· Table of Contents Scientific...

Table of ContentsScientific Program. ............................................................................................................... 3Equine Cryptorchidism........................................................................................................ 6Piroplasmosis under control…...? ................................................................................... 12Complications of Castration............................................................................................. 14Equine Penile Conditions .................................................................................................. 19How to do an endoscopic evaluation of the upper respiratory tract inthe resting horse .................................................................................................................. 23Understanding the dynamics of urt obstructions in equine athletes –what lessons can be learned from the highspeed treadmill? .......................................... 28Control of Veterinary Drugs .............................................................................................. 33Standing surgery of the equine paranasal sinses – when and where should we make

holes in horses’ heads? ................................................................................................ 36Angular Limb Deformities................................................................................................. 43The Surgical Management of the Equine Colic Case – General Points ..................... 48Alimentary system colic ..................................................................................................... 56Pathophysiology of Intestinal Obstruction..................................................................... 67Radiolographic views suggested for pre-purchase examination. ............................... 72How to interpret yearling radiographs ............................................................................. 74How to do ultrasound of the normalequine abdomen ................................................... 75 Ultrasonographic pathology of the gastro-intestinal tract of the horse ..................... 78 Recent advances in understanding and preventing founder......................................... 80Equine Dental Disease ....................................................................................................... 88Endoscopy of the upper respiratory tract of young horses:What does it mean in the context of Pre-purchase examinations? ............................. 104 External Hernias in Horses ............................................................................................ 110Miscellaneous topics: Fourth branchial arch defects, epiglottal entrapment,sub-epiglottal cysts and Arytenoid chondropathy ....................................................... 117How to diagnose high suspensory disease ..................................................................... 123How to investigateand treat cardiac dysrhythmias in the horse .................................. 127A logical approach to the evaluation of dysphagia ........................................................ 132How can the treatments currently used for dorsaldisplacement of the soft palate be rationalised? ............................................................ 141Hock Lameness ................................................................................................................. 146

Axim

Private Bag X169Halfway House1685Tel: (011) 886 3558Fax: (011) 314 0141

Bayer (Pty) Ltd

PO Box 143Isando1600Tel: (011) 921-5911Fax: (011) 921-5379

Instavet Import and Export

P O Box 3040North Riding2162Tel: (011) 462 4463/4Fax: (011) 462 4006

Our Trade Exhibitors,Sponsors and Advertisers

Healthtech Laboratories

PO Box 12285Vorna Valley1686Tel: (012) 657 0471Fax: (012) 657 0675

Intervet SA (Pty) Ltd


Merial SA

P O Box 5924Halfway House1685Tel: (011) 315 8001Fax: (011) 805 1469

Midlands VeterinaryWholesalers

Tel: (033) 263-2310Email: [email protected]

OBP

Private Bag X7Onderstepoort0110Tel: (012) 529 9111Fax: (012) 565 6573

Schering-Plough AH


Stride Distributors cc

PO Box 1247Rivonia2128Tel: (011) 803-3553Fax: (011) 803-7490

Smith and Nephew

P O Box 92Pinetown3600Tel: (031) 710 8309Fax: (031) 710 8106

Virbac RSA

Private Bag x115Halfway House1685Tel: (011) 314-5399Fax: (011) 314-5393

3

Proceedings 36th Annual Congress

3

Annual Equine PractitionersGroup Congress 2004 –

Swadini, SA:Scientific Program.

