The Modern Equine Vet March 2018

The Modern

Equine Vet www.modernequinevet.com

The NittyGritty of Equine Gastric Ulcers Hindlimb Muscle Patterns in Shivers SAA: A Better Way to Monitor Illness?

Technician Update: Nursing Trauma-Induced Injury

Vol 8 Issue 3 2018

TABLE OF CONTENTS

COVER STORY

Nitty-Gritty of

4 Equine Gastric Ulcers Cover photo: michelangeloop/Shutterstock.com

INFECTIOUS DISEASE

Serum Amyloid A Early Indicator of Equine Illness...........................................................12 TECHNICIAN UPDATE

Nursing Trauma-Induced Injury...........................................................14 NEWS

Hindlimb Muscle Patterns Different in Horses with Shivers...... 3 Fair Chance of Returning to Work for Horses with Cranial Nuchal Bursitis...................................................................21

ADVERTISERS Vetquionol..................................................................... 5 Merck Animal Health.................................................. 7

AAEVT............................................................................15

The Modern

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NEWS NOTES

Hindlimb Muscle Patterns Different in Shivers

Courtesy of Equine Veterinary Journal

Abnormal muscle recruitment uncontrolled co-contraction of patterns in the hindlimbs of flexor and extensor muscles in horses with shivers are due to horses with shivers. excessive activation and a loss “In control horses, backof temporal modulation, acward walking resembled cording to researchers at the for­ ward walking (right University of Minnesota. hindlimb peak EMG: backJoshua E. Aman, PhD, of ward: 47.5 ± 21.9%, forward: the Department of Neurology 36.9 ± 15.7%) but displayed at the University of Minnesosignificantly higher amplita and his colleagues aimed to tudes during trotting (76.1 ± characterize hindlimb muscle 3.4%). However, in shivering horses, backward walking activity in horses with shiverwas significantly different ing. They also wanted to idenfrom forward (backward: tify whether degeneration 88.5 ± 21.5%, forward: 49.2 of distal Purkinje cell axons ± 8.9%), and resembled acin the lateral deep cerebellar tivity during trotting (81.4 nuclei (DCN) correlated with ± 4.8%),” the researchers the locomotor abnormalities wrote. seen in this illness.

The horses were also scored Seven draught horses with based on the degree of any loshivers and six normal controls comotion abnormalities preswere included in the study. For ent. Six horses with shivers each horse, the researchers were subsequently euthanized monitored the recruitment acand underwent postmortem tivity of four hindlimb muscles examination with calbindin (biceps femoris, vastus lateimmunohistochemistry being ralis, tensor fasciae latae and performed on the brain tissue. extensor digitorum longus) During this examination, the using surface electromyoresearchers identified axonal graphic (sEMG). The animals degeneration in the Purkinje were asked to perform variThe researchers monitored the recruitment activity of four hindlimb muscles using surface electromyography. cells in the DCN, confirming ous movements such as lifting this relationship. and flexing the hindlimb and Shivering is characterized by abnormally elevated walking backward while being monitored. muscle recruitment particularly in BF and VL musLoss of Temporal Modulation cles during backward walking and associated with The researchers found a marked difference in the muscle selective Purkinje cell distal axonal degeneration the recruitment activity of shivering horses compared with researchers wrote. the controls. The horses with shivers exhibited sustained, The study did have limitations, the researchers admitelevated levels of muscle activation and a loss of tempoted, because they focused specifically on the DCN. There ral modulation—occurring throughout the stride but could be additional lesions that might influence the abparticularly when walking backward. This results in an normal sEMG findings in horses with shivers.

MeV

For more information: Aman JE, Valberg SJ, Elangovan N, et al. Abnormal locomotor muscle recruitment activity is present in horses with shivering and Purkinje cell distal axonopathy. Equine Vet J 2018 Feb 12. (Epub ahead of print). http://onlinelibrary.wiley.com/doi/10.1111/evj.12813/full

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Nitty-Gritty of

Equine Gastric Ulcers FACING THE FACTS AND SEEKING SOLUTIONS Up to 90% of performance

of the Equine Health Studies Program at Louisiana State University.

“We know that acid secretion is the triggering device, but beyond that, there’s a widely diverse group of risk factors with no single factor isolated as causing the problem. It’s no wonder that we continue to seek ways to tackle equine gastric ulcer

horses and up to 50% of all foals develop ulcers and—even with successful treatment—the odds are that the ulcers will recur, sometimes repeatedly, according to Frank M. Andrews, DVM, MS, DACVIM-LAIM, LVMA Equine Committee professor and director

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syndrome [EGUS],” he said.

“We have only one US FDAapproved drug for ulcer treatment in horses,” he said, “but that drug [omeprazole] has proven efficacy.

The trick in creating the best ulcer program for each individual horse is to effectively implement drug treatment and preventive manage-

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Photos courtesy of Frank M. Andrews, DVM, MS, DACVIMLAIM, LVMA

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Figure 1. Ulcer circle of life.

ment measures while also considering the emerging role of nutritional supplements,” Dr. Andrews said at the recent Northeast Association of Equine Practitioners annual meeting in Norfolk, Va.

Back-to-Basics

“It’s important when designing ther­ apy to know how horses secrete acid,” Dr. Andrews stressed. Horses have a smaller stomach, compared with other species, so they are unable to consume large amounts of food.

Grazing allows them to eat frequent small portions over extended periods and produce gastric acid throughout the day without a cumulative effect.

“This differs from you and I,” Dr. Andrews explained. “After we eat, gastric acid [secretion] is stimulated by the presence of food. But in-between meals, there is very little acid secretion in people. In contrast, horses continuously secrete the entire day, even without 6

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the presence of food.”

Horses can produce up to 9 gallons of acid a day, which is neutralized when they are allowed to continuously graze. Most horses are not allowed to graze continuously.

