Miniature Horses American Appaloosa Pinto Arabian Mini Miniature Horse

COLIC - SYMPTOMS - DIAGNOSIS - TREATMENT

An introduction is in order. Dr Terry Gerros is an Equine Internal Medicine specialist that we came to know and rely on when he was at the Oregon State University Veterinary School. Terry's entire veterinary career has been involved with horses. Terry grew up in the Kentucky thoroughbred country and was in private practice at one of the well known farms in Lexington prior to returning to school to further his veterinary education. He then moved to Oregon State University and taught Internal Medicine at the Vet School for 9 years. Since then he has again returned to private practice restricted specifically to equines. The information that follows was published by Dr. Gerros and was graciously provided to us for posting for the readers of our website. It was originally written for practitioners so some of the words are pretty technical but if you can bounce over them there is a wealth of great information related to colic which is probably the most common ailment that faces horses and their owners. This is a long but very comprehensive article explaining the whole range of colic circumstances. Areas of special interest to miniature horse owners are the those that deal with the various forms of Impaction Colic. That is by far the most prevalent problem with our horses. Medical and surgical treatment near the bottom of the article are also very valuable sources of information

Terry C. Gerros, DVM, MS, Diplomate, ACVIM.
Assistant Professor, Large Animal Medicine
Oregon State University

This discussion was originally used as the basis for a lecture series for Veterinary Students. There is a significant amount of technical terminology used throughout. It is hoped that through reading of the material the general information presented will be useful to all individuals regardless of their technical background.

WHAT EXACTLY IS COLIC ?

Colic is the manifestation of visceral abdominal pain and may be acute, chronic, or recurrent. The three basic causes include:

1) Distension of gut with fluid, gas, or ingesta.

2) Pulling on the root of the mesentery.

3) Ischemia or infarction.

Colic occurs less often in ruminants than the horse. Two likely reasons are:

1) Ruminants have a higher pain threshold than does the horse.

2) Dietary shifts occur primarily in the rumen, therefore, intestinal gas is greatly reduced as is the pain induced by gaseous distension.

Why does the horse exhibit colic more than any other species?

The horse appears to have a low threshold of pain and is frequently plagued by minor digestive disturbances that result in distended bowel. Unlike the ruminant, the horse's hind gut serves as the fermentation vat.

WHAT ARE THE SIGNS OF COLIC ?

There are many signs indicative of colic, some of which include:

Restlessness Pawing Treading

Kicking at the abdomen Rolling Groaning/Grunting

Suddenly dropping to the ground in pain Sweating Looking at the flank

Lying down and getting up Bruxism Biting the flank

Anorexia and depression often accompany these signs. You will generally find an elevated heart rate and normal body temperature. Be aware that the clinical and vital signs, and other abnormal physical exam findings will vary considerably between each case. Some of the factors affecting these include etiology, length of illness, prior medications given to the horse, and pain threshold of the individual animal.

The clinical signs of colic may be due to either visceral or parietal pain. Though there are many causes of both kinds of pain, they manifest themselves differently.

Visceral Pain:

The clinical signs of visceral pain are mediated by the sympathetic nervous system. External palpation and pushing on the abdomen does not usually elicit pain unless the affected inflamed or dilated viscus is contacted.

Parietal Pain:

Parietal pain is usually associated with peritonitis and is usually responsive to external pain. The animal with parietal pain is usually reluctant to move and splints the abdomen. Acute peritonitis occurs within minutes following rupture of the stomach or perforation of an ulcer, by the acid contents, while rupture of the colon or rectum may take 12 hours or more before peritonitis is clinically apparent. An animal with pleuritis may show some mild signs of visceral, but on close examination you may notice the horse is actually displaying more signs of parietal pain, a short inspiratory phase, or the animal tenses up when you approach their chest or shy away from you, they may grunt when you auscult or palpate the chest.

Colic due to visceral pain is displayed by bruxism, grunting/groaning, treading with the hind feet, kicking at the abdomen, and anorexia and depression. Pain associated with parietal pain, ie. peritonitis, may be manifested by arching the back, splinting, and exhibiting pain upon deep palpation of the area. These signs are seen most commonly with TRP and abomasal ulcers.

You will be faced with many different presentations of colic. Some will obviously appear surgical and some will obviously appear medical. Some surgical colics will have all the parameters telling you that it can be managed medically, be aware of these. The mare in the early stages with strangulated bowel due to a pedunculated lipoma may only be mildly painful, with all other physical exam findings normal. Go with your gut feeling. Remember, just as on an examination in the classroom, your first impression is usually the correct one. If all the parameters are within normal limits, except pain, and the animal doesn't quite respond the way you think it should, re-evaluate!! Your assessment is likely to be correct, that something else is going on. Use those special senses: sight, touch, smell, hearing. When you are performing a rectal examination, let your fingers be your eyes, try to imagine what the normal anatomy should feel like. Try to visualize what you are feeling. Get a mental picture of the normal anatomy. Again, repetition. All those rectals you did during the breeding season, remember what the normal rectal feels like. In other words, normal placement of organs will put pressure on your arm. You will sense this upon entry into the rectum. When you place your arm in the rectum, your first thought should be, normal or abnormal. Does it feel right? Use your anatomical landmarks; is everything in the right place, do all the structures feel normal. If it doesn't feel right, it isn't right. Once you establish that the rectal is abnormal, then differentiate whether it is small intestine or large intestine, surgical or non-surgical. If you think it's surgical, refer it or take it to your clinic and cut it. Don't dink around.

There are many diseases which cause colic in the ruminant including: mechanical obstruction, functional obstruction, strangulating obstruction, gas distension of a viscus, torsion, volvulus, the list goes on. Extra intestinal causes also exist (just to complicate your life) including: urolithiasis, pleuritis, pyelonephritis, hepatitis, ovarian disease (abscess), impending parturition (a wonderful disease, if all goes right), anaphylaxis, again the list continues.

***Approach to diagnosis and management of colic in the horse:***

1) Take history. Since colic is a common problem, it is often treated either by the owner or the veterinarian before diagnostic efforts are undertaken. You need to know if the owner has treated the animal before your examination since recurrent colic may be an indication of a more serious problem. Examples include: Thromboembolism, sand or other foreign body, tumor, and gastric ulcer, to name a few.

What questions do I ask?

There are a number of questions which will help you to identify the cause.

a) Use and signalment, prior medical history of the horse.

b) The nature and duration of pain.

c) Type and amount of feed, where fed, etc.

d) Any changes in diet, weather, exercise?

e) Breeding history and pregnancy status.

f) Is the horse eating and drinking?

g) Last defecation and character of feces.

h) Has this horse had prior episodes of colic or prior abdominal surgery?

