Equine Colic

what clinical signs might we expect to see in a colicking horse?

subtle behavioral change: loss of appetite, withdrawn from others, excessive recumbency

pain signs: Flehmen, stretching, pawing at the ground, flank watching, bruxism, sweating, trembling, rolling (mild to severe thrashing)

how do you distinguish natural rolling behavior from colic pain behavior?

Rolling in a normal horse is usually seen just once, then followed by standing, a shake and resumption of grazing. Rolling due to colic is seen frequently, and not followed by natural behaviors.

If an owner of a colicking horse calls and asks what do to before the vet arrives, what should you advise?

withhold feed, walk the horse only if it is safe to do so, separate horse from its herdmates to monitor

DO NOT offer feed, give home remedies or any medications, or beer/fizzy drink by mouth

what are the 5 pathophysiological mechanisms that colic can be classified into?

simple distension (eg spasmodic colic or gas colic)

simple obstruction (intra-luminal obstruction or non-strangulating displacements or entrapment)

strangulating obstruction / non-strangulating infarction

inflammatory/toxic

non-GIT (false) colic

What information from a history is likely relevant for an emergency colic investigation?

signs and duration of colic, any medications given, dental history, previous colic history, signalment, fecal output, access to sand, deworming history, any changes in feed, has the horse traveled recently

what are you look for on distance exam of colicking horses?

indications of pain (facial grimace scale), abdominal distension, overall health and BCS

what are you listening for on thoracic auscultation?

any relevant murmurs, arrhythmias, adventitious lung sounds

HR is a good indicator of pain, SIRS or hypovolemia/dehydration

what changes in MM color indicate systemic issue in a horse?

purple, brick red or very pale color — warrants immediate discussion of referral!

Which sedative agents would you use in a colic horse to allow further assessment?

alpha 2 agonists (xylazine, detomidine, medetomidine) — excellent sedation, potent analgesia, fast onset

often given with opioids (eg butorphanol) to potentiate sedation, provide better restraint and greater analgesia

When is it safe to perform a rectal exam in a colicking horse?

good competent handler, sedation is effective, horse shows mild-moderate colic signs but can stand, facilities such as stock are available, spasmolytics such as hyoscine effective

what gut abnormalities might be rectally palpated in colic?

• impacted gut (large colon/cecum)

• large colon gas distension

• large colon displacement (taenial bands in abnormal position)

• distended small intestinal loops

• thickened intestine

**palpation of no abnormalities does not exclude an abnormalitiy!

why should you always pass an NGT in a colic case?

diagnostic and therapeutic!

→ allows us to check for reflux, which may indicate a problem in the proximal intestine

→ allows administration of enteral fluids in indicated (eg large colon impaction)

what is the most common complications encountered with passing a nasogastric tube in a horse?

hitting the ethmoid turbinates resulting in epistaxis

what findings are associated with a normal abdominocentesis?

clear straw colored, total protein <25g/L, total nucleated cell count <5×10^9/L, lactate <1mmol/L

when is abdominocentesis not appropriate in a colic case?

there is increased risk of complications if: there is marked distension of the small or large intestine, sand is present in the large colon or in mid to late gestation pregnant mares

when is gastroscopy indicated?

suspicion of equine gastric ulcer syndrome (EGUS) or gastric impaction

**requires 12-18 hours fasting period to best visualize the stomach

which drugs can be used for initial treatment of pain in a colic case?

NSAIDs (mainly flunixin, but also phenylbutazone or meloxicam can be used, ensure dehydration is corrected first!) or alpha2-agonists (xylazine has the best visceral analgesia properties)

how do you stimulate GI motility in initial treatment of a colic case?

gentle walking (if appropriate), NGT with enteral fluids, stimulating licking and chewing (eg with a salt lick or small amount of molasses)

what enteral fluids can be given for managing simple medical impactions?

water with electrolytes or magnesium sulphate (epsom salts)

• use commercially available electrolytes and make up according to packet

• 1g/kgBW of magnesium sulphate SID

when should you not give enteral fluids?

if there is reflux >2L; leave NGT in place and refer the horse

→ administration of fluid in a horse that is refluxing can make the colic worse and risks rupture

when can colic patients begin refeeding?

no feed allowed until you are sure the colic has resolved; then reintroduce food slowly over 12-48hrs

• reduce volume of hard feeds by ½ initially

• reduce access to lush fresh pasture, slowly increase pasture allowance until back to normal

when is referral indicated for a colic case?