“Frequently, we feed horses only twice-a-day based on our schedule,” he said, “which prevents their stomach from neutralizing the acid produced throughout the day.”

In addition, some of the diets fed twice daily contain high-grain feed that in turn produce volatile fatty acids, which also are known to contribute to ulcer development.

“Studies have shown that horses turned out to pasture with access to roughage have fewer ulcers than do horses confined to stalls and receiving twice-daily feedings,” Dr. Andrews said.

“We also know [from studies] that the pH level of fasting horses is very low, while the pH level in fed horses is very high. This

[higher pH] is what we want,” he stressed, “and we use a pH of 4.0 as the cut-off indicator of damage to non­glandular mucosa.” Of note, doctors likewise keep the pH level above 4.0 throughout the day to heal the esophagus in patients with esophageal reflux disease (GERD).

Up to 80% of ulcers are found in the upper nonglandular region comprised of squamous mucosa.

“This region is predisposed to acid injury, mostly because it doesn’t have the protective and buffering capabilities found in the lower glandular region,” Dr. Andrews explained. The lower region has extensive protective mechanisms, so ulcers are less common and typically heal faster, although there are recent reports of resistance to glandular treatments now, too.

In addition to steady acid secretion, grazing time and high-grain diets, other major risk factors include: • Environmental stress, such as

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Photos courtesy of Frank M. Andrews, DVM, MS, DACVIM-LAIM, LVMA

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D Figure 2. Endoscopy of the nonglandular region showing healthy mucosa (A) and nonglandular ulcers (B). Endoscopy of the glandular region showing healthy (C) and ulcerated pylorus (D).

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travel to a performance or race event, stall confinement, lack of water consumption, change of diet and intensive training • Physical stress, intensive exercise and training, tack changes and shoeing changes which can lead to behavior/attitude changes (especially with overtraining) and poor performance • Medical issues, including pain, musculoskeletal disorders and treatment with nonsteroidal anti inflammatory drugs (NSAIDs).

Ulcer formation associated with NSAIDs typically affects the glandular region, as these drugs can affect the natural protective mucus barrier present in that region.

“Some [colleagues] say that every horse in its lifetime will have an ulcer,” Dr. Andrews said, “What we do know is that the prevalence of equine ulcers ranges from 50% to 90%, depending on the population surveyed and type of athletic activity.” Interestingly, he noted, only 11% of polo horses on a Connecticut farm developed ulcers, possibly because they never really left the farm and were not subjected to the stress, rigors and stress associated with travel.

Thoroughbred racehorses have the highest frequency (80%–90%) of ulcers, followed by endurance horses (70%) and show horses (60%). In foals, an estimated 25% to 50% are susceptible to developing gastric ulcers, with a small percentage of foals developing perforating ulcers, Dr. Andrews said.

“We have seen some with severe ulcers after birth, which might be due to the gastric mucosa not being fully developed at birth.

Clinical signs are vague and nonspecific. “In one study of Thoroughbred horses in race training, gastric ulcers were associated with poor performance, poor or dull hair coat, picky eating habits and colic. In another study involving horses in poor

health, gastric ulcers were found in 88% to 92% of horses showing clinical signs, compared with 37% to 52% of horses with no signs,” Dr. Andrews said, adding that the severity of ulcers may be correlated to the severity of signs.

“Many foals do not show clinical signs until after EGUS becomes widespread or severe,” he explained. “In addition, complications are more frequent and severe in foals, including perforation, reflux and esophagitis.” More often in foals, pyloric stricture can precipitate delayed gastric emptying, he added, which can also be seen rarely in adult horses.

Diagnostics: What We Know Today

Ulcers mimic other diseases, so no laboratory test result can confirm ulcer disease as a diagnosis. The only definitive diagnostic is gastric endoscopy, according to Dr. Andrews, noting that a 2-meter endoscope is needed to visualize the nonglandular mucosa and margo plicatus, while visualization of the glandular pylorus and proximal duodenum requires a 2.5- to 3-meter endoscope in most adult horses.

Patient preparation is important, he stressed, and includes withholding feed from the horse for at least 12 hours, with no access to hay.

“Strip the stall of bedding the evening before gastroscopy and make sure the trailer is clean of all feed before shipping the horse to a clinic for examination. If possible, put a muzzle on the horse while in the stall to prevent it from eating manure,” he added. Water can also be withheld but, in most cases, is not necessary.

Slight sedation with a short-acting tranquilizer may help minimize stress during gastroscopy.

“Once the visual examination is done, ulcers should be scored for severity, which helps practitioners monitor healing and evaluate the efficacy of treatment,” Dr. Andrews explained, noting that

he follows a scoring system developed by the EGUS Council.

Although gastroscopy is minimally invasive and relatively easy to perform, there are drawbacks, including client cost and limited availability, especially in predominantly rural states. “If ulcers are strongly suspected but scoping the horse is cost prohibitive or geographically impractical, consider empirical treatment with omeprazole at a dose of 4 mg/kg for at least 7 days, then observe for resolution of clinical signs.”

If the horse does not respond, referral to a facility with gastroscopy is highly recommended.

Currently there are no hematology or biochemistry markers to diagnose EGUS, but initial evaluation of a sucrose absorption test holds promise, although a later study had mixed results.

Looking for Answers

Treatment should consist of medical therapy and management modi­ fications, Dr. Andrews said, emphasizing the importance of using both interventions to tackle the high rate of ulcer recurrence. Treatment and prevention often rely on initial medical therapy followed by ongoing (lifetime) management intervention.

“If you look at the number of anti-ulcer medications approved for people, you might think a lot of medical options exist for horses.

Not true,” Dr. Andrews said. “A few drugs have been studied, but only one product [omeprazole; GastroGard, Merial] has FDA approval.”