SUNDAY 15 February 2004

17H00: Registration sponsored by SCHERING PLOUGH ANIMAL HEALTH18H30: Welcome Cocktail sponsored by SCHERING PLOUGH ANIMAL HEALTH

MONDAY 16 February 2004

07H30 – 08H00: Late registration

UROGENITAL SESSION Chairman: Vere Allin

08H00 – 08H35: Opening address Prof B Penzhorn08H35 – 08H45: Introduction of speakers J Marais08H45 – 09H30: Cryptorchidism Barrie Edwards09H30 – 09H45: Introduction of Trade Exhibitors Dave Mullins09H45 – 10H00: Piroplasmosis under control…? J Nurton10H00 – 11H00: Castration complications Barrie Edwards11H00 – 11H15: Session speaker Intervet

11H15 – 12H00: Tea SPONSORED BY INTERVET

12H00 – 13H00: Penile conditions Barrie Edwards

13H00 – 14H00: Lunch

UPPER RESPIRATORY TRACT SESSION Chairman: Johan Marais

14H00 – 14H30: How to do an endoscopic evaluation of the upper respiratory tract in the resting horse Patrick Page

14H30 – 15H15: Understanding the dynamics of URT obstructions in equine athletes - what lessons can we learn from the high-speed

treadmill? Geoff Lane

15H15 – 15H45: Tea

4


4

15H45 – 16H30: Management and control of veterinary drugs Rob Sykes16H30 – 17H00: Standing surgery of the equine paranasal sinuses - when and

where should we be making holes in horses’ heads? Geoff Lane17H00 – 18H00: AGM

19H00: Dinner sponsored by MERIAL

TUESDAY 17 February 2004

STUD HEALTH SESSION Chairman: Martin Schulman

07H45 – 08h30: Angular limb deformities Barrie Edwards08H30 – 09H30: Colic Barrie Edwards09H30 – 09H50: Update on treatment of endometritis David Gerber09H50 – 10H05: Session speaker Bayer

10H05 – 10H45: Tea

10H45 – 11H00: Talk to be announced Ceres Vet Hospital11H00 – 11H25: Pre-purchase radiographic views A Carstens11H25 – 11H55: How to interpret yearling radiographs J Marais11H55 – 12H30: Panel discussion on pre-purchase radiographs RG/BE/GL/JM/AC12H30 – 12H50: How to do ultrasound of the normal equine abdomen L Sweers12H50 – 13H10: How to recognise pathology of the equine GIT

ultrasonographically A Carstens

13H10: Lunch

Sports Afternoon!!18H00: Cocktails at the swimming pool - dont miss it! (Sponsored by Bayer)19h00 African Braai in the LAPA (Sponsored by Bayer/OBP)

WEDNESDAY 18 February 2004

CLINICAL SESSION Chairman: Dirk Triegaardt

08H00 – 08H30: How to evaluate and treat cardiac arrhythmias in the horse D Sutton08H30 – 09H30: Practice management – communication styles and skills Katja Bier09H30 – 10H00: Equine perioperative mortalities F Stegman10H00 – 11H00: Dental disease Barrie Edwards11H00 – 11H15: Session speaker Stride

5


5

11H15 – 12H10: Tea

12H10 – 12H25: Session speaker Merial12H25 – 13H15: Endoscopy of the URT as an adjunct to pre-purchase

examinations Geoff Lane

13H15: Lunch

GALA DINNER SESSION Chairman: Allan Bechard

14H00 – 15H00: Hernias Barrie Edwards15H00 – 15H45: Miscellaneous topics Geoff Lane

15H45 – 16H15: Tea

16H15 – 16H45: How to diagnose high suspensory disease I Cilliers16H45 – 17H00: Serological Response of Ponies Experimentally Infected

with Equine Encephalosis Virus Anne Pardini

19H00: Robin Rous Dinner sponsored by VIRBAC (Dress: FORMAL)Guest speaker Brian Jones.Wine sponsored by Midlands Veterinary Wholesalers

THURSDAY 19 February 2004

FINAL SESSION Chairman: Martin Schulman

08H00 – 08H30: A Study of 100 cases of oesophageal obstruction in the horse G Duncanson08H30 – 09H00: Recent advances in understanding and preventing founder James Rowe09H00 – 09H45: A logical approach to the evaluation of the dysphagic horse. Geoff Lane09H45 – 10H30: How can the treatments currently on offer for dorsal

displacement of the soft palate be rationalised? Geoff Lane10H30 – 11H30: Diagnostic Imaging Quiz AC/LS

11H30 – 12H00: Tea

12H00 – 13H00: Hock problems Barrie Edwards

13H00: Lunch

6


6

Definition of a cryptorchid: -failure of one or both testes to fully descend to oc-cupy their normal position in the scrotum. A horseis either a unilateral or bilateral cryptorchid.

