The Practitioner | Issue 2, 2021

Published by the Florida Association of Equine Practitioners, an Equine-Exclusive Division of the FVMA

Issue 2 • 2021

COLONIC ULCERS: A PAIN IN THE HINDGUT! FRANK M. ANDREWS DVM, MS, DACVIM

REPAIR OF TORN EYELIDS IN HORSES ANN DWYER DVM

FACTS AND MYTHS ABOUT MEDICAL TREATMENT OF COLIC DAVID E. FREEMAN MVB, PhD, DACVS

16 ANNUAL th

PROMOTING EXCELLENCE

SYMPOSIUM OCTOBER 21-24, 2021 NAPLES GRANDE BEACH RESORT NAPLES, FLORIDA

The President's Line Greetings fellow practitioners,

EXECUTIVE COUNCIL

RUTH-ANNE RICHTER

BSc (Hon), DVM, MS FAEP COUNCIL PAST PRESIDENT

rrichter@surgi-carecenter.com

ADAM CAYOT DVM

adamcayot@hotmail.com

SALLY A. L. DENOTTA DVM, PhD

s.denotta@ufl.edu

I hope you are enjoying your summer. This is a good time to recover from spring and spend time outside with friends and family.

The long days and warm weather are great for water activities, so get outside and enjoy this beautiful state we call home!

Our 2021 Promoting Excellence Symposium (PES) in October has an excellent lineup of speakers. We're looking forward to welcoming you all back and so excited to get back to hands-on learning. It will be a meeting you won’t want to miss! Naples is also a beautiful area so it's an excellent opportunity to make an event out of it and bring family or friends. Keep an eye on your inbox for more information on this conference!

If you can’t attend the Naples meeting, the 2022 Ocala Equine Conference (OEC) January 20-23, 2022, is a wonderful second chance to get great continuing education. We'll have more updates on this conference soon!

I look forward to seeing you at one of these meetings. Enjoy your summer, appreciate your career and feel fortunate to be caring for such incredible animals.

To get the latest updates on conferences and your equine community, be sure to follow @thefaep on Facebook!

COREY MILLER DVM, MS, DACT

cmiller@emcocala.com

ANNE L. MORETTA VMD, MS, CVSMT, CVA

maroche1@aol.com

Armon Blair, DVM FAEP Council President

A NOTE FROM YOUR FVMA TEAM: If you are not a current FAEP member,

please know you will no longer be receiving this publication in print after this issue. Please contact the FVMA/FAEP at 800-992-3862 for more information.

JACQUELINE S. SHELLOW

If anyone is struggling with mental wellness, please do not hesitate to reach out to colleagues, friends, or the FAEP (call 800.992.3862).

jackie@shellow.com

We are launching a brand new Membership Assistance Program (MAP), which is free for all members. MAP offers personal and professional consultation to help you be your best. For more information, email info@fvma.org

DVM, MS REPRESENTATIVE TO FVMA EXECUTIVE BOARD

Opinions and statements expressed in The Practitioner reflect the views of the contributors and do not represent the official policy of the Florida Association of Equine Practitioners or the Florida Veterinary Medical Association, unless so stated.

Placement of an advertisement does not represent the FAEP’s or FVMA’s endorsement of the product or service.

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2 The Practitioner

Issue 2 • 2021

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COLONIC ULCERS: A Pain in the Hindgut!

FRANK M. ANDREWS | DVM, MS, DACVIM

INTRODUCTION

Ulcers in the equine colon (Right Dorsal Colitis [RDC]) are common in performance horses and lead to decreased performance, vague clinical signs (partial anorexia, rough dull hair coat, intermittent mild colic, and intermittent diarrhea), changes in clinical pathologic data (hyperproteinemia, hyperfibrinogenemia, and an inflammatory leukogram), and may go undiagnosed for months.1 All ages and breeds of horses are susceptible to colonic ulcers and the condition might occur less frequently than gastric ulcers. In a necropsy study of 545 horses, 44% of non-performance horses and 65% of performance horses had colonic ulcers.2 Current therapeutic strategies focus on reducing bulk in the diet and providing coating and conditioning agents to promote healing.

Prevention strategies include providing adequate water to prevent dehydration, avoiding abrupt diet changes, and reducing stress and minimizing the use of non-steroidal anti-inflammatory agents (NSAIDs).

PATHOPHYSIOLOGY

Unfortunately, the exact mechanism leading to the formation of colonic ulcers is unknown, but NSAIDs, stress, dehydration, anatomy, and abrupt dietary changes have been implicated. In addition, other predisposing factors include infection (pathogenic bacteria), an immune-mediated response, behavioral traits and genetic factors.2,3 As with the glandular gastric mucosa, colonic ulcers are probably associated to some extent with NSAID administration and/or stress-induced inhibition of prostaglandins.4 Although, the condition has been seen in horses with no history of NSAID administration. Stress alone and/or administration of NSAIDs may inhibit mucosal-protecting prostaglandin E-2 (PGE-2), leading to hypoxic or ischemic mucosal damage and delayed mucosal healing.2 The right dorsal colon appears to be more susceptible to ischemia when compared to the pelvic flexure or the small intestine.5 In addition, in a previous study, there was a significant decrease in transepithelial resistance across the right dorsal colon mucosa following only 1 h of experimental-induced ischemia.

Unfortunately, PGE-2 concentrations in right dorsal colon mucosal biopsies were not decreased compared to controls.6 However, gastrointestinal mucosal damage may occur from mechanisms other than inhibition of PGE-2. For example, evidence exists that gastric mucosal injury from NSAIDs is associated with adherence of neutrophils to the vascular endothelium; activated neutrophils may release oxygen-derived free radicals and other 4 The Practitioner

enzymes that cause mucosal damage.1,7,8 In addition, PG may act synergistically with nitric oxide (NO) to mediate mucosal protective effects.9 Furthermore, phenylbutazone has been shown to decrease leukotriene metabolites (5-LOX) in the right dorsal colon.10 The leukotriene 5-LOX is necessary for the production of the anti-inflammatory compounds known as lipoxins. A reduction in this leukotriene might lead to chronic inflammatory bowel disease with continued protein loss. When this is coupled with dehydration due to trailering and after competition, ischemia in the right dorsal colon might be exacerbated.

Anatomically, the right dorsal colon has a slower transit time and a narrowed lumen, compared to other segments of the large colon.

This allows roughage feed materials and NSAIDs, if administered, to come in direct contact with the mucosal lining for longer periods of time leading to irritation.4 This is the goal of reducing bulk in the diet to decrease irritation and work in digestion.

In addition to the above factors, horses traveling to competition experience varying degrees of abrupt dietary changes (pasture grass vs. baled dry hay/concentrates), which can disrupt gut microbiota (dysbiosis). The normal gut microbiota maintains the integrity of the gut barrier through release of antibacterial molecules (bacteriocins), production of anti-inflammatory shortchain fatty acids (acetic, butyric, and propionic acids), and by activating essential cell receptors for the immune response.11 Dysbiosis might result in activation of the immune response, decrease epithelial permeability and overgrowth of pathogenic bacteria, which might destabilize intestinal homeostasis favoring intestinal and systemic inflammation.11 In addition, alteration in bacterial flora in the hindgut might lead to a reduction in volatile fatty acids (VFAs), end products of bacterial fermentation, specifically butyrate. Butyrate is considered essential for maintaining health in humans and animal models, where it serves as the main energy source for colonocytes, maintains tight junctions between mucosal cells, has immunomodulatory effects and influences local gene expression.11,12 Highest concentrations of Iso-butyrate and N-butyrate were found in the right dorsal colon compared to other regions of the large intestine.13,14 Abrupt dietary changes might decrease butyrate or other VFA concentrations, acetate and propionate, and could contribute or exacerbate inflammation and alter colonic permeability in the right dorsal colon.