Based on scientific evidence, omeprazole not only reduces gastric acid secretion in adult horses and foals 4 weeks of age or older, it is longer acting and more effective than off-label use of other drug options, including ranitidine. “Although studies support [off-label] ranitidine efficacy, it is less effective than omeprazole and has to be given orally 3 times a day, making owner compliance difficult,” Dr. Andrews said.

Common Signs in Adults & Foals ADULTS • Poor appetite • Dullness • Attitude/behavior changes

• Decreased performance • Reluctance to train • Poor body condition • Poor hair coat

FOALS (Ulcers likely to be severe in foals) • Intermittent colic (after suckling, eating) • Frequent recumbency • Intermittent/interrupted nursing (due to discomfort)

• Weight loss • Excessive recumbency • Low-grade colic • Loose feces

• Diarrhea • Poor appetite • Grinding of teeth • Excess salivation

Scoring Gastric Ulcers GRADE 0 I II III IV

SQUAMOUS MUCOSA The epithelium is intact with no appearance of hyperkeratosis Mucosa is intact but there are areas of hyperkeratosis Small single or multifocal lesions Large single or extensive superficial lesions Extensive lesions with areas of apparent deep ulceration

The Equine Gastric Ulcer Syndrome (EGUS) Council proposed a 0–4 grading system based on size of the ulcer as observed through the endoscope. A small ulcer is one that is less than the diameter of the endoscope; a large ulcer is larger than the diameter of the endoscope.

Adapted from 1999 EGUS Council. Andrews F, Bernard W, Byars D, et al. Recommendation for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine Vet Educ.

1999;11:262-272.

Studies also found that off-label sucralfate really is not effective against nonglandular ulcers either, but its coating effect may be helpful against lesions in the glandular region, Dr. Andrews said. He has used 22 mg/kg of sucralfate 3 to 4 times a day in adult horses with glandular ulcers or inflammatory lesions.

Hands down, the best treatment for existing ulcers is omeprazole, starting at the minimum recommended dose of 4

mg/kg q24h for 28 days.

“Hit them hard and hit them fast,” Dr. Andrews said. “Ulcers heal when patients are on the right dose protocol. If client cost is a factor, consider giving 4 mg/kg for 14 days, then scope the horse to see whether continuation to 28 days is necessary. Using 1 mg/kg as a treatment dose is too low and is not effective, but the preventive dose is 1 mg/kg orally and is sold as nonprescription strength UlcerGard,” notModernEquineVet.com | Issue 3/2018

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Photos courtesy of Frank M. Andrews, DVM, MS, DACVIM-LAIM, LVMA

A

B Figure 3. Gastroscopy findings before and after treatment. Ulceration on diagnosis (A) and ulcer-free mucosa after treatment with GastroGard (B).

ing that the preventive formulation is very useful in curtailing ulcer recurrence associated with stress, such as during transport.

TIP:

Timing is very important during initial treatment, Dr. Andrews explained. “Give the product 45 to 60 minutes before feeding the horse because there is good absorption of GastroGard dur10

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ing fasting; then feed the horse a good alfalfa or grass hay meal that stretches the stomach and stimulates gastric secretion.” Also consider giving the once-a-day treatment in the evening rather than in the morning.

The current thought is that applying the same treatment protocol to all horses is not the way to go. “Start out with the minimum

recommended 4 mg/kg for 28 days, then, as necessary, tailor any additional treatments on an individual basis while implementing your management strategies.”

In general, it may take longer to treat large or more severe ulcers.

If endoscopy is not available, horses should be treated initially for at least 28 days.

Dr. Andrews cautioned against using compounded products. “Compounding is an issue,” he warned, “because we just don’t know if the compounds are truly reliable. So, buyers beware.”

Drug therapy may heal ulcers but once the therapy is discontinued, the ulcers will likely return quickly without management changes. Thus, long-term prevention means constantly modifying management practices that are tailored to the horse.

“What works for one horse won’t necessarily work for all horses that share the same stress level, receive the same feed, graze for the same amount of time and participate in the same events,” Dr. Andrews emphasized. Management intervention is dictated by some of the common risk factors cited earlier.

“First of all is the stress associated with intensive exercise and frequent travel, along with physical stress leading to poor behavior and poor performance. And when you think about the group that has the highest prevalence of ulcers, over 90% are racehorses,” he said. Because of the intense nature of their training program, these horses probably have reduced blood supply to the stomach lining, increased gastric acidity and altered eating behavior, as many are fasted before racing or other athletic activities.

TIP:

Address stress-related factors. If possible, limiting training hours and modifying the number of scheduled events until ulcers have

healed can dramatically improve behavior and performance.

“We know that feeding practices represent a key risk for ulcer development. We also know that stall confinement can lead to gastric ulcers and horses put out to pasture generally have fewer ulcers, depending on pasture quality,” Dr. Andrews said. Feed horses more frequently if possible and provide free-choice foraging.

TIP:

If horses have to be stalled, allow them to see and socialize with other horses. When put out to pasture, try to keep together horses that get along well.

Scientific evidence has also found high-grain diets to be a particular problem. “Grain diets promote a low pH environment and fermentation of grain leads to production of short-chain fatty acids— which predisposes the horse to gastric ulceration. In addition, feeding alfalfa hay or alfalfa hay mixed with grass hay can buffer stomach contents,” Dr. Andrews explained.

TIP:

Feeding alfalfa hay can raise pH levels. Advise clients to provide good-quality hay throughout the

day and night, especially between 11 PM and 4 or 5 AM. Discuss feed changes with clients to ensure that medical conditions are considered before implementing new or revised management practices.

“Lots of dietary supplements on the market boast efficacy in treatment and prevention of equine ulcers. But,” Dr. Andrews stressed, “many products have not been tested in horses and, to date, have little scientific evidence on their efficacy, while other supplements have undergone scientific testing and include ingredients shown to be helpful in ulcer treatment and prevention.” Dr. Andrews, along with colleagues at the LSU Equine Health Studies Program, has been conducting studies on various supplements.

