increased bacterial
concentrations, particularly anaerobic organisms; strong
muscular activity; and increased tissue collagenase activ-
ity may inhibit healing.153.'56. Is7 Portions of the SC are
difficult to exteriorize, and the risk of peritoneal contam-
ination is high.
The preferred technique involves a two-layer hand-
sewn anastomosis. A simple interrupted suture pattern
that excludes mucosa is oversewn with a continuous
Lembert suture using 0-polydioxanone or other absorb-
able suture material (Fig. 36-17). This method produces
significantly larger lumen diameters, better anastomotic
healing, and minimal intra-abdominal adhesion forma-
tion compared with end-to-end triangulated rows of
stainless steel staples.Is8 Extensive mesocolic adhesions
occur with stapled anastomoses. Complications that oc-
cur with single- and double-layer inverting methods of
SC anastomosis included anastomotic leakage and ste-
nosis, respecti~ely.'~~, la Removal of digesta from the
large colon may help minimize stress on the anastomosis
immediately after surgery.

broad ligament, omentum, uterus, and vagina.l19. 124 '"7

Incarcerations of the SC can be diagnosed by rectal

examination but may be difficult to distinguish from Each surgical condition of the large intestine re-
small intestinal lesions. quires specific monitoring and aftercare. Care after large
Intussusception of the SC, a lesion similar to type
IV rectal prolapse, can cause strangulation obstruction.
Rectal examination may reveal the intussusceptum. Ex-
ploratory celiotomy, resection, and anastomosis of the
small colon was successful in one horse (Fig. 36-16).148

NEOPIASIA
Polyps, leiomyomas, and lipomas can occur in the
SC. Polyps can be surgically removed without recurrence
if they are pedunculated. Lipomas can cause strangula-
tion obstruction of the SC in aged horses. Because of a
large amount of fat, the mesocolon may be predisposed
to lipoma f0rmati0n.l~~