Issue 2 • 2021

CLINICAL SIGNS

and albumin in manure as measured by a fecal occult blood test (FOBT; Succeed Fecal Occult Blood Test, Freedom Health, LLC, Aurora, Ohio) was shown to have good positive predictive value (72%) as an ancillary diagnostic test in horses with colonic ulcers.2 A positive test (presence of albumin and hemoglobin) (Figure 1) might provide additional information indicating colonic bleeding, which would support a diagnosis of RDC and colonic ulcers in horses with vague clinical signs. In addition, repeating the FOBT during and after treatment might be helpful to show treatment efficacy.

As mentioned above, the right dorsal colon is susceptible to inflammation and ulceration.

Early in the condition, horses present with non-specific signs of mild intermittent or recurring colic episodes, lethargy, and partial anorexia. However, as the condition worsens clinical signs may include complete anorexia, fever, and intermittent diarrhea. Progression of RDC may lead to dehydration, ventral edema, and weight loss. Horses suspected as having RDC should be evaluated endoscopically because clinical signs might be similar to those associated with gastric ulceration or gastric ulcers might be secondary to the stress of colonic ulcers.1 Differential diagnoses for this condition include Equine Gastric Ulcer Syndrome (EGUS), large colon displacement and/or impaction, infectious causes of diarrhea (Salmonellosis, Potomac Horse Fever, Clostridium), granulomatous enteritis, eosinophilic enterocolitis, and intestinal neoplasia.

Gastroscopic examination of the stomach if negative may help rule-in RDC in horses showing typical clinical signs, especially if there is concurrent hyperproteinemia. Abdominal ultrasonography of the right dorsal colon may show mural thickening (normal < 0.4 cm) (Figure. 2a). The peripheral wall of the right dorsal colon can be scanned percutaneously through intercostals spaces 11 to 15, ventral to the ventral margin of the right lung field.15 With effective treatment, edema in the right dorsal colon wall will decrease or resolve (Figure 2b).

DIAGNOSIS

A presumptive diagnosis of RDC can be made based on history, clinical signs, changes on CBC (mild anemia, toxic changes in PMNs, left shift), hyperfibrinogenemia, hypoalbuminemia, and hypocalcemia, with a normal ionized calcium concentration.

Peritoneal fluid analysis might show a mild increase in WBC count (increased percentage of neutrophils) and increase in total protein concentration. The presence of hemoglobin

Figure 1. Succeed® Equine Fecal Blood Test™ showing positive result (TST) for albumin (A) and hemoglobin (H), denoting hemorrhage from the hindgut (colon) in a horse with colonic edema (on ultrasonographic examination) and right dorsal colitis.

Image courtesy of Dr. Frank Andrews.

Every effort should be made to rule out infectious causes of diarrhea such as, Salmonellosis and Potomac Horse fever (PHF) with diarrhea. Fecal cultures and PHF serology and PCR can be helpful in ruling out these conditions. Horses with Salmonellosis will have signs similar to RDC and these diseases may occur together.

PRINCIPLES OF TREATMENT: ■ Withdraw and/or avoid NSAIDs (especially phenylbutazone) ■ Decrease bulk in diet • Restrict or eliminate hay • Frequent feedings of pelleted diet

■ Coating, supply prostaglandins to repair the colon ■ Implement methods to reduce stress

■ Add supplements containing VFAs, sodium butyrate

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@thefvma | The Practitioner 5

TREATMENT

The use of NSAIDs, especially phenylbutazone, should be discontinued immediately. If pain persists the use of alternative pain medications, such as opioids and/or Alpha-2 agonists, should be used.16 Just as important is decreasing gut fill to allow the colon to rest.

Switching to a pelleted diet and frequent feedings (three to four times per day) will reduce gut fill and decrease irritation. We also recommend eliminating dry hay from the diet and replacing with frequent feeding of alfalfa-based pelleted complete feeds with at least 20 to 30% dietary fiber (Purina® Equine Senior™, Purina

Mills, St. Louis, Missouri). This reduces gut fill and decreases the mechanical load on the colon. The horse can be allowed to graze small amounts of fresh grass (10 to 15 minute intervals four to six times daily) to help maintain body weight. The switch to a complete feed diet should be made over several days to a week to allow the gastrointestinal tract time to acclimatize to the feed change. The complete feed diet should be continued for three to four months or at which time hyperproteinemia and hypoalbuminemia have resolved. In addition, the FOBT (Figure 1) can be used to identify continual bleeding and loss of albumin through the gut wall.

LIVER

RDC

Figure 2. (a) Edema (1.37 cm; yellow box) in the wall of the right dorsal colon in a pony before diet and pharmacologic treatment.

Image courtesy of Dr. Frank Andrews.

Psyllium mucilloid (Equisyl Advantage™, Animal Health Care Products) or psyllium hydrophilic mucilloid (Metamucil®, Proctor & Gamble, Cincinnati, Ohio) can be added to the diet to shorten transit time for ingesta and increase water content of the GI tract. Also, psyllium increases the concentration of shortchain fatty acids in the colon of other species which reduces inflammation and thus may reduce inflammation in the horse colon. Furthermore, corn or safflower oil (one cup, added to feed, q12h) can be added to the complete feed to increase Omega-3 fatty acids. Omega-3 fatty acids competitively inhibit the activity of cyclooxygenase enzyme, which is necessary for eicosanoid production. A diet rich in omega-3 fatty acids may reduce the eicosanoid production, thereby decreasing inflammation.

6 The Practitioner

The use of medication routinely used for gastric ulcers (antacids, omeprazole, or ranitidine) would not be expected to be effective in treatment of RDC. However, sucralfate (22 mg/kg, orally, q6-8h), a sucrose octasulfate, and polyaluminum hydroxide complex, has been used for treatment of RDC. This compound has a strong affinity to bind to gastrointestinal mucosa. It has a greater affinity to bind to ulcer craters when compared to intact epithelial cells. In man, sucralfate is more adherent to duodenal ulcers than gastric ulcers despite the duodenal pH > 4.0. Thus, sucralfate may bind to “ulcer craters” in the colon of horses forming a proteinacous bandage. Furthermore, sucralfate, once bound to the ulcer crater, may stimulate local prostaglandin production, which may exert a “cytoprotective” effect on the colon mucosa.

Issue 2 • 2021

LIVER

RDC

Figure 2. (b) Right dorsal colon in the same pony after two months of dietary and pharmacologic management. Note that the wall of the right dorsal colon is 0.45 cm (yellow box).

Image courtesy of Dr. Frank Andrews.

Misoprostol (2-5 µg/Kg, orally, Q6 to 12h), a synthetic prostaglandin, can be used to improve mucosal blood flow, decrease inflammation and stabilize mucosal integrity. Misoprostol has been shown to decrease lipopolysaccharide-induced tumor necrosis factor alpha secretion in equine leucocytes and may also be useful as a modulator of inflammatory cytokine production.4,17 This drug should not be given to pregnant mares as it could result in spontaneous abortion.

TREATMENT LENGTH

Probably the most concerning issue that faces most clients is “how long do I have to feed my horse the pelleted diet?” This question relates to length of treatment and prognosis of horses with colonic ulcers. The earlier the horse’s condition is diagnosed the better the prognosis and the shorter the treatment period.