Take-Home Message

“Gastric ulceration is multifactorial,” he said, adding that although nutrition is important, nutritional changes are not a panacea.

Therapy goals should eliminate clinical signs, promote healing, relieve pain, prevent secondary complications and prevent recurrence.

The mainstay of treatment is to suppress gastric acid secretion and increase stomach pH. Because of

Dietary Recommendations • Keep horses eating by providing a minimum of 1–1.5 kg/100 kg body weight of long-stem, high-quality forage free-choice throughout the day and night.

• Feed alfalfa hay or a mixture of alfalfa hay to help buffer stomach acid.

• Feed grain and concentrate sparingly, no more than 0.5 kg/100 kg BW of high-starch grain (eg, sweet feed); do not feed grain meals less than 6 hours apart.

• Feed hypertonic electrolyte pastes after exercise with a grain and hay meal to avoid irritation of the gastric mucosa.

• To control acid irritation, consider preventive doses of omeprazole (UlcerGard) in horses performing highintensity exercise or traveling.

• Nutritional supplementation may be beneficial, especially in maintaining stomach health after drug therapy. Only use supplements that have scientific data backing them up. the high recurrence rate in horses, initial drug therapy should be followed by modifying and implementing well-planned and executed management strategies.

“Although our treatment options are somewhat limited today, I believe the scientific breakthroughs of tomorrow will help forge new and exciting diagnostic and treatment strategies,” he predicted. MeV

For more information: Andrews FM, Reinemeyer CR, McCracken MD, et al. Comparison of endoscopic, necropsy and histology scoring of equine gastric ulcers.

Equine Vet J. 2002;34:4775-478.

Andrews FM, Sifferman RL, Bernard W, et al. Efficacy of omeprazole paste in the treatment and prevention of gastric ulcers in horses.

Equine Vet J. 1999;29(Suppl):81-86.

Camacho-Luna P, Andrews FM. Equine gastric ulcer syndrome. In: Sprayberry KA, Robinson NE, eds. Current Therapy in Equine Medicine, ed 7. St. Louis, MO: Elsevier; 2015:280-284.

Franklin SH, Brazil TJ, Allen KJ. Poor performance associated with equine gastric ulceration syndrome in four Thoroughbred racehorses. Equine Vet Educ. 2008;20:119-124.

Kerbyson NC, Knottenbelt DK, Carslake HB, et al. A comparison between omeprazole and a dietary supplement for the management of squamous ulceration in horses. J Equine Vet Sci. 2016;40:94-101.

Malmkvist J, Poulsen JM, Luthersson N, et al. Behaviour and stress responses in horses with gastric ulceration. Appl Anim Behav Sci. 2012;142:160-167.

Sanz MG, Viljoen A, Saulex MN. Efficacy of a pectin-lecithin complex for treatment and prevention of gastric ulcers in horses. Vet Rec. 2014;175:147-151.

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INFECTIOUS DISEASES

Serum Amyloid A Early Indicator of Equine Illness M a r i e

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Serum amyloid A (SAA) is an earlier indicator of illness than rectal temperature and should be added to the health evaluation of traveling horses, according to Marc Oertly, DVM, at the Swiss Institute of Equine Medicine, Vetsuisse Faculty, the University of Berne, Switzerland.

“SAA is a more reliable, early indicator for illness compared with rectal temperature alone in the traveling horses,” said Dr. Oertly at the 63rd AAEP Annual Convention and Trade Show in San Antonio. SAA starts to increase within six to 12 hours post infection “SAA is an acute-phase protein that increases up to 1,000-fold in response to inflammation,” he said. It peaks in 24 to 48 hours, plateaus and clears quickly after the infection is cleared, so it is also a good way to monitor treatment.

To assess if SAA would be a more reliable indicator of sickness in sport horse after long-distance travel compared with clinical status and measurements such as temperature, Dr. Oertly and his colleagues followed 181 high-level warmblood show jumpers between 8 to 17 years of age during several shows. Not every horse went to every show, but some horses went to more than one show, he explained.

They not only wanted to know if SAA would be a reliable indicator of illness, but also the optimal time for measuring SAA after traveling using a stall-side lateral flow immunoassay test. The assay can measure SAA from whole blood or plasma. The researchers used plasma.

There were 28 stallions, 52 geldings and 42 mares, and they were measured at three different destinations: Miami, Mexico and Shanghai, he said.

Fifty-one horses flew into Miami. As soon as they arrived, they received a clinical health check and an SAA reading. At 24 hours, they had another clinical examination and took another SAA measurement.

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Photos courtesy of ARK at JFK

B y

During the entire time, the horses were under strict quarantine, and the rectal temperature was measured twice a day.

After this, they followed horses with an SAA level >15 µg/mL or who had clinical signs of illness, such as fever. Directly from Miami, the horses were flown to Mexico, where 62 horses received the same protocol as the horses in Miami.

They followed 68 horses from Mexico to Shanghai where they received the same protocol, except that these horses spent a quarantine time of two days in Germany before flying to Shanghai.

brinogen. The clinical assessment was performed by different veterinarians and there were limited diagnostics done on the horses with transport-related illness, he said.

“SAA levels of <34 µg/mL at 24 hours can be confidently used to identify clinically sick horse with a sensitivity of 86.7% and a specificity of 91.9%,” he said. “Rectal temperature had a sensitivity of 3.2% and specificity of 100% at 24 hours.”

In sick horses, SAA was above the threshold of 35 µg/mL 24 to 48 hours prior to the first detectable clinical signs, especially when the

more. If the horse is above 35 µg/ mL, he monitors that horse and tests again in 12 to 24 hours. “I found that most develop respiratory signs, so I might give vitamin supplements and cough syrup and monitor,” he said.