I) Treatments given and response to treatment.

j) Parasite control program and date of last deworming.

k) Any changes in degree of pain since you were notified?

l) Is the animal insured? If so, has the insurance company been notified?

These are some of the questions you will need to know to help you identify the problem and how you will manage the case. There are many ways to manage these, economics being one major determining factor.

2) Perform a thorough physical examination. Be consistent in your examinations!!!! Intestinal causes of colic can often be differentiated from colic associated with other organ systems by physical examination (tachypnea may be present in a horse with pleuritis, but the client may have called you to examine the horse because of colic). It is important to note whether the horse has normal borborygmi or if feces are being passed. Rectal examination and passage of a nasogastric tube are an essential part of your physical examination and unless impossible or impractical, should be included in every examination.

What do I look for and how do I assess the animal?

a) Pain - Severity; continuous or intermittent

b) Attitude - Depression, alert, excited.

c) Physical condition - Evidence of colic duration, weight loss.

d) Temperature - Decreased, normal, increased.

e) Pulse - Quality and rate.

f) Respiration - Rate and effort.

g) Mucous membranes-- Oral: Color and capillary refill time.

Nasal membranes: Evidence of chronic discharge, mucopurulent discharge, serosanguinous discharge, epistaxis

h) Eyes: Conjunctiva: Edematous, inflamed. Sclera: Injected, icteric

I) Lymphadenopathy??

j) Nasogastric intubation - Does the tube pass easily?, Presence of gas, fluid reflux (quantity, color, and pH).

k) Auscultation - Intensity and rate of borborygmi;

1) Sounds indicative of sand.

2) Don't forget to listen to the thorax.

There are referred bowel sounds there, listen for dullness.

l) Percussion - Gas caps, tympany, dullness, ballottement.

m) Abdominal distension - Normal, increased.

n) Rectal examination - Bowel distension or displacement, impactions, masses,

mesenteric pain, character of feces, bowel wall thickness, presence of sand, is the mare pregnant.

o) In any intact male, don't forget to palpate the testicles.

3) Ultrasound and radiology may be helpful in your diagnosis. Radiology especially useful in foals or miniature horses. An enterolith maybe detected in the adult with radiography. Ultrasound may be helpful in the identification of tumor or adhesions.

4) Examine the feces! By mixing the stool with water, you can grossly see if there is sand present, if the horse has previously been given mineral oil, it will float. If no feces is being passed, a more serious condition may be present, especially if no GI sounds are heard.

5) Laboratory aids. Of immediate benefit is a PCV, plasma protein (PP), and abdominocentesis. The PCV and PP are useful in assessing the hydration status of the animal. The abdominocentesis helps to assess the peritoneal and visceral surface.

**Gastric dilatation/Grain overload:**

Dilatation of the equine stomach may be primary or secondary. Primary gastric dilatation (GD) is most commonly observed following overeating of highly fermentable feeds, particularly concentrated grain ration, although pelleted and cubed rations have been incriminated. Dilatation is further complicated by an increased osmotic pressure within the stomach and resulting fluid accumulation. Gastric dilatation may result from excessive consumption of water following strenuous exercise or a period of water deprivation. Aerophagia (cribbing) or eating immediately after exercise may produce mild forms of GD. Mom had it backwards, don't eat immediately after swimming. Secondary GD occurs more frequently than primary and results from intestinal reflux into the stomach, most commonly seen with small intestinal obstruction or ileus.

The most common clinical sign is abdominal pain. The severity of which is proportional to the severity and duration of dilatation. In the case of secondary GD, the clinical signs are dependent upon the primary intestinal lesion. Retching and vomiting, though uncommonly observed, may be seen in this condition. Eructation, retching, vomiting, or the presence o ingesta at the nares warrant consideration of severe GD. Hemoconcentration, dehydration, and decreased tissue perfusion is dependent upon the severity and duration of intestinal disease, especially when there is an association with overeating of concentrates.

The diagnosis is best confirmed by passage of a NG tube with subsequent reflux of gastric fluid and gas. Use the largest bore tube you can pass. Remember, if it doesn't fit, don't force it. If the animal becomes painful when the tube nears the cardia, a little lidocaine (30-40 mls) may reduce the pain. Be patient but persistent when passing the tube.

How do you tell the difference between primary and secondary GD?? Decompression of secondary GD only results in partial and temporary resolution of pain. Gastric decompression in primary dilatation should result in correction, if secondary metabolic abnormalities and serious complications such as laminitis and gastric rupture have not occurred.

Management problems such as acute grain overload or excessive water consumption, evidence of cribbing help identify primary gastric dilatation. Rectal examination findings of distended small intestine loops suggest a secondary GD.

Treatment: Decompression by NG tube. Administration of mineral oil or other medications via the NG tube is completely, undeniably, irrefutably, plain and simple, and beyond any reasonable doubt contraindicated!!!! Intravenous fluids and electrolyte maintenance are important for supportive care. Most horses with gastric dilatation and reflux have variable degrees of hemoconcentration, dehydration, hypokalemia, hyponatremia, and hypochloremia. GD is also often associated with alkalosis due to intraluminal sequestration and loss of electrolytes and hydrogen ions. Metabolic acidosis can occur in gastric dilatation following intestinal obstruction. Prokinetic agents have been used in the horse, but conclusive evidence is lacking.

Prognosis again like so many other things, depends upon the etiology, severity, and duration of the disease. Most do well if treated before development of laminitis or gastric rupture. Secondary GD prognosis also depends on the primary cause.

**Duodenitis-Proximal Jejunitis (Anterior enteritis)**

The etiology has yet to be determined, however, Salmonella spp, clostridial toxins, and/or viral agents are thought to play a role in the pathogenesis of this syndrome. This disease is primarily seen in the adult horse. Following an acute case of colic, a chronic state of gastric reflux (3-14 days) occurs, usually without abdominal pain. The clinical signs associated with DPJ include mild to severe colic followed by depression, colic signs when the stomach becomes distended with GIT reflux, obviously gastric reflux (large volumes), and fever (early on). Other clinical features which vary depending upon duration and severity include dehydration, altered mucous membrane color, prolonged CRT, tachycardia, absence of borborygmi, diarrhea (usually during the resolution phase). Rectal examination findings generally are filled but not severely distended small intestine.

The clinical laboratory findings include a leukocytosis with toxic neutrophils or the WBC may be normal, elevated PCV and TP. Hyponatremia, hypochloremia, hypokalemia with a metabolic acidosis occurs in long-standing or severe cases. Abdominocentesis reveals and elevated protein (>3.5 g/dl) and mild to moderate elevation in WBC (<10,000/ml). Fluid is usually yellow and turbid, may be serosanguinous if diapedesis occurs.