Therefore, the main criteria for follow up is below:

LENGTH OF TREATMENT AND PROGNOSIS:

■ Resolving clinical signs

■ Monitor PCV and plasma proteins • Every one-two weeks (more frequent if needed) • Increasing albumin is a good sign ■ Serial ultrasonographic examinations • Every three to four weeks during treatment

■ Treatment and pelleted diet (three to four months)

■ Good to guarded prognosis depending on severity

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@thefvma | The Practitioner 7

PREVENTION Minimizing physiologic and environmental stresses can also be helpful in controlling RDC. Stall rest, reduction of strenuous exercise or training, and reduction in trailering are ways to decrease stress. Horses should always have adequate amounts of clean fresh water and should be provided a mineral/salt mix (added to the diet) to ensure adequate water intake. Water can be flavored or sweetened at home with products like Gatorade or Jell-O packets and then used to flavor water while traveling to increase water intake.

Any dietary changes should be made slowly to provide acclimation of the gut microbiota. We recommend feeding a similar diet that will be fed during traveling and during competition. This might be accomplished by starting to change the diet slowly before traveling so that when the horse reaches its destination the horse is acclimated.

Adding a supplement containing sodium butyrate as well as a prebiotic or probiotic might be helpful to maintain hindgut function and health. It should be emphasized that there is limited data on the effect of supplements on preventing colonic ulcers.

References

1. Cohen N.D. (2002) Right Dorsal Colitis. Equine vet Ed. 14(4), 212-219.

2. Pellegrini F.L. (2005) Results of a large-scale necroscopic study of equine colonic ulcers. J Equine Vet Science 25(3), 113-117.

3. Karcher L.F., Dill S.G., Anderson W.I., King J.M. (1990) Right dorsal colitis. J Vet Intern Med. 4, 247-253.

4. Davis JL. (2017) Nonsteroidal anti-inflammatory drug associated right dorsal colitis in the horse. Eq Vet Educ.

29(2), 104-113.

5. Cook V.L., Cox K.K., Fuller K. and Holcombe S.J. (2013) The effect of lidocaine on recovery of the equine large colon following ischemic injury. Vet Surg. 42, E88.

6. McConnico R.S., Morgan T.W., Williams C.C., Hubert J.D., Moore, R.M. (2008) Pathophysiologic effects of phenylbutazone on the right dorsal colon in horses. Am J Vet Res. 69, 1496-1505.

7. Wallace J.L., McKnight W., Miyasaka M., Tamatani T., Paulson J. 8. Anderson D.C., Granger D.N., Kubes, P. (1993) Role of endothelial adhesion molecules in NSAID-induced gastric mucosal injury. Am. J. Physiol. 265, G993-G998.

9. Wolfe, M.M., Lichtenstein, D.R. and Singh, G. (1999) Gastrointestinal toxicity of nonsteroidal anti-inflammatory drugs. New Engl. J. Med. 340, 1888-1899.adeau JA, et al.

AJVR 2003;64:413–417.

10. Cook, V.L. (2014) The right dorsal colon: why is it different? In Proceedings, International Veterinary Emergency and Critical Care Symposium.

8 The Practitioner

11. Iacob S, Iacob, D.G. (2107) Infectious threats, the intestinal barrier, and its Trojan Horse: Dysbiosis. Fronties in Microbiology. 10, 1-17.

12. Roediger W. E. (1980) Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut 21, 793–798.

13. Dougal K. Harris P.A., Edwards A., Pachebat J.A., Blackmore, T.M., Worgan H.J., Newbold C.J. (2012) A comparison of the microbiome and the metabolome of different regions of the equine hindgut. FEMS Microbiol Ecol. 82, 642-652.

14. Vital M., Gao, J., Rizzo M., Harrison T. Tiedje J.M. (2015) Diet is a major factor governing the fecal butyrateproducing community structure across Mammalia, Aves and Reptilia. The ISME journal. 9(4), 832-843.

15. Jones S.L., Davis J., Rowlingson K. (2003) Ultrasonographic findings in horses with right dorsal colitis: five cases (2000–2001). J Am Vet Med Assoc. 222, 1248-1251.

16. Guedes A. (2017) Pain management in horses. Veterinary Clinics: Equine Practice, 33(1), 181-211.

17. Buchheit T.M. (2014) Effects of the prostaglandin analogue misoprostol on TNF-alpha release by activated equine leukocytes. http://repository.lib.ncsu.edu/ir/ handle/1840.16/9879.

Frank Andrews, DVM, MS, DACVIM Dr. Andrews received his BS in bacteriology and public health and a BS in veterinary science from Washington State University in 1979 and 1983 respectively. He also completed his MS and DVM from Washington State University in 1983. He received a residency certificate in equine medicine and surgery from The Ohio State University in 1987.

Dr. Andrews is LVMA equine committee professor and head of the department of veterinary clinical sciences at Louisiana State University. His research focus is on treatment and prevention of gastric ulcer disease in horses. His research interests include gastric ulcer disease (pathogenesis, treatment, prevention), endocrine diseases (such as pituitary pars intermedia dysfunction and its treatments), neurologic disease (such as equine protozoal myeloencephalitis and the diagnosis, treatment, and prevention of it), and laminitis.

Issue 2 • 2021

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REPAIR OF TORN EYELIDS IN HORSES ANN DWYER | DVM

Equine practices often take calls from owners requesting an emergency visit for repair of a torn eyelid. The owner is usually panicked as the eyelid is found dangling, with bleeding exposed mucosal tissue (Figure 1). Luckily, the prognosis for successful repair is excellent if the injury is promptly attended and carefully repaired.

Figure 2 A,B. The hook at the base of a stable bucket handle is the most common cause of a torn eyelid. When the bucket was new, the metal hook was crimped shut but over time developed a gap wide enough to trap lid tissue. Most eyelid tears could be prevented if all handles were taped closed as shown.

Image courtesy of Dr. Ann Dwyer.

Eyelid repair can be successfully accomplished in the field by any practitioner, as long as they prioritize response time, arrive at the call with the proper tools and supplies, and follow sound wound repair principles.

Wounds that are more than 8-12 hours old undergo swelling that complicates tissue apposition, so eyelid trauma is treated as an urgent emergency and seen as soon as possible. The owner is cautioned against applying any topical “home remedies” and instructed to bring the horse inside.

Figure 1. Torn eyelid injuries are dramatic and alarming, but have an excellent prognosis if repaired promptly and carefully.

Image courtesy of Dr. Ann Dwyer.

Eyelid injuries occur when a horse catches the upper or lower tarsal margin on a fixed object. The stable item most often involved is a water bucket hanging on a stall wall or pasture fence. Water bucket handles are made of round steel that is about 1.5 cm in diameter. The two ends of the handle base are shaped into a “J” that hooks through steel loops embedded on either side of the rubber or plastic bucket. Manufacturers attempt to make bucket handles safe by crimping the blunt steel ends and covering them with rubber or plastic tips. Over time, one or both handle tips may disappear, and the metal hooks tend to spread (Figure 2 A,B). The resultant gap is just wide enough to trap the eyelid margin of a horse rubbing its face. Horses tend to pull back violently, causing the delicate eyelid tissue to rip.

10 The Practitioner

On arrival, the practitioner must rearrange the barn aisle or stall that will serve as the “operating room” to optimize the surgical repair (Figure 3A,B,C,D). Three or four bales of shavings, hay, or straw are stacked and covered with a blanket, creating a table that will support the horse’s mandible just above chest level, as well as provide a stable platform for the surgeon’s elbows. Good lighting is critical; illumination is optimized if the practitioner dons a strap-on LED headlamp and additional light is supplied by either a tripod halogen or LED source, or by an assistant shining a hand-held focal light source on the injured area. Folding tables, tack trunks, or stacked bales are set up to elevate needed drugs, tools, and supplies. A sterile field for surgical tools is created from the inner surface of the drapes that wrap the instrument pack or the paper packaging of surgical gloves.