He treats according to clinical signs.

One veterinarian in the audience asked about measuring SAA in inflammatory airway disease, and Dr. Oertly said there are studies looking at that. Anecdotally, he told of one case of a horse that always had an SAA level above 25 µg/mL, never lower, never higher, but it was

Of the 181 horses, 31 developed clinical signs of illness, including coughing, anorexia, nasal discharge, swollen, painful lymph nodes, sweating and distal limb swelling. At 24 hours, only the horses with sweating had an elevated temperature of more than 101.5° F, but all of the horses with clinical signs had elevated SAA values at 24 hours, he said.

“Healthy horses had a significantly lower SAA at 34 hours than the sick horses,” said Dr. Oertly (P<0.000001).

The study had some limitations. The horses were in quarantine, so the blood samples had to be destroyed right away after SAA, preventing further blood parameter testing, such as CBC and fi-

disease process was causing a respiratory infection.

He explained that 10 of the 15 sick horses developed coughing at 24 hours, but had an elevated SAA when they arrived. “Based on the severity of the clinical signs, seven horses in this study were treated with antimicrobials,” he said. These horses had SAA ≥750 µg/mL. In 10 horses, the administration of NSAIDS had no significant affect in reducing SAA levels within 24 hours.

After these findings, he began to develop a protocol that he uses. He tests at arrival. If the horse is clinically health, looking well, drinking and eating, he repeats the test at 24 hours and if the horse is below the threshold, he doesn’t do anything

©ShutterStock/Lucian Milasan

Serum amyloid A is an acute-phase protein that greatly increases when inflammation is present. It can be an early indicator of equine illness. performing poorly. An endoscopy examination found IAD. The horse received nebulizer treatments, its SAA value went back to zero and his performance improved. “So I think there is a correlation,” he said.

“I’m not saying stop measuring temperature or stop doing other diagnostic testing,” he said, but SAA is another tool that veterinarians can use to evaluate the health of performance horses.

“I do a lot of international show jumpers,” he said. “Normally these horses fly in five to six days before the show starts. If I can detect a horse that is sick as early as possible, I still have the time and the possibility to treat the horse so that it can perform at its highest level,” he said.

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TECHNICIAN UPDATE

Nursing Trauma-Induced Injury to Texas A&M for further evaluation.

At arrival, she was in right lateral recumbency and an accurate neurological assessment was complicated by sedation. She was removed from the trailer, via the sled and moved into a padded, neurologic stall with hoist capabilities. The filly was quiet, and alert during the initial physical and neurological assessment. She had normal vital parameters: a rectal temperature of 100.1° F, a heart rate of 32 beats per minute with a normal sinus rhythm and no murmurs auscultated, and a respiratory rate of 16 breathes per minute. No crackles or wheezes were appreciated during resting thoracic auscultation. Her mucous membranes were pink and moist, with a normal capillary refill time of two seconds. Borborygmi was present in all abdominal quadrants, and digital pulses (DPs) were within normal limits. The eyes were bright and clear with no evidence of ulcerations, despite mild debris in the orbit and conjunctiva.

The physical and neurological findings included: normal mentation, behavior and cranial nerves, and all four limbs were extended out rigidly, but could be manipulated. Normal withdrawal reflex of the front limbs was noted with a hemostat, however, absent reflexes bilaterally in the hindlimbs with cold extremities was noted.

She had normal tail tone with decreased anal tone.

Panniculus was present through the cervical region and stopped at the withers (approximately T3). Point-ofcare blood work results revealed a packed cell volume (PCV) of 29%, total protein (TP) of 6.0 g/dL, a blood

All photos courtesy of Stephanie Wertman, LVT

Stephanie L. Wertman, LVT, VTS-EVN A 10-month-old Quarter horse filly weighing approximately 300 kg presented to the Texas A&M Veterinary Teaching Hospital, Equine Internal Medicine Service with the complaint of recumbency and a history of inability to stand for two days.

During a trailer ride two days prior, the filly fell and was caught under the partition, causing trauma to the cranial aspect of her back at the level of the withers when she tried to rise. Once the owners unloaded her, a one-half gram of phenylbutazone paste was administered orally for pain and inflammation.

There were no wounds or outward signs of trauma and the horse appeared to be ambulating normally; however, the next morning the filly was found in left lateral recumbency in the pasture.

The filly was evaluated by the referring veterinarian on the farm and was administered IV dexamethasone.

Throughout that day the filly attempted to rise, but was only able to â&#x20AC;&#x153;dog sit.â&#x20AC;? She maintained normal bright and alert mentation, a good appetite and continued to pass urine and feces normally. The referring veterinarian examined the filly the following day repeating a second dose of dexamethasone and recommended further evaluation. The filly was sedated with detomidine, loaded onto a trailer using a sled and transported

At home after trauma

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Sedated in trailer for transportation, on slide

AAEV T M E M b E r s h i p Membership in the AAEVT is open to all veterinary technicians, assistants, support staff and those employed in the veterinary health care industry worldwide. Student membership is open to those currently enrolled in an AVMA/CVMA accredited veterinary technology program.

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TECHNICIAN UPDATE

Neurology Consult Day 2

Time in Anderson Sling

The filly fell during a trailer ride.

When she tried to rise, she damaged the cranial aspect of her back at the level of the withers.

glucose of 330 mg/dL, and a blood lactate of 2.9 mmol/L; a lithium heparin sample was submitted for a serum chemistry panel. Muscle enzymes were elevated with a creatinine kinase (CK) >16,000 U/L, and AST of 1,401 U/L, values indicating muscle insult most likely from prolonged recumbency. Mild hypocalcemia (11.5 mm/dL) and hyperbilirubinemia (3.2mg/dL) were most likely due to mild anorexia.