Monorchid –a horse in which only one testis has ever devel-oped. This is a very rare occurrence. The threecases I have encountered have all been shires.

Anorchid –a horse in which neither testes has developed. Thisis even more rare.

The testes normally descend into the scrotum atabout birth (1 week prior to birth to 1 week after-wards).

The testis develops caudal to the kidney and in-creases greatly in size during the 4th – 9th month ofgestation during which time the mare’s circulatingoestrogen level is high. It subsequently undergoesa rapid reduction in size between 9th and 11t h

months prior to descent. The gubernaculum is at-tached proximally at the junction of the tail of theepididymis and vas deferens and distally in the sub-cutaneous tissue of what will be the scrotum. Priorto testicular descent it shortens significantly andincreases in diameter thereby dilating the deep in-guinal ring. As it contracts further, the tail of theepididymis is drawn in to the inguinal canal fol-lowed in normal horses by the testis. The exactcause for failure of one or both testes to descendnormally is not known.

The incidence of cryptorchidism varies betweenbreeds and there is believed to be a hereditary pre-disposition. Approximately 85% of all cryptorchidsare unilateral. When both tests are retained theyare in the same location, i.e. inguinal canal or ab-dominal cavity.Cryptorchids can be classified aseither inguinal or abdominal. The relative inci-dence is approximately 50:50. If the left testis isretained there is a 2:1 chance it is in the abdomen.A retained right testis has a 3:1 chance of being inthe inguinal canal.

Inguinal and abdominal cryptorchidscan be further subdivided: -

Inguinal Retention

It was customary to subdivide inguinal cryptorchidsinto high and low retention but subsequent studiesby Cox et al in the 1970’s concluded that separa-tion into temporary and permanent retention wasmore accurate. In cases of temporary inguinal re-tention, the testis may descend spontaneously fromits inguinal position into the scrotum at any timeduring the first 4 years of life. This occurs irre-spective of what happens to the fully descendedtestis. This type of retention is seen in ponies, butnot all pony cryptorchids fall into this category.

Abdominal Retention

Abdominal cryptorchids are classified as havingpartial or complete retention. In partial abdomi-nal retention, only the tail of the epididymis andpart of the body and vas deferens pass through thedeep inguinal ring to occupy a small vaginal sachigh up in the inguinal canal. This is made pos-sible by the long proper ligament of the testis. Thetestis itself, of necessity, is located close to the deepinguinal ring. In complete retention, the whole ofthe testis and the epididymis are retained withinthe abdomen. In these cases exploration of the in-guinal canal may reveal a small processus vaginaliscontaining only the remains of the gubernaculum or

EquineCryptorchidism

Barry EdwardsUniversity of Liverpool

7


7

the processus may be totally invaginated into theabdomen.

Diagnosis of Cryptorchidism

Cryptorchids may be presented as: -

(a)A young, 1 or 2 year old animal with a knownhistory that no attempt has been made to castrateit. Therefore what is visible and palpable withinthe scrotum is a true reflection of whether or nothe is a cryptorchid.

(b)A horse of unknown history in which only onetestis is present in the scrotum. He could be aunilateral cryptorchid, or a temporary inguinalcryptorchid where the descended testis has beenremoved and the previously retained testis hasdescended.

(c)A horse of any age with no known history re-garding castration, who has nothing palpable inthe scrotum, but whose behaviour has suggestedit could be a cryptorchid.

Behaviour of a CryptorchidCryptorchid horses often show exaggerated malebehaviour. They are noisy. They ‘squeal’ particu-larly in the presence of other horses and are diffi-cult to handle. They will mount other horses at theslightest opportunity.