Issue 2 • 2021

Heavy sedation is required for the delicate repair process. Patient temperament and anticipated duration of the repair dictate effective dose of sedative(s). The following tips are useful: •

Acepromazine administered intravenously at a dose of 0.02-0.05 mg/kg 15 minutes before tissue manipulation will prolong the effects of detomidine sedation

•

Detomidine administered intravenously at a dose of 0.01-0.02 mg/kg is required for sedation that induces the horse to rest its mandible on the table, allow cleaning and administration of regional analgesia as well as surgical repair. If sedation is insufficient, additional dosage is given at half strength.

•

Very fractious horses may require intravenous butorphanol tartrate at a dose of 0.01-0.02 mg/kg in addition to detomidine, but this agent can induce troublesome head tremors.

Regional analgesia follows tissue cleaning; administration of an auriculopalpebral block is given to produce short term akinesia of the upper eyelid, and coupled with a frontal nerve block to desensitize the central portion of the upper eyelid (Figure 4).

These nerve blocks involve injection of mepivacaine or lidocaine through a 25-guage, 5/8 inch needle. The auriculopalpebral block requires 2-3 ml of drug and can be given in one of three sites: (1) where the nerve can be palpated crossing the “dip” of the zygomatic bone just lateral to the supraorbital fossa, (2) over the highest part of the zygomatic arch, or (3) just lateral to the base of the ear. The frontal nerve block requires 1-1.5 ml of drug and is delivered over the depression representing the supraorbital foramen that can be felt in the frontal bone in the superiotemporal region of the orbit. The need for additional local anesthesia of the infratrochlear, zygomatic, and/or lacrimal nerve branches is determined by the location of the traumatized tissue; effective desensitization is achieved by infiltration of a small amount of local anesthetic along the region of the orbital rim that is adjacent to the injured tissue.

Figure 3 A,B,C,D. Proper preparation for field surgery is necessary for a good repair. A. Bales are stacked and covered with a blanket to create a table for head support. After sedation, the horse rests the mandible on the blanket. B. Folding tables are used to hold drugs, supplies, and a sterile instrument field. C. An OPTIVISOR (jeweler’s head loupe) provides helpful magnification. D. Supplemental lighting may include an LED headlamp and/or a tripod construction light.

Image courtesy of Dr. Ann Dwyer.

After sedation, the injured tissue and periocular region is cleansed.

Antiseptics that have soap components, chlorhexidine, or alcohol are never used around the eye; instead the periocular region, injured tissue, and ocular surface are cleaned with a solution of 2-5% povidone iodine. A small amount of povidone iodine is mixed with sterile saline to create a solution that is the color of weak tea, and gently wiped or sprayed onto the injured area and ocular surface though the broken off hub of a needle attached to a syringe. Fortunately, the cornea rarely becomes ulcerated when an eyelid tear occurs, but fluorescein stain is always applied to the cornea to rule out surface trauma; if an ulcer is identified, it is treated accordingly.

Figure 4. An auriculopalpebral nerve block is administered at one of the three sites marked with an orange dot to induce eyelid akinesia. A frontal nerve block is administered over the supraorbital foramen at the site of the green dot to cause desensitization of the upper central eyelid. Additional local anesthetic is injected around the orbital rim near the site of the trauma.

Image courtesy of Dr. Ann Dwyer.

The eyelid tissue has an abundant blood supply which favors excellent healing. However, the tarsal margin and lid stroma must be reconstructed exactly to restore proper function of the lid and maintain a healthy tear film. The surgeon must use appropriate instruments and suture material, take care to debride the damaged tissue minimally, and appose the wound precisely. Box 1 (at the end of this article) lists instruments and supplies used.

Once the horse is adequately sedated and the injury has been cleaned and blocked, repair begins (Figure 5 A,B,C,D,E,F). One assistant, who is positioned on the contralateral side, steadies

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Figure 5 A,B,C,D,E,F. A. Severe tears can be multi-planar. B. Tissue margins have been freshened, but minimal skin was removed. C. A small number of horizontal mattress sutures of 4-0 diameter, Vicryl, or PGS material, were used to appose the subcutaneous layer. D. The skin was then closed with simple interrupted 4-0 sutures. E. The tarsal margin was closed with a figure of eight pattern. Long suture ends were tucked into the loops of adjacent knots to keep them off the cornea. F. Excellent cosmesis and function is evident on the day of suture removal.

Image courtesy of Dr. Ann Dwyer.

the horse’s head which rests on the bale table. The surgeon’s view is illuminated by a headband light as well as available exterior light sources and can be magnified through an inexpensive and rugged jeweler’s head loupe (Optivisor®). The torn eyelid margins are trimmed minimally, using curved Metzenbaum scissors or Stevens tenotomy scissors to remove very thin strips of tissue to expose healthy, bleeding margins. If the injury is multiplanar, the wound border(s) may be slightly revised (extended) to arrange the torn elements for the optimal geometric apposition, but actual removal of tissue must be kept to a minimum. Gripping of the skin with instruments is avoided; instead, the subcutaneous tissue of wound segments requiring manipulation are gently grasped with Bishop Harmon forceps sized with 0.8mm teeth.

The subcutaneous tissue is apposed using horizontal mattress sutures of 4-0 diameter. The suture material should be absorbable, soft, and pliable; Vicryl or PGS are good choices. One author recommends that suture used for eyelid repair be swaged to a P3 reverse cutting needle; this specialized type of needle is widely used in cosmetic surgery (de LINDE HENRIKSEN 2017). The smallest needle holder that is practical in the field situation is used: Derf needle holders are ideal if an assistant is present to cut the suture ends, but good results are also obtained with short (5 ½ inch) Olsen Hegar needle holders. Great care is taken during suture placement to ensure that knots are well buried within the subcutaneous tissue so that no abrasion of the cornea occurs during healing. As eyelid tissue is so well vascularized, only a small number of sutures are placed so as to minimize the 12 The Practitioner

space occupied by suture material. A mental image that aids in judging suture placement is to think of “ties in a quilt” that are spaced at regular intervals: just as the ties keep the quilt stuffing from migrating, the sutures bring the subcutaneous tissue into proximity—but just as the spacing of the quilt ties allow room for the insulation to fluff the quilt, sparse suture placement allows vessels and tissue components to quickly seal and fuse the wound.

It is critical to employ a two-layer closure; a one layer closure can result in the skin functioning as a hinge, with the end result a non-healing, swollen, dysfunctional eyelid (Figure 6).

Skin closure follows apposition of the subcutaneous tissue. Again, suture of 4-0 diameter is used. Many clinicians use nonabsorbable 4-0 nylon suture for the skin layer; the author has used the 4-0 absorbable suture (Vicryl or PGS) deployed for the subcutaneous layer for the skin closure on dozens of cases with good success.

If the subcutaneous layer was carefully reconstructed, the skin margins will line right up without tension or puckering. Some texts advise that the first step in closing the skin layer is to close the tarsal margin with a figure of eight pattern. The rest of the wound distal to the lid margin is then closed with simple interrupted sutures. This author usually closes a portion of the wound away from the tarsal margin with simple interrupted sutures first, leaving the closure of the final centimeter adjacent to, and including, the margin for last.

With either sequence, the figure of eight suture pattern is used to appose the tarsal margin precisely (Figure 6). This suture Issue 2 • 2021

the loops of the adjacent two simple interrupted skin sutures so the tags rest along the skin within the tightened loops. Great care is taken with the entry of the needle into the tarsal plate tissue, aiming to pierce the skin adjacent to the line of dots that mark the Meibomian gland lumens. A helpful mental image is to think of creating a bridge across the lid margin that looks like a tiny staple, with the suture running parallel to and just above the middle of the tarsal edge.