Potassium was borderline normal/ high at 4.2 mmol/L, with the rest of the electrolytes being within normal limits.

A 14-gauge, 5 1/2-inch Mila catheter was aseptically placed in the left jugular vein and secured with 20 Ethilon suture on a straight needle. A 5 L bolus of lactated ringer solution (LRS) was initiated.

Both eyes were thoroughly flushed clean of debris and puralube eye ointment was applied topically to each eye. Although the filly had remained quiet, additional sedation (xylazine) was given IV through the catheter for transportation on a cart to the Large Animal Radiology Service.

A full series (lateral) radiographs of the cervical, thoracic and lumbar spine were taken. The radiologist reviewed 24 radiographs and no fractures, luxations or narrowing of disc spaces were appreciated.

A cause for current clinical signs could not be iden16

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tified, and a myelogram was recommended.

A sonogram of the neck and thoracolumbar area revealed no abnormalities. Lower limb bandages were placed on all limbs for protection. The filly was transported back to the stall, allowed to rest quietly and monitored for any attempts to stand on her own.

Dimethyl sulfoxide (DMSO) was administered as a bolus. DMSO may be used for spinal injuries for its free radical scavenger properties. It decreases inflammation by binding with inflammatory byproducts that damage healthy cells and cause more swelling and inflammation.

The owners were given a poor prognosis that the filly would be a performance horse, and guarded for adequate ambulation; treatment was pursued understanding the complications that could arise.

A definitive diagnosis was undetermined; however, a lesion was localized to the thoracolumbar spine (T3-L3). With the known history of trailer trauma, the rule-outs included T3-L3 trauma (based on a normal cranial nerve examination, the normal reflex response in the front limbs, the lack of reflexes in hindlimbs, and the start/stop location of panniculus response), vertebral fracture, and disc herniation.

Other neurologic concerns included trauma to the

Pressure sores around head, knees

Urine scalding, abrasions from sling

cervical region, rabies, West Nile virus, equine protozoal myeloencephalitis, cervical vertebral stenotic myelopathy (Wobbler’s Syndrome), eastern equine encephalitis and western equine encephalitis, equine herpesvirus-1 and neoplasia.

A treatment plan was formulated for the evening to include continuation of IV fluid therapy, puralube eye ointment applied topically to both eyes every 6 hours, manual manipulation to her opposite side every four to six hours and observation overnight.

Medications added included flunixin meglumine, dexamethasone, acepromazine and vitamin E as a free-radical scavenger. She was offered Purina Equine Senior mashes every four hours with mineral oil to aid in the prevention of an impaction, one flake of alfalfa, and water every two hours. Overnight, the filly was noted to dog sit with her hindlimbs stretched in front of her, was unable to rise. She could rotate herself from side to side, readily ate, drank water and urinated and defecated normally.

The following morning, the filly’s condition was stable with normal vitals. Neurological evaluation showed decreased tone to her hindlimbs resulting in increased flexion of the hindlimbs and increased extension of the forelimbs as noted with a Schiff-Scherrington phenomenon; she could dog sit and had improved anal tone as compared with the tone upon arrival.

The filly was assisted to stand with the UC Davis lift several times throughout the day. She was very uncooperative with assistance, and once lifted, was unable to properly place her hindlimbs, keeping them in a flexed position underneath herself with

increased extension of the forelimbs. Multiple clinicians and technicians were required with ropes for manual manipulation of the hindlimbs with minimal manipulation of the forelimbs.

Once up, the filly tolerated the lift/sling process.

She was lifted every four hours, with periods of standing dependent on her tolerance and capability ranging from only a few minutes to an hour. A neurology consult was sought and the neurologist concurred with a suspect lesion between T3-L3.

A myelogram was recommended in seven to 10 days, to allow the current inflammation to subside and to obtain more diagnostic images. Due to decreased urine output—despite adequate hydration and continued fluid therapy—a urinary stallion catheter was aseptically passed with a fair amount of normal colored urine evacuated from the bladder. Fresh grass was picked and added to her diet. The remaining treatment plan was unchanged.

Two days after admittance, the filly was febrile with a rectal temperature of 102.4° F, had a heart rate of 52 bpm, and a respiratory rate of 32 breaths per minute. Her mentation was quieter than on previous occasions with decreased feed intake overnight. All other physical examination parameters were within normal limits. Fluid rate was increased due to her hyporexia overnight. Differentials for fevers included meningitis, aspiration pneumonia, colitis, encephalitis, cystitis and tissue necrosis.

To rule out central nervous system inflammation or infection, a dorsal and lateral recumbent lumbar sacral spinal tap was attempted. Due to positioning ModernEquineVet.com | Issue 3/2018

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TECHNICIAN UPDATE

Post sponge bath; air drying; rewrapping legs; bedding stall

First time off lead shank, seven weeks from admission

The filly's hind end ataxia improved significantly over the next several weeks thanks to multiple medical and rehabilitation efforts.

in the sling, decreased ability to sedate properly and hesitation to completely anesthetize the filly, the tap was unsuccessful; an atlantooccipital tap was not attempted due to concern about anesthesia and lesion localization caudal to AO space. Samples including a nasal swab and EDTA blood samples were sent out for quantitative polymerase chain reaction (qPCR) testing for EHV-1, and a fecal sample was also collected and sent for qPCR Salmonella test.

Minocycline was added due to possible meningitis (for its antibacterial, anti-inflammatory, and neuroprotective properties), and prophylactic omeprazole for gastric ulcers was added as well. A tapering dose of dexamethasone was continued. The use of the Anderson sling was initiated for its long-term value, allowing the filly to stay up for four hours at a time.

Manipulation of the hindlimbs with ropes was still necessary, as the filly moved around the stall.

