5. 5
Several classification systems of equine colic have been
described including a disease-based system classifying the
cause of colic as:
Obstructive
Obstructive and strangulating
Non strangulating infarctive
Inflammatory (peritonitis, enteritis)
12. 12
Colic cases can also be classified on the basis of the
duration of the disease: acute « 24-36 h), chronic (> 24-
36 h) and recurrent (multiple episodes separated by
periods of > 2 days of .normality)
13. 13
Equine colic accurs world wide.
The incidence rate: 3.5-10.6 percent
Mortality: 2.5 percent
The case fatality rate:
6-13 percent
14. 14
1) intrinsic horse characteristics
2) Management
those associated with feeding practices
medical history
parasite control
15. 15
Age
Horses 2-10 years of age are 2.8 times more
likely to develop colic that horses less than 2
year.
16. 16
Breed
There is a consistent
finding that Arabian
horses are at increased
risk of colic, but the
reason for this apparently
greater risk has not been
determined.
18. 18
Horses with a history of colic are 6
times more likely to have colic again
Previous abdominal surgery are 5
times as likely
19. 19
Inadequate parasite control programs have been estimated to put
horses at 2-9 times greater risk of developing colic.
20. 20
The features common to severe colic, and often
present to a lesser degree in milder colics, are pain,
gastrointestinal dysfunction, intestinal ischemia,
endotoxemia and compromised cardiovascular
function (shock )
21. 21
Distension of the gastrointestinal tract stimulation
of stretch receptors and pain → inhibits normal gut
motility and function → accumulation of ingesta
and fluid further destination and pain
22. 22
Alterations to motility or absorptive function
Examples
spasmodic colic→ severe contraction of intestine
Impaction → blockage of the intestine
23. 23
Ultimately → most forms of lethal colic involve some degree of ischemia
of the intestine because of loss of barrier function
24. 24
► because of restricted respiration by pressure on the diaphragm and reduced venous return to
the heart because of pressure on the caudal vena cava
► endotoxemia and hypovolemia
30. 30
↑pulse rate with ↓pulse amplitude
Endotoxemia → bright red mucous Membranes
Terminal stages of disease→ cold, purple, dry
mucous with CTR of more than 3 seconds and toxic
line
34. 34
Patient history and signalment
Physical exam
Rectal palpation
Naso-gastric intubation
Ultrasonography
Radiology
CBC, biochemistry
Exploratory surgery
35. 35
Patient history and signalment
Physical exam
Rectal palpation
Naso-gastric intubation
Ultrasonography
Radiology
CBC, biochemistry
Exploratory surgery
36. 36
All four quadrants of the abdomen should be
examined for at least 1 minute at each site.
Continuous, loud borborygmi→ intestinal
hypermotility
Absence of sounds→ ileus
42. 42
All four quadrants of the abdomen should be
examined for at least 1 minute at each site.
Continuous, loud borborygmi→ intestinal hypermotility
Absence of sounds→ ileus
43. 43
The structure is often compressible, akin to
squeezing a fluid-filled tubular balloon, and slightly
moveable. is suggestive of a small-intestinal obstructive lesion
or anterior enteritis
44. 44
Gas and fluid distension of the large colon is evident as large
(> 20 cm) taut structures often extending into pelvic canal.
Tenial bands are often not palpable.
Impaction is evident as columns of firm ingesta. The most
common site is the pelvic flexure
48. 48
1-Ultrasonography
2-radiology
3-Course of the disease
Spasmodic and gas colic: usually resolves within hours of onset.
Horses with strangulating lesions have severe clinical signs and
usually die within 24 hours of the onset of signs.
Horses with non strangulating obstructive lesions : have longer
courses, often 48 hours to 1 week
49. 49
Hematocrit and plasma total protein
blood leukocyte:
Combination of leukopenia and a left shift are
consistent with the endotoxemia
Hyperkalemia → in horses with severe acidosis
50. 50
Hypokalemia → in horses with more long-
standing colic
Hypocalcemia and hypomagnesemia →severe
colic
(GGT)→its activity is elevated in 50% of
horses with right dorsal displacement of the
colon (compression of bile duct).
51. 51
Serum urea nitrogen and creatinine Prerenal azotemia is common
in horses Acid-base status: Most horses with severe colic have
metabolic acidosis
52. 52
Abdominocentesis
The presence of intracellular bacteria, plant
material and degenerate neutrophils is
indicative of Gastrointestinal rupture
53. 53
Arterial systolic blood pressure →90 mmHg (12 kPa) having
a 50% chance
below 80 mmHg→ fewer than 20%
Capillary refill time: 3 seconds or more→30%
HR: 8O/min →50% chance of survival
50/min → has a 90% chance
54. 54
The nature of the necropsy findings depends
on the underlying disease
57. 57
1-Provision of analgesia
2-Correction of fluid, electrolyte and Acid-
base abnormalities
3- Gastrointestinal lubrication or
administration of fecal softeners
4-Treatment of underlying disease