Surgical Procedures
COLOTOMY
Enterotomy of the SC should be performed through
the antimesenteric band, resulting in a quicker comple-
tion of the colotomy; easier, more accurate apposition;
and less hemorrhage and inflammation than in those
performed adjacent to the band.lS0,151 Bursting wall
tensions of antimesenteric band colotomies are signifi-
cantly greater than colotomies of the sacculated por-
tion.lS1 The colotomy location is more important than
the surgical technique used. Closure of the mucosa as a
separate layer facilitates seromuscular layer closure but
does not affect the postoperative healing response or
lumen diameter in normal horses.'50
FIGURE 36-17. Small colon anastomosis using a 2-layer technique
RESECTION AND ANASTOMOSIS with 0-suture material. (A), The first layer is a nonmucosa penetrating
simple interrupted pattern. (B), The second layer consists of a contin-
Strangulation obstruction of the SC requires reset- uous Cushing suture pattern interrupted at 180 degrees to prevent a
tion and anastomosis. The SC may be prone to anasto- pursestring effect.
404 ALIMENTARY SYSTEM
colon resection and anastomosis is different than care
after enterolith removal, for example. General consid-
erations include antibiotic administration, oral fluid ther-
apy, and dietary and management changes.
Antimicrobials
Many of the surgical procedures performed in the
large intestine require opening the bowel and perform-
ing clean-contaminated surgery. Peritoneal soiling, es-
pecially with particulate digesta, should be limited.
Copious, continuous lavage and use of appropriate
serosal covering with laparotomy sponges can limit con-
tamination, even when the bowel cannot be completely
exteriorized. The concentration of bacteria, particularly
anaerobic species, increases in aboral direction, and
contamination of the surgical field with pathogenic bac-
teria may occur. Therefore, broad-spectrum intravenous
antibiotics such as gentamicin (2.2 mglkg, IV, QID) and
potassium penicillin (22,000-44,000 IUIkg, IV, QID)
are usually sufficient and should be given before and
continued 3 to 5 days after surgery. Metronidazole (15
mglkg, PO, QID) may be useful if anaerobic infection
is suspected but is not given routinely. Contamination
during enterotomy or resection and anastomosis may
theoretically contribute to an increased wound infection
rate, but this problem has not been observed clinically.
Any clean-contaminated procedure, of course, may con-
tribute to wound infection or other complications such
as hernia formation.
Management Changes
Management changes may help prevent recurrence
of diseases after surgery. If sand impaction occurs, a
change in housing arrangements and feeding programs
may help prevent recurrence. Avoiding abrupt feeding
changes may decrease the potential for motility changes,
tympany, and subsequent displacements or volvulus of
the colon. Impactions or other simple obstructions of
the large intestine occur in horses after shipping, a
change in training program, or are associated with other
unrelated gastrointestinal or musculoskeletal problems.
Horses resting for orthopedic problems may be prone
to development of large intestinal diseases. Careful
attention should be paid to vague or subtle signs of
gastrointestinal disease in these horses. Avoiding abrupt
dietary changes in broodmares and providing fresh clean
water to all horses, particularly during the winter
months, are important considerations.
Feeding horses after large intestinal surgery should
be carefully considered. Motility dysfunction may cause
diseases of the cecum, the ventral colon, or the RDC.
Normal motility may not return for several days after
surgery. Therefore, the surgeon cannot expect normal
motility to return immediately, particularly if an enter-
otomy and evacuation of accumulated digesta were
performed. Although this particular surgery removes
accumulated feedstuffs, it certainly does nothing to
correct the primary problem. Feeding, therefore, should
be staged, and the horse should be slowly reintroduced
to its normal diet. Feed is withheld for a minimum of
24 hours. If gastric distention does not occur, oral fluid
intake can begin approximately 12 hours after surgery.
Laxative diets may be considered, but a slow reintro-
duction of the horse's regular diet is preferred. Pelleted
feeds may increase fecal water content and decrease
intestinal transit time, but some horses do not readily
consume the diet.
Pharmacologic Stimulation
Occasionally, motility dysfunctions persist and
reimpaction may occur, particularly after enterotomy
for impaction of the ventral or small colon. Medical
management is therefore required for these conditions.
The use of neostigmine (0.0125 to 0.025 mglkg, SC, IV
or IM) to stimulate motility of the large intestine may
improve motility after surgery, but if an enterotomy or
resection and anastomosis have been performed, the
surgeon should proceed with caution. Neostigmine in-
creases progressive motility of several segments of the
large intestine, but strong contractions might be detri-
mental to healing of the intestine.
Immediate general complications after surgery in-
clude dehydration, endotoxemia, peritonitis, ileus, mo-
tility dysfunctions, and death. Complications specifically
associated with the large intestine include recurrence of
the initial problem or inherent complications associated
with resection, anastomosis, or colotomy incisions. Be-
cause problems of the large intestine can be mild at
first, a prolonged clinical course before surgery predis-
poses the horse to the development of enterocolitis,
caused by Salmonella sp. ~ndotoxemia,thrombophle-
bitis, and laminitis may then become apparent. Nonin-
fectious enterocolitis, associated with mucosal damage
of the large intestine, is common after nonstrangulating
displacement or early strangulation obstruction of the
large colon and can persist for 48 to 72 hours. Leuko-
penia is common, but horses are generally bright and
afebrile, unlike horses with infectious enterocolitis.
Fever on day 1 or 2 after surgery in horses with left
dorsal displacement of the large colon occurs, but no
firm evidence has been given to explain this response.
Recurrence of nonstrangulating displacement and stran-
gulating VLC has led to development of colopexy and
resection techniques.
Adhesions, although certainly possible, are gener-
ally not as severe in large intestinal surgery as they are
in small intestinal surgery. Omental adhesions occur on
exposed staple or suture lines at anastomotic sites or
colotomy incisions. Obstructive disease due to adhesions
occurs but to a lesser extent than after small intestinal
surgery.

In general, the prognosis for horses with surgical
lesions of the large intestine is better than that associated
with lesions of the small intestine. Long-term survival
rates (21% to 42%) for horses with VLC compare
f a v o r a b l y with those after small intestinal surgery (11%).
Survival in horses with nonstrangulating lesions of the
large intestine may approach 80% to 90%, depending
on the initial condition. The long-term survival rate in
horses with large intestinal disorders (56.7%) is signifi-
cantly higher than for horses with small intestinal dis-
orders (33.8%).29In horses with large bowel diseases
requiring surgery, if inoperable cases are excluded, a
survival rate of 73.3% is seen.28Horses with nonstran-
gulating displacements of the colon are found to have
an overall survival rate of 71%.85 Survival rates are
sufficiently high to attempt surgical intervention and
correction of the lesion.
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