The primary rule out is intestinal obstruction.

The diagnosis is based upon history, clinical and lab findings, and rectal examination. The definitive diagnosis is made at surgery or necropsy.

Treatment is a critical factor here. Gastric decompression is an absolute must. It is imperative that you repeat this frequently, placing an indwelling stomach tube is indicated, but do not be lulled into the concept that this all you need do to keep the stomach from over distending. You may find that you get continuous drainage, but most importantly is that it prevents gastric rupture. What else must I do, you ask? Maintain hydration status, electrolyte and acid-base balance. Let your laboratory values be your guide. Analgesics are important, AFTER you rule out obstructive disease. Antibiotics may be indicated, again use your clinical judgement (don't worry, it will come) and CBC findings. Surgical intervention: These guys are poor general anesthetic risks. Update by the surgeons.

Oh yes, don't let us forget about the complications which may follow. Just when you thought you had resolved the problem. Thank you very much. The include laminitis, renal dysfunction (the two most common), pneumonia, pleuritis, hepatitis, multi focal abscessation of lymph nodes, intraperitoneal adhesion, and of course, diarrhea. Sounds like a referral case to me.

**Small intestinal strangulation obstruction**

Interruption of the blood supply to the bowel with simultaneous luminal blockage produces intestinal strangulation obstruction characterized by congestion and edema of the wall, accumulation of hemorrhagic fluid in the lumen, and loss of mucosal integrity of the affected segment of bowel. Damage to the mucosal barrier, which may be severe after only THREE, yes count them 3, hours of strangulation obstruction, allows penetration of bacteria and endotoxin through the bowel wall and their release into the peritoneal cavity. Left untreated, the horse becomes hypovolemic, develops endotoxemia and metabolic acidosis, and suffers circulatory collapse. Death follows within 24-48 hours. Guess what? Early recognition is paramount for successful treatment!!

The clinical findings with this condition:

Pain: Moderate to severe, intermittent to unrelenting, can be accompanied by depression.

Cardiovascular status:

a. Heart rate: >60 bpm and higher

b. Pulse: Weak, thready, or not palpable

c. Mucous membranes: Injected, muddy, or cyanotic

d. Capillary refill: >2.5-3 seconds

e. Packed cell volume: >50 and increasing

f. Plasma protein: >8g/dl; decreased if protein lost in bowel lumen or peritoneal cavity

Intestinal motility: Hypomotile or silent (amotile)

Nasogastric tube: Continuous small intestinal reflux; tube should be fixed in place to allow gastric decompression and prevent rupture, pH > 6.0, large volumes

Rectal: Distended loops of small intestine

Abdominocentesis: Serosanguinous, cloudy fluid >5-10,00 WBC, >2.5 g/dl protein, intracellular or free bacteria. Ingesta on repeated taps indicated RUPTURE.

Blood gases: Metabolic acidosis, increased blood lactate

Response to medication: Short-lived analgesia, lack of auscultable peristalsis, increased PCV/TP despite intravenous fluids and bicarbonate

Examples of small intestinal strangulation obstructions:

I. Volvulus

II. Intussusception

III. Internal hernias

a. Epiploic foramen

b. Mesenteric defect

c. Gastrosplenic ligament

d. Nephrosplenic ligament

e. Cecocolic ligament

f. Broad ligament

g. Omental defect

h. Fibrous bands and adhesions

IV. Diaphragmatic hernia

V. External hernias

a. Inguinal hernia

b. Umbilical hernia

VI. Pedunculated lipoma

Treatment: Exploratory laparotomy.

Prognosis: This completely depends upon how soon the condition is discovered and how soon the animal gets operated on. Reported survival rates after correction range from 27-70 per cent.

Postop complications include gastrointestinal distension and ileus, peritonitis, and adhesion

formation at the operative sites. Yes, of course, laminitis and diarrhea.

**Intussusception:**

This condition is most frequently seen in young horses and are the result of abnormal peristalsis. The jejunal, ileal, and ileocecal intussusceptions are the most common types seen. The condition presents as an acute, complete luminal obstruction, although subacute and chronic forms have been reported. Congestion and edema lead to infarction and necrosis. The causes include dramatic dietary changes, enteritis, ascarid infection, verminous arteritis, and tapeworm attachment (A. perfoliata) at the ileocecal orifice. It can also follow small bowel enterotomy or anastomosis. Signs of complete small intestinal obstruction usually develop, reread the last topic. Rectal examination may elicit pain when palpating the ileocecal region, if it is involved. Devitalization of the intussusception is reflected in peritoneal fluid changes associated with strangulation. With an ileocecal intussusception, the ileum is contained within the cecum and peritoneal fluid changes may not reflect the degree of necrosis.

Intussusception of the large colon is an unusual cause of intestinal obstruction in horses. Most frequently reported in the young horse less than 2 years of age, it has been reported in older animals. To date, all reported cases have involved the left colon. Clinical signs resemble those of impaction or nonstrangulating colon displacement early in the course of the disease, including mild to moderate colic, slow progression, reduced or absent fecal output, reduced intestinal sounds, slight tachycardia, mild dehydration, with normal CRT and mucous membrane color. Rectal exam reveals a gas and ingesta filled left colon.

Medical management until there is a lack of response to therapy, progressive intestinal tympany, or increasing severity of abdominal pain dictate surgical intervention.

Treatment: Exploratory laparotomy.

*Spasmodic colic*

How do you diagnose this one? Good question. Lets call it acute intestinal inflammation characterized by pain which is usually intermittent. This becomes a frequent diagnosis and is predisposed by poor management, dietary changes, fatigue, chilling, parasites, weather changes, and from drinking cold water. Irritation and/or fermentation leads to spasm and mild "gas cramps", lasting any where from 5-15 minutes and repeats. This is a very mild form of colic and places minimal stress on the animal. You frequently hear hyperperistaltic borborygmi and loose feces may be noted. Treatment is fairly simple, analgesics, lubricants (mineral oil) and you may want to even add an antifermentative (turcapsol). The prognosis is favorable.