A complete blood count (CBC) revealed a severe leukopenia with a white blood cell count of 1.8/uL (an absolute neutropenia of 1134/uL and lymphopenic of 630/uL), and heat precipitation fibrinogen of 400 mg/ 18

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dL. The qPCR EHV-1 testing was negative. Although afebrile, the filly continued to have a dull mentation and hyporexia. Mild diarrhea was observed and is the most common differential for fevers, hyporexia and leukopenia/neutropenia in our hospital population.

Mineral oil, steroid and antibiotic therapy were discontinued after the evening treatment.

Manipulations and physical therapy with the sling continued.

On Jan. 29, 2017, the filly remained afebrile (maintained on flunixin meglumine), diarrhea was evident (causing mild rectal prolapse with rectal tearing), and Salmonella qPCR result was positive, confirming colitis. Isolation protocol (boots, gloves, gowns, perimeter, footbath, etc.) was initiated for all personnel entering stall and/or treating this filly.

Physical therapy in the Anderson sling was continued, with improvement in strength and placement of both hind feet, right hind better than left hind, decreased hyperextension of the front limbs, and continued knuckling of the left hind fetlock when not assisted, as well as crossing over in her hindlimbs when turned. Complications related to repeated lifting and prolonged recumbency

Back at home!!

included significant pressure sores and urine scalding. A pressure sore over the left front fetlock was concerning due to its depth. An aseptic arthrocentesis with joint distention using sterile saline was performed with no communication of the wound and the joint. No joint fluid was obtained and amikacin was infused into the joint.

Daily intensive care included cleaning, treating with topical antibiotics, bandage changes, constant repositioning of the filly, changing and adding more padding, repositioning of sling, etc.

A notable change occurred when the filly no longer wanted to lie down when the sling was lowered, learning to rest completely in the sling. She continued to gain strength and mobility within the sling and supporting her own weight (the sling was dropped about 6–8 inches below the abdomen).

The filly’s hind end ataxia was most notable when turning around or with sudden movements; she continued to cross her hindlimbs, lose her balance and fall over with the sling catching her, but continued to show increased strength in her hindlimbs. Due to improved clinical signs and resolution of the diarrhea, a repeat CBC (normal WBC 7.6 uL) was performed. She continued to have low-grade fevers of about 101.5° F. Due to continued low-grade fevers, significant improvement in neurological status, and inherent risk, a myelogram was delayed.

Physical therapy included lowering and rising the sling to encourage flexion and extension (to mimic

standing-up motions), moving the filly around the stall as much as the sling would allow; forward, backward and turning both directions (opening the side doors—without breaking protocol—to the “outside” world and seeing other horses encouraged this activity—food was also a great motivator). The filly’s pressure sores began resolving; the urine scalding required sponge baths, drying, topical SSD and constant changing of the padding and the rear piece of the sling. All medications were discontinued except for flunixin meglumine, vitamin E and omeprazole.

Treatment of the hocks and left front fetlock continued with “silver” impregnated bandages. Edema developed in the hindlimbs and hydrotherapy and sweat wraps or full limb bandages were applied as necessary.

At this point, the filly’s neurologic status plateaued and consults with the neurologist said this was expected at four to six weeks post injury in other species.

Recommendations of continued physical therapy and time were given; the filly continued to stay standing most of the day with periods of rest while in the sling. Four weeks after admittance, the Anderson sling was replaced with the UC Davis sling, followed by moving the filly around the stall. She was noted to be weight-bearing on all limbs, although weaker on the left hindlimb. The sling was then removed and she was manually supported by clinicians and technicians while encouraged to move slowly around the stall. She stood for 90 minutes, eating and drinking, ModernEquineVet.com | Issue 3/2018

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TECHNICIAN UPDATE

Shutterstock/nelelena

Teaching Moments Management of a recumbent or slung horse for an extended time requires exquisite attention to nursing care, monitoring and prevention of potential common complications (eg, aspiration pneumonia, corneal ulcers, cystitis, ileus, impactions, pressure sores and self-trauma) to be successful. I was involved in this case from the moment this filly arrived and was aware of the guarded prognosis. Although she was willful, stubborn, and threw temper tantrums, she was sweet as well. Patience, horsemanship and TLC were required to learn her quirks. This filly could not be forced into anything. This case was aggravating at times but her progression was exciting to watch.

It was a case that took a huge team effort from the senior clinicians, house officers, ICU technicians and veterinary students. Despite not having a definitive diagnosis, her outcome was deemed a success with smiles all around when she was able to walk onto the trailer by herself!

A multitude of nursing skills were necessary on this case: these included unloading her in a recumbent position off the trailer, manually placing the patient from one “slide” onto a second “slide” to transport, placing an IV catheter while in lateral recumbency, maintaining lateral recumbency under sedation (not anesthesia), and positioning/assisting with cervical, thoracic and lumbar spinal radiographs in lateral recumbency. Other skills needed were set-up and administration of IV fluids through a gravity feed fluid line in a recumbent patient (and in a sling), placement of head and tail ropes to assist with initial lifts and positioning and padding of a recumbent but not stationary patient. A working knowledge to set up and safely care for a horse in a sling (duration of one month) was paramount.

It was necessary to reposition this recumbent filly to place both the UC Davis Lift and Anderson Sling to lift and for physical therapy using the electric hoist. Constant adjustment of the sling straps and padding was required, changing of soiled padding and leg wraps, repeated sponge bathing and drying of the filly, and topically treating pressure wounds while in the sling, especially while in “isolation.” Set-up and assistance with the lumbar-sacral tap was needed in both the dorsal “sitting” in sling position and in lateral recumbency, with the filly restrained under light sedation. Blood collection via the cephalic and jugular veins (filly was not good with needles) for serial blood work (PCV, TP, lactate). Serial fecal samples for Salmonella testing, blood and nasal swabs for EHV-1 PCR testing, and hair samples for genetic testing for HYPP (per owner’s request) were collected. Maintaining and removing isolation protocol once serial Salmonella testing was negative was required. An aseptic urinary catheter was placed, and a left front fetlock arthrocentesis was set up and assisted with. Each rotation of veterinary students was retrained every two weeks on her care (quirks, different kinds of rehabilitation, how to get her up, how to give her medications, draw blood, assist with her hand walks, etc.). Above all TLC was foremost!! with normal urination and defecation observed before falling/lying down in right lateral recumbency.

