EQUINE COLIC (ADULT HORSES)

Gastrointestinal disease causing signs of abdominal pain in

horses is commonly referred to as colic.
Colic is a frequent and important cause of death and is
considered the most important disease of horses
encountered by practicing veterinarians.
It is estimated to cost the horse industry in the USA
approximately $115 000 000 annually.

ETIOLOGY
Several classification systems of equine colic have been
described including a disease-based system classifying the
cause of colic as:
1.
2.
3.
4.

Obstructive.
Obstructive and strangulating.
Non-strangulating infarctive.
Inflammatory (peritonitis, enteritis).

1.Simple obstructive
Simple obstructive colic are those in which there is
obstruction to the aboral passage of ingesta but no
ischemia or strangulation of bowel. In the terminal
stages there is often ischemia caused by distension
of the intestine.

2. Obstructive and strangulating

Diseases that cause both obstruction and
strangulation as an initial event, such as torsion of
the small intestine or volvulus
of the large colon, result in severe and unrelenting
pain that is little relieved with analgesics.
Obstruction causes distension
and strangulation causes ischemia, loss of barrier
function and endotoxemia. These diseases have a
short course, usually less than 24 hours and

3.Infarctive
Infarctive diseases, such as thromboembolic
colic, are characterized by ischemia of the
intestinal wall with subsequent alterations in
motility and absorptive and barrier functions.
Ileus causes distension of the intestines and
stomach and altered barrier function causes
endotoxemia. The course of the disease is
usually less than 48 hours and is terminated
by cardiovascular collapse and death.
4.Inflammatory
Inflammation of the intestine or peritoneum
alters gastrointestinal motility and absorptive
function leading to accumulation of fluid and
ingesta, distension and abdominal pain.

 Colic cases can also be classified on the basis

of the duration of the disease: acute (< 2436 h), chronic (> 24-36 h) and recurrent
multiple episodes separated by periods of >
2 days of normality) .
Another classification system is anatomically
based.

PATHOGENESIS

The pathogenesis of equine colic is variable depending on

the cause and severity of the inciting disease.
A horse with a strangulating lesion involving 50% of its
small intestine has a much more rapidly evolving disease,
with severe abnormalities, than does a horse affected with
mild spasmodic colic or impaction of the pelvic flexure of
the large colon.
While equine colic often involves changes in many body
systems, notably the gastrointestinal, cardiovascular,
metabolic and endocrine systems, there are several
features and mechanisms that are common to most
causes of colic and that depend only on the severity of the
disease for the magnitude of their change.
The features common to severe colic, and often present to
a lesser degree in milder colic, are pain, gastrointestinal
dysfunction,
intestinal
ischemia,
endotoxemia,
compromised
cardiovascular
function
(shock)
and
metabolic abnormalities.

1. Pain
.Pain is the hallmark of gastrointestinal disease in horses and

is attributable to
1)
2)
3)

Distension of the gastrointestinal tract and stimulation of

stretch receptors in the bowel wall and mesentery.
Stretching of mesentery by displaced or entrapped bowel.
Inflammation and irritation of the bowel, peritoneum or
mesentery.

.The intensity of the pain is often, but not always, related to

the severity of the inciting disease. Horses with mild
impaction of the large colon of short duration (< 24 h) often
have very mild pain, whereas a horse with a strangulating
lesion of the small intestine will have very severe pain.
.Gastrointestinal pain has an inhibitory effect on normal
gastrointestinal function, causing a feedback loop in which
the pain inhibits normal gut motility and function, allowing
accumulation of ingesta and fluid, resulting in distension
and further pain.
.Horses can respond very violently to abdominal pain and
may injure themselves when rolling or thrashing.

2. Gastrointestinal dysfunction
.Colic is almost invariably associated with
impaired gastrointestinal function, usually
alterations to motility or absorptive function.
1) Gastrointestinal motility may be increased, as is

presumed to be the case in spasmodic colic.

2) Altered in its character or coordination, as in
some cases of impaction colic, or absent, such as
in ileus secondary to inflammation or ischemia of
the bowel or to the presence of endotoxemia.
.Increased or uncoordinated gastrointestinal

motility probably causes pain through excessive

contraction of individual segments of bowel or
distension of bowel because of the loss of
normal propulsive activity.

The absorptive function of the intestine may be

decreased by inflammation or ischemia, which
results in distension of the small intestine or large
colon, pain and potentially rupture of the
stomach or colon.
Impairment of the barrier function of the
gastrointestinal mucosa by inflammation or
ischemia can result in leakage of endotoxin into
peritoneal fluid and endotoxemia.

3. Ischemia of the intestinal wall

Ultimately, most forms of lethal colic involve
some degree of ischemia of the intestine.
Ischemia may be the result of
1.Impaired blood flow to or from the intestine
because of torsion or volvulus of the intestine,
entrapment of the intestine, strangulation
such as by a pedunculated lipoma, or
thromboembolic disease.
2.Ischemia may also result from severe
gastrointestinal distension, such as occurs in
the terminal stage of severe colon impaction.

Mild ischemia probably impairs

intestinal motility and function.

normal

4. Endotoxemia
Death in fatal cases of colic in which the affected
viscus ruptures secondary to distension, or when
ischemia and/or infarction damages a segment of
bowel wall, is due to the absorption of endotoxins
from the gut lumen into the systemic circulation.
Rupture of the stomach or intestine is also a

characteristic termination of distension of the

intestine in the horse. The resulting deposition
of large quantities of highly toxic ingesta or
fecal contents into the peritoneal cavity
causes profound shock and death within a few
hours.