*Flatulent colic*

This is a form of enteritis characterized by excessive gas formation due to fermentation. The predisposing factors to gas formation include both primary and secondary causes. Primary causes include feeding highly fermentable feeds: green alfalfa or excessive grain and dietary changes or errors. Secondary causes are related to obstructive disease or ileus. Of course there is the ever present "idiopathic" etiology. The clinical picture is an acute onset of severe pain which tends to be a continuous and violent colic. There is abdominal distension (you can see this, distended paralumbar fossa) which is usually associated with large bowel involvement. Owner may tell you the horse has been passing gas and/or scant feces. Heart rate generally is elevated. Depending upon the amount of distension, the animal may be dyspneic possibly progressing to cyanosis. Auscultation of the abdomen reveals decreased intestinal sounds with metallic sounds. Abdominocentesis is unremarkable. Rectal exam-guess what- gas distended bowel. Treatment is a bit more complex. Control the pain, relieve the distension: stomach tube, stimulate motility (parenteral medication ?, oral lubricant), cecal trocharization. You may have to use surgical decompression.

*Thromboembolic colic*

The exact pathogenesis is unknown. A "low flow" state may exist due to thrombus formation in the cranial mesenteric artery and major branches especially the ileocecolic artery?? Strongylus vulgaris has been incriminated in the condition due to larval migration, which induces intestinal and vascular damage, leading to lesion formation and intestinal dysfunction. Vascular lesions include wall thickening, thrombus formation, and dilatation of the arterial lumen. The sites most frequently affected include the cecum, colon, and small intestine. Hey, that gives the rectum a rest.

The clinical signs seen in this form of colic are much like so many of the others we've already discussed, including: mild to moderate visceral pain, which occasionally is severe, ofttimes the pain is intermittent but recurrent. There is mild intestinal distension that is slow to develop, and is secondary to ileus. Gastric reflux may be present, and if so, is due to ileus. Other physical examination findings include depression, weight loss, and diarrhea. Rectal palpation is usually unremarkable, however, there may be mild SI distension and you may detect abnormalities in the cranial mesenteric artery and its branches.

Laboratory findings include a neutrophilia �eosinophilia, unless toxemia is present, and we all known what that looks like, right? Abdominocentesis is variable. You may see some degree of peritonitis, mild to moderate elevation of WBC and protein. Remember, the character of the fluid may change with progression of the disease. Want to get really aggressive, run a serum protein electrophoresis, you may see and elevated IgG (T) globulin spike. Fecal egg counts may or may not be helpful.

Treatment consists of relieving the immediate signs of abdominal discomfort, restoring hydration and electrolyte, and acid-base imbalances, and treating the peritonitis if present. When the acute crisis resolves, use larvicidal doses of anthelmintics, ie fenbendazole 50 mg/kg SID for 3 days, or 30 mg/kg SID for 5 days. You may need to repeat this monthly for up to 3 months.

**Ascariasis (Ascarid Impaction):**

Heavy infestations of Parascaris equorum is foals, weanlings, and yearlings can lead to small intestinal impaction, particularly after the administration of a high efficacy anthelmintic such as ivermectin, piperazine, or organophosphate. These non-benzimidazole drugs inhibit neuromuscular transmission and paralyze the ascarids, thereby promoting impaction. Organophosphates cause lysis of the cuticle which reportedly produces hypomotility when absorbed.

Clinical signs: The ascarid mass accumulates producing a partial or complete obstruction of the small intestine. This presents as a mild to severe colic. Nasogastric reflux may contain ascarids. The foal or weanling may be pot-bellied, dull hair coat, the animal may not shed its winter coat. The diagnosis is based upon evidence of heavy ascarid infestation, signs of small intestinal obstruction, and a history of recent deworming.

Treatment: Use of low efficacy dewormers, ie thiabendazole 44 mg/kg or fenbendazole 5 mg/kg in those foals suspected of heavy roundworm infestation. This followed by a high efficacy dewormer. Impactions are treated with lubricants (mineral oil) and analgesics if the obstruction is incomplete. Occasionally surgical intervention is required to remove the impaction..

Prevention: Good deworming program, be religious!

**Enteroliths:**

These little jewels occur in various parts of the U.S., from Florida to as far north as Wisconsin, and as far west as California. California appears to be plagued with this condition more than anyplace else in the U.S. There is no sex or breed predilection. Most of these horses are between 5 - 10 years of age, however, it has been reported as young as 11 months. Yes, that's correct, 11 months. They are generally composed of struvite (magnesium ammonium phosphate). Many different things have been found in the center of these; hair, metallic objects, foreign objects. Silicon dioxide is the most common nidus. Historically, these horses have periodic bouts of abdominal pain. The pathogenesis is unclear, but may be related to diet. High Mg⁺⁺ concentration in the diet. Alfalfa hay, with its high protein content, may contribute as a result of increased ammonia nitrogen load to the intestine. The jury is still out on this one.

Enteroliths occur in various places in the gut. The most frequent locations are: right dorsal colon, transverse, and small colon. They may be single or multiple. The diagnosis is based upon history, physical examination, and rectal exam. The degree of pain is variable depending on the extent of distension and vascular compromise. The horse generally continues to pass scant amounts of liquid feces, gas, and mineral oil. Abdominocentesis will be normal until pressure necrosis occurs from the lith. Radiographs may help in the diagnosis. Surgery is the treatment.

**Large colon impactions:**

This is one of the MOST COMMON causes of colic in the horse. The cause for impaction formation is unclear, but may be related to coarse feed, poor dental maintenance or worn teeth, inadequate mastication, dehydration, alterations in colonic motility, and in my experience, more common when the weather changes and reduced water intake can occur. Impaction occurs at two sites of narrowing, the pelvic flexure and the transverse colon. Both are sites where motor centers can induce retention to aid mixing of food. This natural retention of ingesta appears to predominate, overriding the normal aboral flow.

These horses present with mild to moderate pain and decreased fecal output. The amount of pain will increase with complete obstruction or pressure necrosis of bowel around the impaction. The feces are often hard, dry, and mucus covered. The history includes progressive anorexia and decreased water intake.

Diagnosis is made by rectal examination and based on the presence of a large, firm, ingest-filled colon. Some right dorsal and transverse colon impactions have inconclusive rectal findings. In these horses you may only find left colon and pelvic flexure gas distension but normal anatomic location. When you can't confirm this by rectal examination, you back into the diagnosis with you physical exam findings and by ruling out other possibilities.

Miniature horses frequently have small colon impaction!!!

**Colon displacements and colon volvulus:**

The equine large colon if freely movable within the abdominal cavity because of the single mesenteric attachment to the body wall. The normal position of the colon, maintained by contact with other abdominal organs, may be deranged by altered motility or altered digestive mechanisms. The derangements may lead to a variety of displacements, volvulus, and eventual strangulation.