After four weeks of standing in the sling, the filly rested quietly for approximately 12 hours with minimal attempts to stand and was lifted easily the following morning with the UC Davis lift and remained standing most of the day.

Repeat Salmonella qPCR testing (5 negatives samples) released the filly from isolation. For the first time, the filly was walked outside briefly with four “spotters.”

Clinically, the filly’s hind end ataxia improved significantly over the next several weeks; there was improved accuracy of hind feet placement, normal crossing over of her hindlimbs, improved balance, she was able to get up/down on her own, walk up and down curbs, back-up (this remained the most difficult), and circle both ways. Her left hindlimb continued to be weaker than the right, with intermittent hock effusion. The urine scalding and pressure sores 20

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were resolving with daily care, except at the point of hocks (bilaterally). The hocks remained an issue due to the dog sitting positioning of the filly when attempting to rise. These were treated daily and the stall was heavily bedded.

One slight set-back occurred when the filly was vaccinated for WNV + VEWT, Calvenza Flu/Rhino, and Imrab Rabies IM. This resulted in a suspect cellulitis of the LF pastern and fetlock and a rectal temperature of 103.1° F. This was resolved with NSAIDs and a sweat bandage. Although the filly remained ataxic in the hindlimbs, she continued to improve in strength, balance and coordination—eager to walk every day.

The left hind hock continued to be effusive.

Bilateral tarsal radiographs performed on March 22, 2017, showed bilateral osteochondritis dessicans/osteoarthritis (OCD) lesions. This disorder of cartilage and bone development resulting in bone fragment and joint effusion requires surgical inter-

vention. Due to the filly’s current neurologic status, surgery and general anesthesia were not recommended at this time. The filly was maintained on phenylbutazone as necessary.

At the time of discharge in April, the filly’s neurologic status was significantly improved from admission. Definitive diagnosis was never determined, however, spinal trauma with concurrent spinal shock at T3-T4 was suspected due to clinical signs and diagnostics. A myelogram could possibly have further differentiated a cause of clinical signs but due to risks of anesthesia, continued low-grade fevers, inherent risk of the procedure itself (worsening neurologic signs, seizures, recovery) and improvement in clinical signs, this was not pursued. At presentation, the filly was unable to stand, with Schiff-Scherrington phenomenon, loss of motor to the hind limbs, first absent panniculus and decreased anal tone.

At discharge, the filly was walking, trotting, trying to buck, able to turn and walk up/down curbs.

While evidence of ataxia is still present, and backing up continues to be difficult, she can navigate in a stall and ambulate reasonably.

Stall confinement or very small paddock turnout was recommended with continued rehabilitation ex-

ercises for four to six weeks (similar to hospital care); walking three times daily with added small inclines, tight and wide circles, backing up, and possibly walking in a pool with water (swimming is not recommended at this time). It is recommended to have the filly re-evaluated in one to two months to monitor her progress and make further rehabilitation recommendations. MeV

ACKNOWLEDGEMENTS

Thank you to Cristobal Navas de Solis, LV, PhD, DACVIM, Assistant Clinical Professor (LAIM), Texas A & M University, Michelle Coleman, DVM, PhD, DACVIM, Assistant Professor (LAIM), Texas A & M University, & Rodolfo Madrigal, DVM, Texas A & M University.

A very special thank you to Ron & Jan Adams for their dedication and determination to this beautiful little filly.

Thank you for the images and videos provided.

About the authors

Stephanie L. Wertman, LVT, VTS-EVN, is the Equine Internal Medicine, Tech II at Texas A&M Veterinary Medical Teaching Hospital in College Station, Texas.

Fair Chance of Returning to Work for Horses with Cranial Nuchal Bursitis Horses with cranial nuchal bursitis have a fair prognosis for returning to their previous level of work, but recurrence of clinical signs is common, according to a recent study.

This retrospective case series analyzed medical records of horses diagnosed with cranial nuchal bursitis to further characterize associated diagnostic, management and prognostic factors.

Thirty horses met the inclusion criteria, 21 of which were geldings and nine were mares. The most common presenting clinical signs were swelling over the cranial nuchal bursa, pain upon poll palpation, reduced flexion of the neck and abnormal head carriage.

Radiographs were obtained in 27 cases; 22 of which had radiographic abnormalities. All horses underwent ultrasonography, which showed synovial effusion in most cases.

Ten horses were treated with medication only (box rest and NSAIDs or intrabursal injection of corticosteroids), 16 underwent surgery (bursoscopic debridement and lavage) and four underwent surgical treatment following failed medical management.

Of the 24 horses for which there was follow-up information, 10 had recurrence of clinical signs— the most common of which was residual swelling of the poll region.

Horses that underwent surgery after a failed response to medical treatment were more likely to have a recurrence of clinical signs, while horses that underwent surgical treatment only were less likely to have recurrence, according to the researchers.

There was no significant difference between the different treatment groups and the likelihood of return to their previous level of work.

MeV

For more information: Bergren AL, Abuja GA, Bubeck KA, et al. Diagnosis, treatment and outcome of cranial nuchal bursitis in 30 horses. Equine Vet J 2017 Dec. 19 [Epub ahead of print]. http://onlinelibrary.wiley.com/doi/10.1111/evj.12787/full ModernEquineVet.com | Issue 3/2018

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