Equine Colic

Colic Pathophysiology

Colic refers to any type of abdominal pain or signs consistent with abdominal pain. While most cases are due to GI issues, other body systems (neuro, musculoskeletal, renal, respiratory) can cause signs of “colic”. Colics can be divided into 4 main types

Strangulating obstructions

A twist or entrapment leads to obstruction along with a compromise to the vascular supply.  The intestine is damaged or dead due to the strangulation of blood supply; obstruction occurs but is a secondary problem. Many conditions are often non-strangulating initially but rapidly lead to strangulating conditions due to swelling and fluid buildup (e.g. a loose entrapment becomes tight)

Examples : large colon volvulus, strangulating lipoma, epiploic foramen entrapment

Associated complications:

  • Hypovolemic shock  –Fluid (SI & LI) and/or gas distension(LI) occurs proximally.  Large volumes of sequestered fluid results in shock.
  • Severe pain due to traction on mesentery and distension of gutpain increases rapidly until unrelenting and severe. Pain changes to depression if intestines become devitalized (pain often subsides).
  • Intestinal damage – venous occlusion leads to increased venous pressure and subsequent intestinal edema and net secretion of fluid. The occlusion also leads to decreased arterial inflow, resulting in intestinal necrosis. Necrosis starts with the mucosa as it is the most metabolically active section. See table below.
  • RBC leakage – Red blood cells leak out of altered capillaries, causing intramural hemorrhages and serosanguineous peritoneal fluid. Hemorrhages in mesentery can cause fibrosis, shortening of mesentery, and adhesions.
  • Hypoproteinemia – protein leaks out of bowel due to damage. This leads to a PCV /TPP mismatch : High PCV, low TPP. Compare this to blood loss with both low PCV and low TPP or dehydration with both values being high. The mismatch is hard to treat- if you give fluids to lower PCV and you severely lower the TPP. We usually give colloids first and then fluids.
  •  Endotoxemia– ischemia causes progressive damage, starting with the metabolically active mucosa. Once this mucosal barrier is lost, endotoxin can leak across to the peritoneum and be absorbed into circulation.  Horses may have a “toxic line” (darker line) around the teeth or have brick red mucous membranes.
  • Reperfusion injury may occur in the small intestine.  The return of oxygen to previously ischemic area leads to formation of free radicals which cause further damage. Presently we have no effective means of preventing or treating reperfusion injury.
  • Abdominal distension if large intestinal lesion.
  • Reflux if small intestinal lesion.
  • Death due to endotoxic and hypovolemic shock


Small intestine – Villi lost early on. Completely denuded by 3 hours

With time, the crypt cells will migrate to cover lost villi (within 12 hours), then rapid recovery occurs.

If ischemia continues for 4-5 hours, the loss of mucosa includes the crypts

By 6-7 hours of ischemia, degeneration has passed outward beyond muscle layers. This is bad news; recovery is very difficult as no mucosal cells remain. This section of the bowel needs to be removed surgically.

Large intestine -Complete ischemia induces cellular necrosis. Groups of 3-5 surface epithelial cells loosen and slough.

Cellular degeneration actually becomes irreversible before sloughing occurs. Irreversible mucosal damage occurs after 3-4 hours of  complete ischemia

Sloughing of 97% of the surface epithelium and 50% of glandular epithelium is associated with death.

Strangulating lesions require surgery. General surgical complications include :

  •  Postoperative ileus (especially small intestinal lesions)
  •  Diarrhea
  • Laminitis
  • Adhesions
  • Peritonitis
  • Incisional infections
  • Incisional hernias

Nonstrangulating obstructions

Simple obstructions may be physical (something in the way) or functional (not moving despite no physical obstruction, eg due to neurotransmitter issues or other problem). Intestinal distension occurs secondary to the obstruction or lack of motility.  Gas, fluid and ingesta increase proximally to obstruction. This distension can compress intestinal veins and capillaries. Edema occurs due to increased capillary filtration. Distension pressures of 25cm H20 for 120 minutes can cause jejunal damage with adhesions possible due to the damage. Motility initially increases proximal to obstruction. As distension increases, spasms develop causing intermittent pain. Prolonged distension leads to  continuous pain due to stimulation of stretch receptors.

The specific pathology that results depends upon the site of the obstruction.

Examples : large colon impactions, enterolithiasis

Small intestinal obstruction

  • Reflux due to fluid buildup in the stomach. Horses do not vomit. If gastric decompression isn’t performed via nasogastric intubation, the stomach will rupture.
  • Electrolyte abnormalities and dehydration due to increased secretions
  • Tachycardia due to dehydration
  • Pain due to intestinal distension and spasms. Pain gradually worsens.        

Large intestinal obstruction

  • Bloat due to gas buildup.
  • Dehydration due to altered water resorption.
  • Pain due to intestinal distension and spasms. Pain is generally mild but gradually worsens.
  • Impaction due to buildup of ingesta and removal of water from the ingesta.

 Cecal obstruction

  • Bloat due to gas buildup.
  • Dehydration due to altered water resorption.
  • Pain due to intestinal distension and spasms. Pain is generally mild but gradually worsens over several days.
  • Impaction due to buildup of ingesta and removal of water from the ingesta.

Small colon obstruction

  • Pain  – more severe than large intestinal obstruction due to more rapid distension
  • Reflux is possible. Duodenal compression? Gastrocolic reflex?
  • No bloat.

Non-strangulating lesions carry a better prognosis than strangulating lesion due to less toxemia and fewer complications.

Inflammatory conditions

Intestinal inflammation causes hyperplasia and hypertrophy in smooth muscle. This may cause ileus due to alterations in neurotransmitter function. Infectious agents often lead to secretory response and may also damage the absorptive capabilities of the gut.

Inflammation in the small intestine often leads to hypoproteinemia due to leakage of protein (loss) and less absorption through the villi due to the greater diffusion distance between the nutrients and capillaries. Horses may have weight loss and ventral edema.

Inflammation in colon (colitis) leads to mucosal permeability and signs of endotoxemia, especially tachycardia, shock, changes in mucous membrane color, and fever. Ulcerations can cause colic signs.

Inflammation also alters ability of gut to protect self from intestinal contents. Overwhelming gut inflammation can lead to systemic inflammatory response syndrome (inflammation in other organs).

Examples : equine proliferative enteropathy (Lawsonia), right dorsal colitis, Salmonellosis

Nonstrangulating infarctions

With nonstrangulating infarctions, the intestine is devitalized but no twist or entrapment is present. These conditions are less painful than those involving intestinal distension and entrapment until secondary distension develops. Toxemia leads to tachycardia and depression. These generally carry a very poor prognosis!

Examples : mesocolon tear, intestinal infarctions from Streptococcus equi infections or large strongyles (this may become a problem again with increasing anthelmintic resistance)


Lawsonia intracellularis and Equine Proliferative Enteropathy, 2014 VCNA

Nonsteroidal anti‐inflammatory drug associated right dorsal colitis in the horse, 2015 EVE



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Large Animal Surgery - Supplemental Notes Copyright © by Erin Malone, DVM, PhD is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, except where otherwise noted.