Figure 6. Schematic of eyelid margin closure. The conjunctiva has been apposed with a minimal number of simple interrupted sutures. Small gauge suture (4-0) is passed through the skin in the numeric sequence shown, then carefully tightened. The tarsal margin is bridged by a length of suture that emerges at the level of the meibomian glands. The knot for the pattern is tied between the suture entry (1) and final exit (4) so that the tags are away from the cornea. The tags can then be tucked under the knot of the adjacent skin suture more distal to the eyelid margin.

Image courtesy of Dr. Ann Dwyer.

pattern accomplishes several goals: it bridges the tarsal plate with a span of suture that applies enough tension to align the edges in a straight line, then the suture that crosses over in an X pattern further into the tissue exerts slight outward pressure to keep the margin from inverting, and the knot that secures the suture is tied away from the lid margin, reducing the risk that the suture ends will abrade the cornea. The cut ends of knot suture can be further secured if they are left a little long, and enclosed within

A tetanus toxoid booster is administered if needed, and systemic antibiotics such as trimethoprim sulfa (25 mg/kg P.O., q 12 hours) are prescribed for five-seven days. An intravenous dose of a non- steroidal anti-inflammatory agent is administered at the visit (Flunixin meglumine, 1 mg/kg) and additional oral NSAIDs are prescribed for five-seven days. Whether absorbable or nonabsorbable material was used to close the skin, a suture removal visit is scheduled in 10-14 days. A fly mask is advised to cover the horse’s face for the duration of time that the skin sutures remain in place.

If the steps described in this article are followed exactly, functional results of the eyelid repair will be excellent. The horse will quickly return to normal eyelid cosmesis and the owner will be delighted.

However, if any of the steps listed are skipped or ignored—e.g. if too much tissue is removed, if the suture used for the repair is too large, or if the wound is closed in a single layer or left with a stepped apposition of the tarsal margin—the horse may suffer lifelong debilitating consequences. Adverse outcomes range from eyelids that do not close normally, creating a tear film deficiency and exposure keratitis, to eyelash trichiasis that causes constant pain and recurrent corneal ulcers. Difficult blepharoplastic procedures are indicated for such complications, and they may not succeed in fixing the problem.

FUNCTION

ITEM

NOTES

Tissue debridement

Curved Metzenbaum Scissors and Stevens Tenotomy Scissors

Use smallest instrument to trim least amount possible

Tissue grasping

Bishop Harmon Tissue forceps and Adson Tissue forceps

BH: 0.8 mm teeth is best size for subcutaneous tissue Adson: 1 x 3 teeth

Suture placement

SHORT (5”) Olsen Hegar needle holders or Derf needle holder with small suture scissors

If no assistant, will need Olsen Hegars to cut sutures—use GENTLY

Suture for subcutaneous layer

4-0 Vicryl or PGS

P3 reverse cutting needle is advised

Suture for skin

4-0 Vicryl or PGS or 4-0 Nylon

P3 reverse cutting needle advised

Illumination

LED Headlamp and Finnoff transilluminator or tactical flashlight

Models sold at camping stores or equine dentistry supplier

Magnification

OPTIVISOR: rugged headband loupe

Sold for jewelry repair, 4x or 6x magnification lens

Continued on Page 16 www.faep.net |

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Continued from Page 13 Finally, as gapped bucket handles are the source of most eyelid tears, these injuries are often preventable. Practitioners will do their clients and patients a great service if they point out gapped bucket handles when performing routine farm calls. The remedy is simple and inexpensive: a few twists of duct or electrical tape is all that is needed to cover the gap(s), eliminate the hazard, and save an emergency call!

Recommended Reading

de Linde Henriksen, M. Standing ophthalmic surgery—How to perform standing surgery of the periocular region in the field. In: Proceedings of the American Association of Practitioners, 2017; 63: 139-153.

Dwyer, AE. Ophthalmology in equine ambulatory practice.

In: Vet Clin N Am, Ambulatory Practice, Ramey DR and Baus, MR, eds. 28; 2012: 155-174.

Dwyer, AE. Practical field ophthalmology. In: Equine Ophthalmology, 3rd ed. Gilger BC, ed., 2017: 72-111.

Ann Dwyer, DVM Dr. Ann Dwyer has been an equine practitioner at Genesee Valley Equine Clinic in Scottsville, New York, since completing her DVM at Cornell in 1983. She is an honorar y member of the American College of Veterinary Ophthalmology and has authored many articles and book chapters on equine eye problems. She lectures widely and is active in organized veterinary medicine, having served as president of the American Association of Equine Practitioners in 2013.

Gelatt, KN and Gelatt JP. Veterinary Ophthalmic Surgery.

Elsevier Saunders, 2011

16 The Practitioner

Issue 2 • 2021

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FACTS AND MYTHS ABOUT MEDICAL TREATMENT OF COLIC DAVID E. FREEMAN | MVB, PhD, DACVS

TREATMENT PLAN FOR MEDICAL COLIC

Remove food, allow water. This is extremely important but rarely done. Additional food will only contribute bulk to the impaction and make it more difficult to remove.

Give laxatives and water by nasogastric tube.

Monitor progress.

Give analgesics as indicated, without masking changes.

Repeat laxatives if necessary.

Only allow food when impaction has fully resolved.

Evaluate management, dentition, diet.

ANALGESIA

7. To facilitate transport to a clinic for further treatment.

8. To facilitate administration of IV fluids.

9. To distinguish between medical and surgical types of colic.

Control of pain is crucial in horses with colic (flunixin meglumine and/or xylazine). Pharmacologic control of pain can be supplemented, as indicated, by other procedures, such as decompression of the stomach by nasogastric tube. Although decompression of the colon/cecum by enterocentesis is an option, this is recommended largely for horses with no surgical option, and with full regard for possible complications. Handwalking is used to prevent rolling and associated injury to the horse and others.

Owners will walk horses endlessly because this interrupts the signs of colic and gives them the false sense of security that it is of benefit, when it is really only masking signs of a persistent or worsening problem. All forms of pain control should be interrupted so that progress can be monitored repeatedly and frequently. Persistent pain under any circumstances indicates a need for referral. The goals of pain control are (order of importance varies with each case):

The concern that flunixin meglumine can mask signs of surgical colic is valid, but most veterinarians can recognize clinical deterioration even when the horse responds favorably to this drug. This concern emphasizes the need for close observation of a horse with colic. Although the drug insert once stated that flunixin meglumine could be given IM or IV, the IM route is not recommended because it can cause severe and fatal myositis in the injection site.

1. To provide restraint.

2. To prevent self‑mutilation, injury to personnel, and damage to equipment.

3. To provide brief, pain‑free periods for observation and evaluation of disease progress.

4. To provide pain‑free periods to allow other medication to take effect (e.g. laxatives).

5. To provide humane care.

6. To treat intestinal spasm (if present).

The concern that flunixin meglumine can interfere with mucosal repair and cause endotoxemia in horses after surgery for small intestinal strangulation is the product of in vitro studies. However, this potential adverse effect has not been confirmed in multicenter controlled clinical trials when compared with other NSAIDs with more COX-2 selective profiles (e.g. firocoxib, meloxicam) that do not interfere with mucosal repair in vitro. The in vivo situation is considerably more complex and involves many factors that the

20 The Practitioner

FLUNIXIN MEGLUMINE

Flunixin meglumine (Banamine; 1.1 mg/kg IV (SID or BID)) is a nonsteroidal anti‑inflammatory drug (NSAID) that blocks the production of prostaglandins. Benefits are pain relief, inhibition of endotoxin effects, and improved cardiovascular status.

Issue 2 • 2021

in vitro studies cannot address. Also, in the equine large colon, FM does not inhibit barrier recovery. The one unanswered question is the source of endotoxin after surgery in a horse with strangulating small intestinal diseases, and the focus should be on this.