The displacements include:

I. Left dorsal displacement

a. Also termed nephrosplenic (renosplenic) entrapment

1) Colon moves through the nephrosplenic space

2) Colon moves up between the body wall and spleen

b. More common in large breeds of horses

1) Warmbloods

2) Thoroughbreds

c) Clinical signs: mild to moderate pain, no gastric reflux

d) Rectal examination

1) Distended large colon

2) Caudomedially displaced spleen

3) May palpate colon over the N-S ligament

e) Management

1) Conservative

i) If only pelvic flexure involved, deny feed, may see spontaneous resolution

ii) Short-acting anesthesia, right lateral, hoist by legs, hold 1 min., back to dorsal recumbency, slowly turn and position in left lateral, completing 360-degree rotation

2) Surgical

i) Ventral celiotomy

II) Right dorsal displacement

a)Etiology/pathogenesis unknown, mechanisms likely for other displacements

1) Nutrition

2) Feeding practices

3) Alterations in colonic motility and function leading to changes in weight

4) Gas formation w/in sections of the colon

b) Clinical signs similar to left dorsal displacement

c) Rectal examination

1) Large gas-distended colon

2 Can not find pelvic flexure

3 Cecum may be medial to colon-ABnormal

d) Management

1) Conservative

i) Maintain hydration

ii) Withhold feed to allow self correction

2)Surgical intervention

i) Ventral celiotomy

Colonic volvulus:

A volvulus greater than 270 degrees causes vascular obstruction, often resulting in severe colonic devitalization. There is no breed predilection, adult horses and broodmares have the highest incidence. Volvulus is most common during the summer months, with lesser incidence in the spring.

The exact cause of is unknown. It is speculated that hypomotility due to pain, intestinal fatty acid content, or electrolyte abnormalities may initiate the movement. Gas distension of the ventral colon may allow it to displace dorsally with the dorsal colon moving ventrally, thus potentially inverting the entire colon. Volvulus is most commonly observed at the base of the colon. However, the twist may occur at any point of the large colon. The sternal and diaphragmatic flexure is the second most common location. Looking from the rear of the horse, the twist usually is clockwise. The cecum may or may not be involved.

Two types of vascular insults occur to the colon during a volvulus. Venous obstruction is the initial insult because of the common clinical observation of extensive colonic edema, congestion and hemorrhage. A volvulus may result in a pale grey serosa with minima edema, congestion and hemorrhage, indicating the initial vascular insult is both arterial and venous obstruction.

The clinical signs of volvulus depend upon the degree of twisting, duration of vascular compromise, and the length of colon involved. The onset is usually acute and the pain severe. These horses often present with severe abdominal distension and evidence of shock. Tachycardia and tachypnea are present. Rectal examination reveals a large, gas-distended colon, an edematous colonic wall may be detected. The results of an abdominocentesis are highly variable, and when compared to the changes in the abdominal fluid from a small intestinal strangulating obstruction, is of little value in determining the severity of bowel damage.

Treatment: Surgical intervention.

Prognosis: Depends upon the severity of the vascular compromise and the damage to the colon.

**Cecal Impaction**

This syndrome can be divided into types of impaction, 1) a dehydrated or firm mass fills the cecum, the cecum is tightly stretched over the food mass, but is still able to stretch with gas or fluid. The second type is more a dysfunction since the cecum is filled with ingesta that has a fluid consistency.

With a firm impaction, diets high in corncobs, kernel corn, or coarse hay or straw are implicated. No specific cause is known when the problem arises with the horse on a normal hay and grain diet.

There is no known cause for cecal dysfunction with distension. There is hyperemia and thickening of the cecal wall, but the cause of ileus is unclear. Once distension occurs, mural ischemia prolongs the ileus making the cecum prone to rupture.

The clinical exam findings with a firm cecal impaction are mild to moderate intermittent pain. Heart rate and borborygmi are variable. Rectal examination is the most remarkable in that the cecum generally is palpable full of feed including the cecal base. The mass is firm and may be dented with your fingers - Don't push to hard!! The cecum is in normal position.

Cecal dysfunction generally presents with a much more severe pain due to the massive distension of the cecum. A resonant ping may be heard in the right paralumbar fossa. The heart rate varies, what else is new. Gut sounds are reduced or absent. Rectal exam finds the cecum to feel tympanic except the cecum is pulled cranial due to the weight of the food and fluid.

Treatment: Cecal impaction can be handled medically. Those that are treated medically generally do well, as long as it resolves fairly rapidly. Those that are managed initially medically, then require surgery because lack of resolution, generally don't do as well due to the length of the illness. It is better to stay out of that abdomen, but when clinical signs dictate........ Surgical intervention as discussed by our surgeons. The prognosis for cecal impaction is good, and for cecal dysfunction, guarded.

**Sand Impactions**

Horses that have short or nonexistent grass in their pasture or insufficient roughage in their diet are prone to consume sand while attempting to gather bits of feed from the ground. The composition of the soil also has an effect on the incidence of sand colic. There is a higher incidence of sand colic in California, Florida, Michigan, and coastal regions.

The clinical signs are similar to large colon impaction. (Just when you thought this might be easy to figure out.) Often the weight of the sand will cause intermittent colic, which responds to analgesics, only to recur in a few days or weeks. Horses will stretch out and stand in this position for long periods of time. This may be an attempt to reduce tension on the intestine. In some horses you will see intermittent diarrhea from the irritation caused by the sand. Vital signs vary. Auscultation of the abdomen may reveal the sound of "pouring" sand. Rectal examination may be normal. Coarse sand may be felt with your fingers during palpation, however, fine sand may not be felt.

In order to diagnose this condition, simply place fecal material in a sleeve or bucket and add water to float the feces. The sand will settle out. Any amount of sand settling out is abnormal. Note: Some sand may be normal, depending upon the area in which you practice. These impactions usually form in the right dorsal and transverse colon. Sand will also accumulate in the ventral colons. Peritoneal fluid usually is normal or may have a slight elevation in protein. The colons are heavy and can be easily penetrated by either needle or teat cannula. In this case, you will likely see sand in the sample. Diagnostic but not good for the horse.

PERITONITIS IN THE HORSE

Definition and etiology: The peritoneum is composed of a single layer of mesothelial squamous cells overlying loose areolar connective tissue and adipose tissue. It lines the peritoneal cavity and covers the intra abdominal viscera. Function primarily is as a bidirectional semipermeable barrier to the diffusion of water and low-molecular-weight solutes between the blood and the abdominal cavity. It secretes a serous fluid that lubricates the abdominal cavity, minimizes intraabdominal adhesion formation, and has minor antibacterial properties. Peritonitis is characterized by exudation of serum, fibrin, and protein into the peritoneal cavity.

Peritonitis may be classified according to origin ( primary or secondary), onset (peracute, acute, chronic), region affected (diffuse, localized), and presence of bacteria (septic, nonseptic). Primary peritonitis may result from hematogenous spread and be associated with impaired host defenses. It usually is a secondary condition.