• owner request referral

• violent colic signs and presents with HR of 100bpm

• FLASH shows dilated loops of small intestine

• peritoneal fluid is orange in color, has a total protein >25g/L

• mild colic signs not responding to medical treatment

• horse shows colic signs and you palpate moderate/severe abnormalities on rectal examination

• patient has brick red MM

• obtaining >2L of net reflux after NGT is passed

what is a non-strangulating obstruction and what are some examples?

lesions preventing the aboral movement of ingesta, gas, and fluid without compromising the arterial blood supply

Examples: duodenitis-proximal jejunitis, ileal impaction, muscular hypertrophy of the ileum, ascarid impaction, gastroduodenal obstruction, neoplasia, intestinal inflammation and fibrosis, miscellaneous simple luminal obstructions

what are strangulating obstructions and what are some examples?

SI volvulus, pedunculated lipoma, intussusception, mesenteric rents, inguinal or scrotal herniation, diaphragmatic hernia, epiploic foramen entrapment, vitelline anomalies, entrapment through the gastrosplenic ligament

what is duodenitis proximal jejunitis (DPJ)?

aka anterior or proximal enteritis; a medical colic

main features: inflammation and edema of the duodenum and proximal jejunum, excessive intestinal fluid secretion, large volumes of enterogastric reflux

what distinguishing features favor DJP?

• fever

• pain improves after decompression, and HR often decreases

• generalized but non-taut small intestinal distension on rectal exam

• increased wall thickness (>6cm) on ultrasound, usually generalized rather then focal

what bloodwork findings can indicate DJP?

• hemoconcentration (increased PCV and TP)

• leukopenia

• electrolyte disturbances: hypocalcemia, hyponatremia, hypochloremia, hypokalemia

• elevated hepatic enzymes (GGT, AST, ALP)

what abdominocentesis findings may indicate DJP?

peritoneal protein >35g/L and peritoneal WBC >5x10⁹/L

what are the key features of DJP treatment?

gastric decompression (most important) via NGT, every 1-2hrs to prevent rupture

aggressive fluid therapy with IV crystalloids

flunixin-meglumine (use judiciously in case of azotemia)

antimicrobials may be considered in cases of neutropenia

parenteral nutritional support (IV dextrose then amino acids and lipids)

lidocaine and metoclopramide (prokinetics, only after ruling out surgical obstruction)

digital cryotherapy and NSAIDs to prevent laminitis

when is surgical exploration of DJP warranted?

uncontrolled pain, reflux >7 days, suspicion of obstruction

what is equine proliferative enteropathy (EPE)?

an infectious intestinal disease that primarily affects weanling foals, caused by Lawsonia intracellularis, which invades proliferating crypt epithelial cells in the ileum

what is the pathophysiology of EPE?

L. intracellularis is transmitted via fecal-oral route, organism invades crypt cells in the distal small intestine, resulting in severe mucosal hyperplasia, corrugated thickening of the intestinal wall, decreased absorptive capacity, protein-losing enteropathy, weight loss and hypoalbuminemia

what clinical signs are typically seen in foals with EPE?

lethargy, anorexia, fever, peripheral edema (ventrum, sheath, distal limbs), weight loss/poor doers, colic, diarrhea

what clinical and laboratory findings indicate EPE?

appropriate signalemt (weanling or young horse), compatible clinical signs (weight loss, edema, diarrhea, colic), hypoproteinemia due to hypoalbuminemia (TP often <50g/L, albumin often <20g/L)

what tests can be used to confirm EPE in a weanling?

PCR detection of L. intracellularis in feces or rectal swabs

serology via ELISA, IFAT, or IPMA

how is EPE treated in weanlings?

antimicrobial therapy for 2-3 weeks (oxytetracycline, doxycycline or minocycline, macrolides ± rifampin)

supportive care: IV fluids, plasma transfusion, nutritional support, anti-ulcer therapy

how can EPE be prevented and controlled?