ALPHA2 AGONISTS AND SEDATIVES

Xylazine (0.2‑1.1 mg/kg IV or IM) is sufficient for most cases and detomidine (5‑20 micrograms/kg IV) might be required for severe pain. Xylazine can be give repeatedly in low doses as needed, because its short duration of effect allows almost continuous assessment of progress.

The ability of xylazine to reduce intestinal blood flow and motility could be of clinical importance in impaction colics. However, xylazine might relieve spasm, which could help with removal of the impaction. Also, the motility effect is short lived.

Butorphanol (Torbugesic, 0.02 to 0.08 mg/kg IV) is usually used with xylazine, but at recommended doses, side effects include inhibition of motility. This effect is short and appears to be siteand dose-dependant. Motility side effects can be minimized by continuous infusion of 23.7 μg/kg/hr, after a loading dose of 17.8 μg/kg.

LAXATIVES Laxatives might need to be given repeatedly. Sometimes reflux through the stomach tube makes it impossible to give laxatives

and can signify another problem or a longstanding impaction (check for gastric reflux before giving any laxative). The horse colon accounts for a greater proportion of its total body weight than does the human colon, and so human doses for laxatives on a body weight basis are underdosing for horses. However, increasing the dose increases toxicity.

MINERAL OIL

Mineral oil (half to one gallon to a 450‑kg horse) is an effective fecal softener. Its presence on the perineum, tail, and hind limbs, usually ≥ 12 hours after administration, indicates that the intestinal tract is partly or completely patent (Figure 1). Mineral oil can pass around some obstructions, such as enteroliths, but without removing any feces.

Mineral oil has been advocated as a cathartic in cases of intoxication. However, its use in cases of blister beetle toxicity may be contraindicated because it can increase the absorption of cantharadin. Careful attention must also always be paid to placement of the nasogastric tube because deposition of mineral oil in the lungs can cause a fatal lipoid pneumonia.

One concern with mineral oil is failure to penetrate an impaction the same way that water does. This can be demonstrated with fecal balls immersed in water or mineral oil in fecal cups overnight (Figure 2). However, this demonstration fails because the oil in the colon does permeate colon contents under the massaging effect of abdominal contractions during breathing and other activities in the live horse. At surgery, oil can be found deep within the impacted mass in the colon. Also, water

Figure 1. Presence of mineral oil on the tail and perineum at ≥ 12 hours after administration indicates that an obstruction of the gastrointestinal tract is incomplete or has resolved. Mineral oil can pass around an enterolith.

Image courtesy of Dr. David Freeman.

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@florida_vma | The Practitioner 21

Figure 2. The nonsense test proposed to demonstrate that water-based solutions can break down a fecal ball and mineral oil cannot. This fails because it is a lifeless system without abdominal movements and motility and assumes that all the water reaches the site of impaction.

Mineral oil can be found at surgery fully penetrated into an impaction, contrary to what this test proposes.

Image courtesy of Dr. David Freeman.

can be absorbed by the small intestine and colon and not reach the impaction in the volume infused, either directly or through secretion, whereas all the oil given will reach the impaction.

Mineral oil can be given to a horse that might go to surgery, despite the earlier concern that it would increase the risk of contamination and peritonitis if the intestine has to be opened.

Current methods for emptying the colon are very effective and clean.

MAGNESIUM SULFATE

Magnesium sulfate is classified as a saline laxative, assumed to increase fecal bulk and water content through an osmotic response to the poorly absorbed magnesium ion. It is given at a dose of 1 mg/kg (1 lb to a 500-kg horse). It reflexly stimulates equine colonic function, possibly through the gastrocolonic reflex, and the osmotic effect on fecal bulk is unlikely. The gastrocolonic reflex is associated with increased colonic motility and defecation. Magnesium sulfate can be given once or twice daily for two‑three days with little risk of a toxic effect. Repeated doses can cause weakness, collapse, and tachycardia from the absorbed magnesium ion, especially if it is administered with DSS (see below). Treatment of toxicosis is diuresis with IV fluids and IV calcium.

DIOCTYL SODIUM SULFOSUCCINATE

DSS is an anionic surfactant that has been classified as a wetting agent, irritant laxative, or fecal softener. It can increase mucosal permeability (increases Mg absorption if given with magnesium sulfate) and cause mucosal damage and inflammation. It should not be infused directly into intestine at surgery because it will induce transmural inflammation and adhesions. In one study 22 The Practitioner

in horses, DSS was ineffective as a laxative and caused mucosal injury at the recommended dose.

PSYLLIUM HYDROPHILIC MUCILLOID

Psyllium hydrophilic mucilloid is a bulk laxative used to remove or prevent a sand impaction at a dose of 1 g/kg or 500 g in six to eight L of water through a nasogastric tube two‑three times daily. It is difficult to administer because it has a tendency to gel.

Feeding psyllium pellets at four times the recommended amount can cause gastric bezoar formation and rupture.

There is conflicting evidence as to efficacy of psyllium on a daily basis to prevent or remove a sand impaction. Of twelve ponies with sand surgically placed in the cecum, six were treated with 1g/kg psyllium and six were untreated. All were euthanized 11 days later with no significant difference in the amount of sand retrieved between the treatment and control groups. More recent work showed that horses given psyllium (0.5 kg q12h) in addition to mineral oil (2L q24h) had increased sand clearance relative to those administered mineral oil alone (51.0% vs 26.1% total sand removal) suggesting that the combination may improve sand clearance. There is some concern that colonic flora will degrade psyllium after chronic exposure, thus decreasing any laxative properties. This has led to the common practice of only feeding psyllium for one week out of every month for sand prevention in endemic areas.

WHEAT BRAN

A bran mash is traditionally regarded as an excellent laxative for horses and could prevent colic. In one study, it was concluded that the laxative qualities of wheat bran may be exaggerated, Issue 2 • 2021

based on the finding that wet and dry bran mashes did not change water content of feces in ponies compared with other diets.

INTRAVENOUS FLUIDS Intravenous fluid therapy is a lifesaving treatment that replaces essential water and electrolytes in horses with diarrhea, colic, shock, hemorrhage, dehydration, “tying up,” kidney failure, and a variety of other diseases. Intravenous fluids are expensive, require an indwelling intravenous catheter with the associated risk of thrombophlebitis, and may be impractical in many settings (Figure 3).

The notion that horses with impactions should be treated with IV fluids in large volumes to drive water into the impaction and soften it has not been consistently validated. Most available evidence indicates that this is highly unlikely with the largest volumes that can be administered, even in a hospital setting. In fact, horses given three times maintenance IV fluids had increased urine production and Na+ loss, which could contribute to electrolyte abnormalities as well as rebound dehydration when fluids are discontinued. Horses with impactions can become dehydrated because of decreased fluid intake, fluid loss into the bowel in response to laxatives, and altered absorption of fluids by the obstructed intestine. IV fluids could be of some benefit to offset this level of dehydration and to prevent water movement out of the intestine to correct dehydration.

Horses with severe colic should not be stabilized at home with IV fluids before being transported to a referral hospital for possible surgery. Firstly, it takes time to administer fluids at the farm and, therefore, delays arrival at the hospital for assessment and treatment. Secondly, some horses can appear to improve after fluid therapy and analgesics, which can create a false sense of recovery.

This only adds to the delay. Thirdly, fluid therapy at home adds to the cost and could put surgery out of the owner’s financial reach.

Fourthly, it often fails to improve the horse’s condition and can create problems through catheter-related complications and fluid overload.

The volume of fluids delivered might be based on overestimates of needs, because water requirements were determined on fed horses. In the fed state, horses need to draw huge volumes of water from the extracellular space to support digestive processes, which are intense in a herbivore of this size. Most horses that require IV fluids are not fed, so findings of a recent study are highly relevant to them. Failure to recognize this could lead to overhydration.