In the horse, peritonitis is usually acute, diffuse, and secondary to traumatic or chemical insults or to infectious disease processes. Some infectious agents have an affinity for serosal surfaces and predispose the horse to the development of peritonitis, these include strangles, influenza, EVA, and AHS. Chemical peritonitis may progress to septic peritonitis. Localized peritonitis is most frequently associated with abdominal abscess.

Pathophysiology:

1) Release of catecholamines, histamine, and other vasoactive amines

2) peritoneal vasodilatation and hyperemia

3) increase in peritoneal and vascular permeability

4) influx of protein-rich fluid, macrophages, PMN cells, humoral opsonins, natural antibodies, and serum complement into the peritoneal cavity

5) chemotactic phagocytosis

6) depression of peritoneal fibrolytic activity

7) fibrin deposition

8) reflex ileus of the GIT

Clinical signs: The clinical signs depend on the primary disease process, infectious agent, and extent of disease. The range varies from localized peritonitis with little systemic involvement to generalized peritonitis with severe toxemia/septicemia. Most often clinical signs are suggestive of GI dysfunction and are nonspecific.

Common presenting signs include: Colic, ileus, pyrexia, anorexia, weight loss, and diarrhea. Profound toxemia, weakness, depression, tachycardia, tachypnea, circulatory failure, rapid deterioration and death within 4 to 24 hours is seen with peracute peritonitis seen with rupture of the intestine or uterine perforation.

Peracute peritonitis with viscus rupture or abscess rupture results in overwhelming sepsis, cardiovascular collapse and death. Blunt and to the point!

Acute diffuse peritonitis reveals clinical signs of abdominal pain, sweating, pawing, muscle fasiculations, tachycardia, tachypnea, thready peripheral pulse, red-to-purple mucous membranes, prolonged CRT, dehydration, depression, and anorexia (sounds alot like toxemia). Body temperature is variable, but usually you will find pyrexia. Both visceral and parietal pain are evident during the early stages of the disease. However, parietal pain predominates in most cases, splinting the abdomen, shys away from you. Ileus frequently occurs resulting in intestinal distention, gastric reflux, and abdominal discomfort. Decreased fecal output, constipation (or diarrhea), and impaction (due to dehydration) result because of reluctance to perform and abdominal press because of pain.

Rectal examination findings reported include:

1) a gritty feeling to the serosal and parietal surfaces from fibrin deposition.

2) dull, dry texture to the peritoneum.

3) decreased fecal or dry fecal material in the intestine.

4) pain on palpation of fibrous adhesions, mesenteric bands, inflamed surfaces of the peritoneum.

5) intestinal impaction or distension secondary to ileus.

6) abdominal mass (abscess or neoplasia).

Horses with localized, subacute or chronic peritonitis may show signs of chronic or intermittent colic, depression, anorexia, weight loss, intermittent fever, ventral edema, exercise intolerance, decrease or absent borborygmi, and mild dehydration. Heart rate, respiratory rate, and fecal output may be normal. Polydipsia/polyuria have been reported in association with chronic peritonitis. Pyrexia and abdominal discomfort are not consistent findings.

Clinicopathologic alterations:

1) Acute peritonitis

a) leukopenia with left shift

b) +/- hypoproteinemia

c) elevated PCV

d) +/- hyperfibrinogenemia

2) Subacute, chronic or localized

a) neutrophilic leukocytosis, maybe normal

b) hyperproteinemia, hypergammaglobulinemia, hypoalbuminemia

c) hyperfibrinogenemia

) +/- normocytic, normochromic anemia

3) Electrolyte and acid/base abnormalities vary depending upon underlying cause and stage

4) Peritoneal fluid analysis

a) confirm presence of peritonitis

b) +/- information on underlying cause

c) elevated WBC count

1) acute phase primarily polymorphonuclear cells

2) later mononuclear cells and macrophages

d) elevated protein

e) +/- bacteria free or phagocytized in leukocytes

f) analysis of fluid

1) cytology

2) gram stain

3) culture and sensitivity

4) electrolytes, creatinine (uroperitoneum)

g) organisms commonly isolated from peritoneal fluid in horses

1) obligate anaerobes (B. fragilis common)

2) enteric bacteria (E. coli common)

3) Strep. zooepidemicus

Differential Diagnosis: See list provided

Treatment:

1) treat the underlying disease process

2) correct the hydration status

3) correction of electrolyte and acid/base abnormalities

4) plasma if hypoproteinemic

5) treatment of accompanying endotoxemia

6) appropriate antimicrobials

a) base upon culture and sensitivity

b) broad spectrum including anaerobic coverage

7) intermittent drainage of abdominal fluid to remove bacteria and toxic by products

8) analgesia

9) antiinflammatory agents or heparin to decrease adhesion formation

10) high protein, low CHO diet

Complications:

1) Laminitis

2) Abdominal adhesions

3) Abdominal abscess

4) Renal dysfunction

5) Septic emboli to other organs

6) Recurrent colic

7) Ill thrift

Prognosis: Unfavorable with generalized or prolonged peritonitis especially if gross bacterial contamination is evident.

Medical Management of Colic

In practice well over 90% of the cases of colic you will see will be managed medically, with the remainder requiring surgical intervention. Keeping this in mind, it should be obvious that a thorough clinical examination to determine the cause and location of abdominal pain is imperative. It is therefore equally important that your selection of medications is such that they will act directly to alleviate the cause and relieve pain without untoward side effects. You will develop certain protocols for handling specific etiologies, however, please remember to treat each case individually. If and when you get complacent, that will be the time that you will make errors which could result in litigation against you and even worst, the death of an animal or someone's companion. The classes of medications used in the management of colic include analgesics, tranquilizers, GI protectants, laxatives, lubricants, anti-fermentatives, anti-ulcer medicants, and electrolytes, including intravenous and oral preparations.

With that in mind, what is the approach to medical management of the acute abdomen. We have discussed various etiologies, clinical signs, and ways to differentiate between those managed medically and those which require surgery. Proper medical management requires that you understand the causes and mechanisms of abdominal pain. An increase in intramural pressure is the primary pain stimulus to the GI tract, regardless whether it is caused by distension, associated with impaction, displacement, and excessive fermentation, or, spasm, associated with irritation or ischemia. Your goal will be to relieve the distension or spasm which may require that you relieve the pain until that has been accomplished.

THE NEED FOR SURGERY

Only a small percentage of colics the average equine practitioner sees will be considered for colic. It is safe to say that about 95% of your cases can be adequately managed at the farm or the stable. With the exception of a few equine clinics, surgical and complicated medical cases must be referred to a hospital with complete surgical and anesthetic facilities and a staff experienced in equine abdominal surgery. Those medical cases which require diagnostic and therapeutic management beyond the capabilities of the owner or the practice setting are also candidates for referral.