• early detection of clinical cases

• isolation of affected foals

• monitoring serum protein levels

• pest control to reduce wildlife contamination

what is ileal impaction?

a non-strangulating small intestinal obstruction that is geography dependent (uncommon in NZ but very common in SE US and some parts of Europe)

what are key predisposing factors of ileal impaction?

• sudden change in hay feeding practices

• feeding coastal Bermuda hay

• Infection with the intestinal tapeworm Anoplocephala perfoliata

what diagnostic test findings are associated with ileal impaction?

• may palpate a firm, dough-like mass on the right side of the abdomen just medial to the cecum

• peritoneal fluid analysis can help assess intestinal viability and determine whether a strangulating lesion is present

how is ileal impaction treated?

gastric decompression (less reflux volume than DPJ)

IV crystalloids

flunixin megulimine

anthelminitics once horse is stabilized (praziquantel or pyrantel pamoate)

what might cause a simple obstruction in a horse?

food impactions, strictures, foreign bodies, bezoars (solid masses of indigestible material), or parasitic boluses

→ these prevent aboral progression and gradual accumulation of ingesta, fluid and gas, resulting in luminal distension

what do horses with strangulating lesions often exhibit?

acute, continuous, severe abdominal pain with minimal to no response to analgesics

tachycardia

congested MM and prolonged CRT

elevated PCV and TP (hemoconcentration)

small intestinal distension on rectal palpation

significant gastric reflux (often >2L)

what is small intestinal volvulus?

rotation of the intestine ≥360° around its mesentery; affects horses of all ages and is relatively common in foals (2-4mo)

what findings might indicate small intestinal volulus?

nasogastric reflux, distended amotile small intestinal loops on ultrasound; distension of SI on rectal examination; abdominocentesis shows serosanguinous fluid, TP >20-25g/L, cell count >10 × 10⁹/L, lactate >7.7mmol/L

how is small intestinal volvulus treated?

exploratory celiotomy via a ventral midline incision

• if the intestine remains viable, the volvulus is corrected (untwisted)

• if devitalized, the ischemic segment must be resected, followed by anastomosis

what is a pedunculated lipoma?

benign fatty tumors suspended from the mesentery by a stalk of variable length → the length of the pedicle determines the risk of strangulation

• long pedicles may wrap around one or more loops of small intestine, occluding the lumen and vasculature, leading to ischemia, necrosis and rapid clinical decline

how is a pedunculated lipoma treated?

exploratory celiotomy, cutting the pedicle of the lipoma to release entrapped bowel and remove the lipoma, resection of non-viable intestine when necessary

what might cause intussusception?

any factor causing disruption of normal peristalsis including: enteritis, ascarid infection, tapeworm infection (Anoplocephala perfoliata), abrupt dietary changes

how is intussusception diagnosed?

ultrasound findings are characteristic, revealing the classic “bull’s eye” or target sign on transverse view

what are the treatment options for intussusception?

manual reduction or resection and anastomosis depending on lesion location

what causes scrotal or inguinal hernias?

increased intra-abdominal pressure from trauma, strenuous exercise, or copulation

what are some complications of herniation?

bowel incarceration, strangulation, and compression of testicular vessels (resulting in cold, firm, edematous testes)

how are hernias treated?

inguinal incision to:

• reduce herniated intestine and unilateral castration

• assess viability of intestine

• closure of EXTERNAL inguinal ring to prevent recurrence

OR midline celiotomy may become necessary when needing to resect and anastomoze devitalized intestine

what is the difference between primary and secondary cecal impactions?

primary - firm, dry ingesta

secondary - fluid distension of the cecum due to impaired motility

how do you diagnose cecal impaction?

palpation of a firm impacted cecum or distended fluid-filled cecum; a taught ventral cecal band can be suggestive of ileal impaction

what is the initial treatment for dry ingesta cecal impactions?