5. Shock
The usual cause of death in severe colic is
cardiovascular collapse secondary to endotoxemia
and hypovolemia.
In less severe colic, hypovolemia and cardiovascular
dysfunction may contribute to the development of the
disease, and rapid correction of hypovolemia is central
to the effective treatment of colic.
Hypovolemia is due to the loss of fluid and
electrolytes into the lumen of the gastrointestinal
tract or loss of protein from the vascular space with
subsequent reduction in the circulating blood volume.
Hypovolemia impairs venous return to heart and
therefore cardiac output, arterial blood pressure and
oxygen delivery to tissues.
Cardiorespiratory function is impaired if there is
severe distension of gut, such as in large-colon
torsion.

6. Coagulation and fibrinolysis

Severe
colic, especially that involving
ischemia or necrosis of intestine, is associated
with abnormalities in coagulation and
fibrinolysis characterized by hyper-coagulation
of blood and decreases in rate of fibrinolysis.
Disseminated intravascular coagulation is
common among horses with ischemia or
necrosis of the gut and is a good prognostic
indicator of survival.

CLINICAL FINDINGS
The purposes of the clinical examination are
diagnostic and prognostic.
A. Behavior
Pain is manifested by
1. Pawing.
2. Repeatedly getting up and lying down, often

with exaggerated care.

3. Looking or nipping at the flank.
4. Rolling, and lying on the back.

Pain may be continuous or, more commonly,

intermittent with bouts of pain lasting as long

as 10 minutes interspersed with similar
periods of relaxation.

B. Posture
The posture is often abnormal, with the horse standing
stretched out with the forefeet more cranial and the hind
feet more caudal than normal - the so- called 'saw-horse'
stance.
Some horses lie down on their backs with their legs in the
air, suggesting a need to relieve tension on the mesentery.
C. Abdomen size
Distension of the abdomen is an uncommon but important
diagnostic sign .
Symmetrical, severe distension is usually caused by
distension of the colon, sometimes including the cecum,
secondary to colon torsion, or impaction of the large or
small colon and subsequent fluid and gas accumulation.
If only the cecum is distended the abdomen may show an
asymmetrical enlargement in the right sub-lumbar fossa.

D. Defecation and feces

Defecation patterns can be misleading. It is
often mistakenly assumed that there is no
complete obstruction because feces are still
being passed. But in the very early stages of
acute intestinal obstruction there may be
normal feces in the rectum, and the animal
may defecate several times before the more
usual sign of an empty rectum with a sticky
mucosa is observed.

E. Physical examination
1. Heart and respiratory rates
. The heart rate is a useful indicator of the severity
of the disease and its progression but has little
diagnostic usefulness.
. Horses with heart rates less than 40/min usually
have mild disease whereas horses with heart rates
above 120/min are usually in the terminal stages of
severe disease.
. Horses with obstructive, non strangulating disease
often have heart rates between 40 and 60/min,
whereas horses with strangulating disease or
necrotic bowel will usually have heart rates over
80/min. However, heart rate is not an infallible
indicator of disease severity, as horses with torsion
of the colon can have heart rates of 40-50/min.
. The respiratory rate is variable and may be as high
as 50/min during periods of severe pain.

2. Mucous membranes and extremities

Mucous membranes of normal horses and of horses without
significantly impaired cardiovascular function are pink, moist
and regain their normal color within 2 seconds after firm
digital pressure is removed.
Dehydrated horses have dry mucous membranes, although
the capillary refill time and color are normal.
Horses with impaired cardiovascular function have pale, dry
mucous membranes with delayed capillary refill (> 2 s) .
Endotoxemic horses will often have bright red mucous
membranes with normal or delayed capillary refill. As the
disease becomes more severe the mucous membranes
develop a bluish tint and capillary refill is longer than 3
seconds.
Cool extremities may be indicative of compromised
cardiovascular function.
Sweating is common in horses with severe abdominal pain
and, when present in a horse with cool extremities and signs
of cardiovascular collapse, is indicative of a poor prognosis.

3. Auscultation
loud borborygmi distributed in all or most
quadrants are indicative of intestinal hyper-motility
and consistent with spasmodic colic, diarrhea or the
very early stages of a small-intestinal obstructive
strangulating lesion.
Hypo-motility of absence of sounds are consistent
with intestinal impaction, intestinal tympany.
The absence of sounds, or the presence of
occasional high-pitched, brief sounds, sometimes
with a splashing character, is consistent with ileus.
These sounds should not be mistaken for the
rolling, prolonged sounds of normal peristalsis.
4. Rectal examination
A careful rectal examination is probably the most
important part of the clinical examination in colic

CLINICAL PATHOLOGY
1. Hematology (hematocrit and plasma total protein
concentration is useful in assessing hydration
status).
2. serum biochemistry
a. Serum urea nitrogen and creatinine concentrations
are useful indicators of hydration status and renal
function.
b. Measures of serum electrolyte concentration
(hypokalemia,
hypocalcaemia
and
hypomagnesaemia).
c. serum gamma glut amyl transferase (GGT) activity
is elevated.
d. serum and peritoneal alkaline phosphatase activities
are higher in horses with ischemic or inflammatory
bowel disease than in horses with other forms of
colic.

PROTOCOL FOR EVALUATING A

COLIC PATIENT
1. Behavior; the following should be assessed:
severity of pain, frequency and duration of
attacks.
2. Clinical and clinicopathological observations
a)Elevated pulse rate with a fall in pulse
amplitude are among the most reliable
indicators of the state of dehydration or
shock.
b)Respiratory rate.
c)Mucous membrane color and capillary refill
time are assessed.
d)Temperature.

e)
f)
g)
h)
i)
j)
k)

Intestinal sounds.
Rectal findings.
Amount and nature of feces.
Reflux through a nasogastric tube.
Visible distension of the abdomen.
PCV and plasma protein.
Skin turgor.

Thank you for

attention
With my best wishes
for you all