The decision to refer a horse with colic involves the logical assessment and correlation of a number of clinical parameters. Consideration of these parameters individually can be very misleading. Rapid referral of a surgical case can literally mean the difference between life and death.

The correct decision to refer only part of your job as a veterinarian. Inappropriate or inadequate preparation of the patient for transportation can result in the death of an otherwise salvageable animal. It far better to refer the wrong case well than to refer the right case poorly.

THE DECISION TO REFER:

1) Those caused by a surgically correctable lesion.

2) Those requiring management beyond the scope of the owner or the practice setting.

3) Those in which the available diagnostic parameters do not clearly differentiate between medically or surgically manageable conditions, but in which the horse may benefit from immediate access to surgical facilities if the clinical parameters deteriorate.

The recommendation to refer ultimately is made by the veterinarian on the spot in consultation with the owner.

Accurate interpretation of clinical signs that may indicate the need for surgery depends on localizing the disease to a system. Colic is defined as acute abdominal pain and, as such, can be induced by any disease process causing pain within the abdomen. Other diseases however, may be misdiagnosed by the owner as colic. In these cases, it is up to you to evaluate which body system is affected. Abdominal sources of pain are more common than non-abdominal sources. Owners tend to identify acute behavioral changes typical of pain as "colic". When evaluating a horse that the owner says is "colicy", remember that extra-abdominal disease of the musculoskeletal, cardiovascular, respiratory, and central nervous systems can mimic colic (see table 1 below).

The next step evaluating a potential referral candidate with abdominal pain is to localize the pain to a system within the abdominal cavity. Although colic is generally attributed to lesions of the intestinal tract, disease of the urinary or genital tracts also may present with signs of colic. Some of the diseases seen in these systems fall into the referral category (surgical or intense medical management), whereas others may be managed on the farm.

Although you should evaluate each case of colic based on the clinical signs present at the time of the exam, the duration of the current episode and its relation to any previous episodes can alter the prognosis and your decision to refer. Most intestinal accidents probably begin with less than complete luminal and vascular obstruction, progression may be rapid. Complete occlusion of small intestinal vasculature with luminal obstruction, for example, can cause irreversible bowel damage within 3 hours. Strangulating obstruction must be identified early in the course of the disease for an acceptable outcome. On the other hand, persistent impaction which has failed to resolve with 3 - 4 days of aggressive medical therapy may be a candidate for surgery to prevent irreversible bowel wall damage from chronic distension and pressure. Finally, a horse with chronic colic that needs frequent veterinary treatment or that interferes with the animal's function may benefit from being referred for exploratory surgery.

Is surgical therapy indicated? Some cases of medical colic require extensive diagnostic or therapeutic management, but most horses are referred with the idea that surgery may be required.

During the initial examination, cases tend to fall into three categories based on available clinical signs:

1) Those cases that definitely need surgery.

2) Those that definitely do not.

3) The grey zone, including horses that either do not have parameters diagnostic for a surgical lesion at the time of examination, or that may be managed either conservatively or surgically.

I use a set of parameters which help me make a logical decision in identifying those case which require surgery (see tables 2 & 4 below, alternatively uses Figure 1). Clinical signs and their severity depend on the nature of the lesion and its duration. Remember, you can not consistently rely upon any one parameter for either a diagnosis or prognosis. These are just guidelines and should only be considered as such. Often times you must go with your gut feeling, making the decision based solely upon your physical exam findings and without any laboratory data.

As a rule of thumb, positive indicators of a surgical lesion are marked pain which responds briefly to analgesics, palpable distension of the small intestine with fluid, or significant gastric reflux (>1 liter). Palpation of a large colon displacement indicates a surgical lesion regardless of the presence or absence of other signs. Other parameters that support the presence of a surgical lesion include an elevated pulse (>60 bpm), elevated PCV and TP, and elevated WBC and RBC counts in the peritoneal fluid.

The longer the lesion is present, the greater the number of positive surgical indicators and the likelihood that the lesion will require surgical correction. Unfortunately, the prognosis decreases the longer the lesion remains uncorrected. Obviously, the quicker you ascertain a surgical problem, the faster it's referred and operated, the greater the chance for survival. Oftentimes a decision for against referral must be made before a surgical lesion can be definitely identified. The farther away from the referral center, the earlier you must make the decision.

Once you make a decision to refer, you should explain the situation to the owner and give them your reasons for recommending referral. Communication here is the key. For animals which have a high sentimental or financial value, it may pay you in the long run to refer the case even though you are not sure of a diagnosis. The aggravation of an unnecessary trip with a happy ending is often minimal compared with the stress of delay and the potential for an adverse outcome.

Some cases of mild but recurrent colic cannot be resolved without surgical intervention. These include enteroliths and some intestinal adhesions among others. Mild colic are less of an emergency, in these cases, a more thorough examination and preparation can be done.

Optional surgery? Three categories exist is this situation:

1)Those that are caused by a known lesion, but which may be treated medically or surgically (ie. certain impactions).

2) Those for which surgical exploration is desirable for diagnostic and perhaps therapeutic purposes.

3) Those that lack definitive indications for or against surgery.

Consider the pelvic flexure impaction which remains static or increases in size in the face of aggressive medical management. Surgery may be indicated to prevent pressure damage to the bowel. Surgical intervention of cecal impaction currently carries little better prognosis that medical therapy.

Recurrent cases of colic that respond temporarily to medical therapy bur which recur with sufficient frequency or severity that they interfere with the animal's function, may need surgical intervention in hopes of correcting the lesion or diagnosing the cause. Be sure your owner is aware that once identified, the lesion may not be correctable (ie. tumor) or that a lesion may not even be identified. Note, even though they may be in good physical condition prior to surgery, unexpected complications can occur.

Many horses with a lesion that can be repaired surgically do not show definitive indicators for surgery during the early stages of the disease. Will delay in referral compromise the prognosis if surgery is indicated? There is no clear-cut way to make this decision for all cases.

Non-strangulating obstruction develop more slowly and definitive surgical indicators appear more gradually,. Fortunately, irreparable damage also develops more gradually if adequate fluid support and gastric decompression are provided.

What if the owner elects to delay referral? The economic or sentimental value of the horse to the owner may influence the decision of when to refer. Should the owner elect to delay referral, you should instruct the owner the monitor the animal for continued or increasing degree of pain, also the pulse can be monitored every 30 - 60 minutes for increase suggesting progressive damage.