fluid therapy to hydrate the impaction, analgesics (flunixin or phenylbutazone) and oral laxatives (magnesium sulfate)

if the cecum is severely distended or medical therapy fails, surgical evacuation is recommended

where do large colon impactions typically occur?

at anatomical narrowing points — pelvic flexure or right dorsal colon

what risk factors are associated with large colon impaction?

decreased water intake (often seen in winter), feeding very dry roughage or large concentrate meals, sudden restriction of exercise

what clinical signs are associated with sand impaction of the large colon?

recurrent mild colic, weight loss or reduced appetite

chronic colitis and diarrhea

large colon impaction or obstruction in severe cases, resulting in more severe abdominal pain

how are sand impactions usually treated?

administration of psyllium, with fluids, magnesium sulfate or mineral oil, to facilitate the passage of sand

surgical intervention may be necessary if a complete obstruction develops

what is spasmodic colic?

simple distension colic caused by abnormal intestinal motility resulting in painful intestinal spasms

colic signs are intermittent and mild to moderate in severity

what are some predisposing factors for spasmodic colic?

sudden dietary changes, ingestion of lush pasture or high-concentrate diets, stress or changes in routine, transport, intestinal parasitism

how is spasmodic colic treated?

analgesics (flunixin) and antispasmodic agents (eg buscopan) to reduce intestinal spasms

what are enteroliths?

mineral concretions (mainly struvite) that form around a foreign nucleus (stone, nail, rope), commonly found in the right dorsal colon or transverse colon

diagnosed with abdominal radiography and treated surgically

what risk factors are associated with development of enteroliths?

high-magnesium diets and feeding predominantly alfalfa hay

what are non-strangulating displacement?

colon displacements that obstruct the lumen without initially compromising blood supply (but may later on if they become strangulating)

mild to moderate colic and large colon distension on rectal examination

what does right dorsal displacement result from and how is it diagnosed?

abnormal movement of the colon, usually involving counterclockwise rotation

rectal palpation identifies gas-distended large colon lateral to the cecum and absence of the pelvic flexure (depending on RDD type)

what does left dorsal displacement result from?

the left dorsal and ventral colon migrate dorsally and laterally, rotating 180° and becoming entrapped between the spleen and the kidney over the nephrosplenic ligament

what will you find upon rectal palpation of a horse with left dorsal displacement and nephrosplenic entrapment?

colon positioned between spleen and left kidney, unable to palpate the left kidney, ventral and medial displacement of the spleen

how do you treat left dorsal displacement and nephrosplenic entrapment?

exercise — may facilitate correction in early stages of entrapment

administration of phenylephrine for splenic contraction prior to exercise or rolling under GA

or surgical correction when conservative methods fail

what is the pathophysiology of large colon volvulus?

may occur at multiple sites, including the base of the cecum, the cecocolic ligament or the sternal and diaphragmatic flexures

twists typically occur clockwise when viewed from behind

what clinical signs are associated with non-strangulating large colon volvulus?

mild pain, mild gas distension, normal vital signs

what clinical signs are associated with strangulating large colon volvulus?

severe pain, marked distension, tachycardia, prolonged CRT, endotoxemia, shock

what risk factors are associated with large colon volvulus?

broodmares 0-3 months post-partum, recent dietary changes, recent access to lush pasture

how is large colon volvulus diagnosed?

rectally — massive gas distension and tight colonic bands

ultrasound — edematous intestinal walls (thickness >9mm)

abdominocentesis — findings vary with duration

how is large colon volvulus treated?

rapid stabilization with hypertonic saline and isotonic fluids prior to exploratory midline celiotomy

what causes rectal impactions?

dry, firm fecal matter becomes difficult to pass or when the rectal lumen becomes narrowed

causes: reduced intestinal motility or stasis, dehydration, consumption of coarse/poorly digestible forage, perirectal abscesses or masses, neurological problems, rectal trauma or scarring

what clinical signs are associated with rectal impaction?

straining to defecate, reduced or absent fecal output, mild to moderate colic signs, restlessness or repeated attempts to pass manure

how are rectal impactions treated?

lubrication and softening of feces, enemas, fluid therapy to correct dehydration, manual removal or fragmentation during rectal examinations