The consequences of overhydration in equine practice are infusion of an excess of Na+ which causes an intense diuresis that can waste Ca++ and K+ in the urine. The resulting hypocalcemia and negative K+ balance can impair recovery. Overhydration can also damage capillaries and cause fluid loss from plasma to the interstitium. This is an area of growing concern because of adverse effects of overhydration on gastrointestinal function.

Figure 3. Fluids IV can be lifesaving in many situations, but cost and consequences of overhydration need to be considered.

Image courtesy of Dr. David Freeman.

ENTERAL FLUIDS Fluids by nasogastric tube are effective means of rehydrating horses with impaction, and may reflexly stimulate colonic secretion and/or motility. One to one and a half gallons BID or TID is recommended if the horse’s stomach has the capacity to hold these volumes. Fluids delivered by nasogastric tube can reach the cecum and large intestine within one-two hours in most normal horses.

Also, intermittent bolus delivery can increase the volume delivered to the colon as it will overwhelm the small intestine’s capacity for absorption. Nasogastric administration may also stimulate the gastrocolic reflex, thus increasing motility.

Enteral fluids are considerably less expensive and easier to prepare than IV fluids because they do not need to be sterile. Enteral fluid therapy is also slightly more forgiving than intravenous fluids.

However, large volumes of plain water or hypotonic solutions may cause marked electrolyte abnormalities including hyponatremia, hypokalemia, and hypocalcemia and a mild hemodilution. Most

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@florida_vma | The Practitioner 23

average size horses can tolerate 6-10L/h of intragastric fluids, although some show signs of discomfort. Many horses treated with enteral fluids for an impaction will develop self-limiting diarrhea due to excretion of fluids as the impaction resolves.

Cecal rupture has been reported, most likely when the cecum is impacted.

A balanced electrolyte solution for enteral therapy containing 5.27g NaCl, 0.37g KCl, and 3.78g NaHCO3 per one liter of water produces a solution with 135 mmol Na/L, 5 mmol K/L, 95 mmol Cl/L and 45 mmol HOC3-/L. In normal horses, a balanced electrolyte solution and sodium sulfate resulted in the best hydration of RDC contents, while sodium sulfate, magnesium sulfate, and balanced electrolyte solution resulted in the most hydrated feces. Sodium sulfate caused hypocalcemia and hypernatremia, while plain water caused hyponatremia. In conclusion, the balanced electrolyte solution is the safest and most effective option with impaction colics.

PROKINETIC DRUGS Prokinetic drugs are usually not needed nor recommended to treat impactions, and are rarely effective for motility disorders in horses. Neostigmine, a cholinesterase inhibitor, stimulates progressive motility in the cecum, large colon, and small colon.

Bethanecol has been used to stimulate motility in horses and seems to be most efficacious in promoting gastric emptying.

LIDOCAINE

Despite the original claim that lidocaine has prokinetic effects, subsequent studies have demonstrated the absence of such an effect and that lidocaine might even delay intestinal transit.

Studies on equine small intestine subjected to ischemia and reperfusion demonstrated a positive response to lidocaine on smooth muscle contractility in vitro; however, this response could only be achieved with higher concentrations of lidocaine than can be safely achieved in plasma. The anti-inflammatory effects of lidocaine, which have been offered to explain its ability to promote motility in inflamed intestine and after colic surgery, have not been demonstrated in equine jejunum and colon after ischemia and manipulation. Based on recent studies, lidocaine appears to be an ineffective prokinetic drug and ineffective anti-inflammatory drug. If it does have a benefit, this might be through its visceral analgesic effects.

References 1. Banse HE, Gilliam LL, House AM, et al. Gastric and enteric phytobezoars caused by ingestion of persimmon in equids.

J Am Vet Med Assoc 2011;239:1110-1116.

2. Bauck AG, Freeman DE, Morton AJ, Groshe A, Graham AS. Effects of a continuous rate infusion of lidocaine on mucosal injury and intramural inflammation after mechanical manipulation of equine jejunum. Vet Surg 2015;44:E42.

3. Bergstrom TC, Sakai RR, Nieto JE. Catastrophic gastric rupture in a horse secondary to psyllium pharmacobezoars.

Can Vet J. 2018;59:249-253.

24 The Practitioner

4. Cohen ND. Right dorsal colitis. Equine Vet Educ 2002;14:212-219.

5. Cruz AM, Li R, Kenney DG, et al. Effects of indwelling nasogastric intubation on gastric emptying of a liquid marker in horses. Am J Vet Res 2006;67:1100-1104.

6. Dabareiner RM, White NA. Large colon impactions in horses: 147 cases (1985-1991). J Am Vet Med Assoc 1995;206:679-685.

7. Freeman DE, Ferrante PL, Palmer JE. Comparison of the effects of intragastric infusions of equal volumes of water, dioctyl sodium sulfosuccinate, and magnesium sulfate on fecal composition and output in clinically normal horses.

Am J Vet Res 1992;53:1347-1353.

8. Freeman DE, Mooney A, Giguere S, Diskant P, Burrow J, Evetts C. Effect of food deprivation on daily water requirements in healthy horses. 11th International Equine Colic Research Symposium, Dublin, Ireland, 2014, p. 30.

9. Hammock PD, Freeman DE, Baker GJ. Failure of psyllium pucilloid to hasten evacuation of sand from the equine large intestine. Vet Surg 1998;27:547-554.

10. Jochle W, Moore JN, Brown J, et al. Comparison of detomidine, butorphanol, flunixin meglumine, and xylazine in clinical cases of colic. Equine Vet J supplement 1989;7:111-116.

11. Lester GD, Merritt AM, Kuck HV, et al. Systemic, renal, and colonic effects of intravenous and enteral rehydration in horses. J Vet Intern Med 2013;27:554-566.

12. Lopes MA, Moura GS, Jose FD. Treatment of large colon impaction with enteral fluid therapy. Proceedings. Am Assoc Equine Pract 1999;45:99–102.

13. Lopes MAF, Walker BL, White NA, et al. Treatments to promote colonic hydration: enteral fluid therapy versus intravenous fluid therapy and magnesium sulphate. Equine Vet J 2002;34:505-509.

14. Lopes MAF, White NA, Donaldson L, et al. Effects of enteral and intravenous fluid therapy, magnesium sulfate, and sodium sulfate on colonic contents and feces in horses.

Am J Vet Res 2004;65:695-704.

15. Monreal L, Navarro M, Armengou L, et al. Enteral fluid therapy in 108 horses with large colon impactions and dorsal displacements. Vet Rec 2010;166:259-263.

16. Peek SF, Semrad SD, Perkins GA. Clostridial myonecrosis in horses (37 cases 1985-2000). Equine Vet J 2003;35:86-92.

17. Sanchez LC, Elfenbein JR, Robertson SA. Effect of acepromazine, butorphanol, or N-butylscopolammonium bromide on visceral and somatic nociception and duodenal motility in conscious horses. Am J Vet Res 2008;69:579-585.

18. Sellon DC, Roberts MC, Blikslager AT, et al. Effects of continuous rate intravenous infusion of butorphanol on physiologic and outcome variables in horses after celiotomy.

J Vet Intern Med 2004;18:555-563.

19. Ziegler AL, Freeman CK, Fogle CA, Burke MJ, Davis JL, Cook VL, Southwood LL, Blikslager AT. Multicentre, blinded, randomised clinical trial comparing the use of flunixin meglumine with firocoxib in horses with small intestinal strangulating obstruction. Equine Vet J. 2019;51:329-335.