When is surgery not indicated? Four reasons:

1) The lesion can be managed better conservatively.

2) The lesion has no effective surgical therapy (ie. enteritis, pleuritis)

3) The prognosis with surgical intervention is grave (ie. bowel rupture)

4) The owner is unwilling or financially unable to consider surgery.

Euthanasia should always be recommended on humane grounds for animals with untreatable and progressive lesions.

Preparing the patient for transport.

The ultimate goal is to get the animal to the referral center in the best possible condition so that the veterinarians there can accurately evaluate it and take appropriate therapeutic measures.

1) Pain relief: Insurance of adequate pain relief is mandatory, not only from the standpoint of humane care, but also to ensure safety of the animal and the driver during transportation. There are many to choose from.

2) Sustaining the pain relief: Analgesics given immediately before loading may not last the entire length of the trip. If you must dispense a few doses of an analgesic, be sure your client knows how to administer them. Be sure you warn them about the animal's potential for violent and unpredictable behavior.

An intravenous catheter with a long extension set attached may be placed so the client does not have to enter the trailer during transport. Explain to the owner how the catheter is used, including how to use a heparin flush after each injection and how to close the catheter to air after administration.

3) Gastric decompression: May be the most important thing you do for the horse. Gastric decompression alone may be enough to relieve pain without use of analgesics. However, the mere presence of a tube placed in the stomach does not guarantee decompression. Use a large bore tube with side and end ports and suction or siphon. It may take up to 10 - 20 minutes to establish flow. If you detect small intestinal distension during rectal examination, taking the time to establish flow will be well spent. Leave the tube in place during transport! Gastric rupture is fatal and failing to take this simple precaution may be a fatal mistake for the horse.

4) Cardiovascular support: Reestablishing an adequate circulating volume is not only important for survival during transportation but is important for survival during anesthesia. Prognosis is inversely proportional to the PCV. The most common acid-base picture is metabolic acidosis with normal to low electrolyte values. Lactated Ringers is generally a good choice. Fluids must be infused rapidly to expedite referral, and restoration of fluid volume alone does much to alleviate acidosis. If necessary, a fluid jug can be hung in the trailer. This only advisable if the owners are capable of managing complications that may arise with the fluid line or catheter and if the trip will take more than 2 hours.

Fluids are the mainstay of CV support. Nonsteroidal antiinflammatories will inhibit vasoactive products of ischemic bowel and can clinically improve CV parameters and relieve pain. They also are effective in relieving clinical signs of colic without affecting the primary problem, resulting in delay of the decision for surgery. Be sure you write down your findings and treatment and tell the client to give these notes to the referral center staff. Your client may not remember what you told them, no matter how many times you tell them!!

Client preparation: Communication is the key!! The client should understand the reasons for referral and what can be reasonable expected from the referral process. The decision is the clients, but based upon your assessment and recommendations. This decision is usually if not always made under stressful conditions. Let your client know what he should expect.

The cost: Surgical management of colic requires lab support, general anesthesia, a full surgical team, and facilities for intensive monitoring and postoperative care. Preoperative stabilization may require iv fluids, analgesic, NSAIDS, antibiotics, and other medication. Shortcuts rarely save money and will likely hinder the outcome. Initial management of even an uncomplicated case requires a significant financial commitment by the client.

The minimum cost for an uncomplicated nonstrangulating obstruction which does not require enterotomy or resection and anastomosis, hospitalization for 3 - 5 days typically may cost $1,500 - 2,500.00, depending on the cost of materials and care at a specific referral center. Obviously, more complicated cases require more intensive care and prolonged therapy, which results in higher costs.

Inform your client about the complications. Enteritis, laminitis, and incisional dehiscence occur in some cases, regardless of the precautions taken. Again should any of these occur they will only add to the expense.

The prognosis: Dependent upon three things;

1) The lesion.

2) The treatment.

3) The complications.

Small intestinal lesions generally have a poorer prognosis than large intestinal lesions, and they also have more complications. The speed and efficacy of the therapy strongly influences the morbidity and mortality caused by the primary abdominal lesion, as well as the frequency and severity of complications. Commonly recognized complications include, laminitis, peritonitis, endotoxemia/septicemia, intraperitoneal adhesions with recurrent colic, and incisional dehiscence, infection, and herniation.

Give your client a general education as to the problems which may be encountered. They should also be made aware that a high percentage of animals with certain types of surgical colic recover from surgery and are able to resume their previous activities.

The insured horse. Have your client try to contact the insurance company. It is not your responsibility, but it may be helpful if you do it. It is best to contact them before general anesthesia is induced. This ensures compensation should the horse die during anesthesia.

Your client should expect the animal to receive another physical examination before anything is done. This helps in further identifying any additional changes which may have occurred since your examination. In some cases , initial examination may demonstrate a lesion that has such a grave prognosis that further therapy is futile. Sometimes, a noncorrectable lesion may not become apparent until the surgery is in progress.

Management of surgical colic is expensive. Ofttimes the decision is made in the heat of the moment and without consideration of the financial responsibility. Most referral centers require a deposit. Informing the client that a deposit will be required may help prepare the client for the investment, the request for deposit, and remind him to bring his checkbook.

Signs of Colic in the Horse

Pawing Sweating Looking at the abdomen

Kicking w/ back legs Kicking the abdomen Rolling

Getting up and down Bruxism Abrasions of head/points

Depression Anxiety Yawning

Phlegmon reaction Dyspnea (blowing) Dirt on the back

Distended abdomen Stranguria Tenesmus

Treading back legs Playing in water bucket Biting the flank

Groaning/grunting

Stall is messed up (as if the horse has been stall walking)/restlessness

Suddenly dropping to the ground (throw themselves down)

Laxatives (full-sized horses)

Mineral oil

2-4 liters with 2-4 liters warm water

If impaction firm, mineral oil will move around the impaction and not penetrate it.

Dioctyl sodium sulfosuccinate

Anionic surfactant that carries water and fat into intestinal contents. More effective than mineral oil in softening and promoting passage of colonic impactions. 10-20 mg/kg in 1-2 liters warm water. Do not administer with mineral oil (oil embolism). Do not administer if horse appears to have any clinical signs of toxemia. It will worsen the condition and put the horse into septic shock.

Magnesium or Sodium sulfate

Saline cathartic, retains water osmotically in the intestinal lumen. 0.5 mg/kg in 2-4 liters warm water. Usually about 1 pound/450 kg. May induce diarrhea (transient).

Psyllium

Used primarily to treat sand impactions. 2 cups in 8 liters of water. Forms a gelatinous mass with water that physically pushes intraluminal contents distally. May be used prophylactically.