Issue 2 • 2021

David E. Freeman, MVB, PhD, DACVS David Freeman graduated from the Veterinary College of Ireland, Dublin, in 1972 and then worked in private practice in Ireland for 10 months. He did an equine internship at New Bolton Center of the University of Pennsylvania in 1974 to 1975 and this was followed by a residency in large animal surgery at New Bolton Center from 1975 to 1977. He was awarded a PhD from the University of Pennsylvania in 1985. From 1981 to 1994, he was an equine surgeon at New Bolton Center, University of Pennsylvania. He became a board certified surgeon in the American College of Veterinary Surgeons in 1989. He joined the faculty at the University of Illinois, College of Veterinary Medicine, in 1994 and became head of equine medicine and surgery in 1998. In 2004, he joined the Department of Large Animal Clinical Sciences at the University of Florida, College of Veterinary Medicine, as professor of equine surgery and associate chief of staff, and subsequently as service chief in large animal surgery. He was also interim department chair in large animal clinical sciences at the University of Florida from 2009 to 2012. He gave the Sir Frederick Hobday Memorial Lecture by invitation to the British Equine Veterinary Association in 2004, and he was recognized by the Federal University of Minas Gerais, Brazil, for “outstanding contributions to the development of equine surgery worldwide” in 2011. He is currently the Martha and Arthur Appleton Endowed Professor in Equine Studies, and director of the Island Whirl Equine Colic Research Laboratory, University of Florida. David’s main area of clinical interest is improving survival after gastrointestinal surgery in horses and reducing postoperative complications and the associated expense.

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Brief Summary of Prescribing Information. ®

(detomidine hydrochloride)

Sedative and Analgesic For Use in Horses Only Sterile Solution 10 mg/mL CAUTION: Federal law restricts this drug to use by or on the order of a licensed veterinarian.

INDICATIONS: Dormosedan® is indicated for use as a sedative and analgesic to facilitate minor surgical and diagnostic procedures in mature horses and yearlings. It has been used successfully for the following: to calm fractious horses, to provide relief from abdominal pain, to facilitate bronchoscopy, bronchoalveolar lavage, nasogastric intubation, nonreproductive rectal palpations, suturing of skin lacerations, and castrations. Additionally, an approved, local infiltration anesthetic is indicated for castration.

CONTRAINDICATIONS: Dormosedan® should not be used in horses with pre-existing AV or SA block, with severe coronary insufficiency, cerebrovascular disease, respiratory disease, or chronic renal failure. Intravenous potentiated sulfonamides should not be used in anesthetized or sedated horses as potentially fatal dysrhythmias may occur.

Information on the possible effects of detomidine hydrochloride in breeding horses is limited to uncontrolled clinical reports; therefore, this drug is not recommended for use in breeding animals.

WARNINGS: Do not use in horses intended for human consumption. Not for human use. Keep out of reach of children.

HUMAN SAFETY INFORMATION: Care should be taken to assure that detomidine hydrochloride is not inadvertently ingested as safety studies have indicated that the drug is well absorbed when administered orally. Standard ocular irritation tests in rabbits using the proposed market formulation have shown detomidine hydrochloride to be nonirritating to eyes. Primary dermal irritation tests in guinea pigs using up to 5 times the proposed market concentration of detomidine hydrochloride on intact and abraded skin have demonstrated that the drug is nonirritating to skin and is apparently poorly absorbed dermally. However, in accordance with prudent clinical procedures, exposure of eyes or skin should be avoided and affected areas should be washed immediately if exposure does occur. As with all injectable drugs causing profound physiological effects, routine precautions should be employed by practitioners when handling and using loaded syringes to prevent accidental self-injection.

PRECAUTIONS: Before administration, careful consideration should be given to administering Dormosedan® to horses approaching or in endotoxic or traumatic shock, to horses with advanced liver or kidney disease, or to horses under stress from extreme heat, cold, fatigue, or high altitude. Protect treated horses from temperature extremes. Some horses, although apparently deeply sedated, may still respond to external stimuli. Routine safety measures should be employed to protect practitioners and handlers. Allowing the horse to stand quietly for 5 minutes before administration and for 10–15 minutes after injection may improve the response to Dormosedan®.

Dormosedan® is a potent α2-agonist, and extreme caution should be exercised in its use with other sedative or analgesic drugs for they may produce additive effects.

When using any analgesic to help alleviate abdominal pain, a complete physical examination and diagnostic work-up are necessary to determine the etiology of the pain.

Food and water should be withheld until the sedative effect of Dormosedan® has worn off.

ADVERSE REACTIONS: Occasional reports of anaphylactic-like reactions have been received, including 1 or more of the following: urticaria, skin plaques, dyspnea, edema of the upper airways, trembling, recumbency, and death. The use of epinephrine should be avoided since epinephrine may potentiate the effects of α2-agonists. Reports of mild adverse reactions have resolved uneventfully without treatment. Severe adverse reactions should be treated symptomatically. As with all α2-agonists, the potential for isolated cases of hypersensitivity exist, including paradoxical response (excitation).

SIDE EFFECTS: Horses treated with Dormosedan® exhibit hypertension.

Bradycardia routinely occurs 1 minute after injection. The relationship between hypertension and bradycardia is consistent with an adaptive baroreceptor response to the increased pressure and inconsistent with a primary drug-induced bradycardia. Piloerection, sweating, salivation, and slight muscle tremors are frequently seen after administration. Partial transient penis prolapse may be seen.

Partial AV and SA blocks may occur with decreased heart and respiratory rates.

Urination typically occurs during recovery at about 45–60 minutes posttreatment, depending on dosage. Incoordination or staggering is usually seen only during the first 3–5 minutes after injection, until animals have secured a firm footing.

Because of continued lowering of the head during sedation, mucus discharges from the nose and, occasionally, edema of the head and face may be seen.

Holding the head in a slightly elevated position generally prevents these effects.

OVERDOSAGE: Detomidine hydrochloride is tolerated in horses at up to 200 mcg/kg of body weight (10 times the low dosage and 5 times the high dosage).

In safety studies in horses, detomidine hydrochloride at 400 mcg/kg of body weight administered daily for 3 consecutive days produced microscopic foci of myocardial necrosis in 1 of 8 horses.

HOW SUPPLIED: Dormosedan® is supplied in 5- and 20-mL multidose vials.

NADA #140-862, Approved by FDA Manufactured by: Distributed by: Zoetis Inc. Kalamazoo, MI 49007 Revised: January 2013 107224US-10A&P Made in Finland

NO TWO DAYS SPENT TREATING EQUINE PATIENTS ARE THE SAME. As the #1 vet-trusted equine sedative1, DORMOSEDAN® (detomidine hydrochloride) gives you predictability you can rely on.

Make the trusted choice1 for consistent results backed by industry-leading support from Zoetis.

Contact your Zoetis representative for more information or visit DORMOSEDAN.com today.

IMPORTANT SAFETY INFORMATION: Do not use DORMOSEDAN STERILE SOLUTION in horses with pre-existing

atrivoentricular (AV) or sinoatrial (SA) block, with severe coronary insufficiency, cerebrovascular disease, respiratory disease or chronic renal failure. Intravenous potentiated sulfonamides should not be used in anesthetized or sedated horses. Careful consideration should be given to horses approaching or in endotoxic or traumatic shock, to horses with advanced liver or kidney disease, or to horses under stress from extreme heat, cold, fatigue, or high altitude. Do not use in horses intended for human consumption. Handle dose syringes with caution to avoid direct exposure to skin, eyes or mouth. See Brief Summary of prescribing information on page [26].

1.

Data on file: 2020 Equine Pain & Sedation Market Research Study.

All trademarks are the property of Zoetis Services LLC or a related company or a licensor unless otherwise noted. Dormosedan is a registered trademark of Orion Corporation distributed by Zoetis Inc. © 2021 Zoetis Services LLC. All rights reserved. GEQ-00748

All trademarks are the property of American Regent, Inc. © 2020, American Regent, Inc. PP-AI-US-0375 02/2020