Examination- Restraint.- Sedate.- Restrain with its offside against the wall. Stand

at its shoulder and grip the mane at the witheswith your left hand.

- Introduce your right hand to the scrotal regionhaving run it progressively and firmly down itsflank.

- Should the horse move, maintain your grip onits withers. In this way you won’t loose con-tract with the horse and find yourself be hind its

hind feet.

(a)If no testes are palpable in the scrotum, the ani-mal is a bilateral cryptorchid. When one testishas descended, which one can be determined bypalpating the cord and identifying which side ofthe penis it passes.

Now palpate the inguinal canal on the side thetestis is missing from the scrotum. Introducefingers in a spatula fashion feeling for an objectwhich may be small at the end of your finger-tips. This may be testis or could be the tail ofthe epididymis if the testis is a partial abdomi-nal one. Repeated examination may cause thetestis to be withdrawn due to contraction of thecremaster muscle. Even under sedation it maynot be possible to palpate an inguinally retainedtestis in the standing horse. Therefore, reserveyour judgement.

(b)Again determine which testis is present in thescrotum. Palpate the scrotum on the other sidefor evidence of a scar. Even though the castra-tion incision has healed by second intention, theresidual scar cannot usually be palpated andeven with the horse in dorsal recumbency is al-most impossible to see. However, in some caseswhere the end of the vaginal sac has becomeadherent to the subcutaneous tissues, contrac-tion of the cremaster muscle results in a pal-pable and visible scar attached to which is apencil-like core of scar tissue.

In the absence of any recognisable scar, palpatethe inguinal canal as described in (a).

(c)Palpate both sides of the scrotum for scars. Ifnot present, explore both canals. Remember thatthe presence of a scar simply indicates that theskin has been incised – it does not mean that thetestis was located. As many as 7 scars havebeen found a horse which still had a retainedtestis in its abdomen.

8


8

Remember too, that horses which have had bothtestes removed, can behave like entires, not onlymounting mares, but also achieving intromission.

Rectal Examination may aid in determining thelocation of the testes but since most cryptorchidhorses presented for castration are young and frac-tious, the amount of diagnostic information to beobtained from rectal examination should beweighed against the potential for rectal injury aswell as injury to the examiner.

The vaginal rings are identified and palpated. Ifthe epididymis can be palpated in the caudomedialaspect, the tail of the epididymis must have passedthrough the vaginal ring with or without the remain-der of the epididymis and testis. In this situation,the testis may be in the abdomen, in the canal, ormay have been previously emasculated. The mo-bility and flaccid nature of the ‘Normal’ (i.e. Non-terratomatous) testis makes identification per rec-tum very difficult.

Pecutaneous Ultrasonography of the inguinal re-gion or transrectal ultrasonography may assist inlocating a retained testis in the inguinal canal orabdomen. Transrectal ultrasonography using a5MHz, linear transducer can be carried out safelyin a calm animal. Scans begin at the pubic brimand proceed cranially in a sweeping pattern be-tween the midline and the abdominal wall. Cryp-torchid testes appear less echogenic than normaldescended testes.

Diagnostic Blood Tests

Until diagnostic blood tests were developed by Coxin 1970, the only way it could be proved that ahorse had been castrated was to search each in-guinal canal and identify the remains of the sev-ered cords.

(a) Testosterone stimulation testBecause the levels of testosterone vary con-

siderably in entire animals, taking a single samplefor testosterone assay in unreliable. Therefore 20mlof blood are taken into a plain tube. While the needleis in the jugular vein, 500IU of HCG are injected.No sooner than 40 minutes later and not later than 1hour, a second sample is taken. Both are submittedfor testosterone assay. The second sample, if froma horse with a retained testis, will show a signifi-cant rise in testosterone level compared to the first.

b) Oestrone sulphate assayAlternatively a single sample of blood may betaken and submitted for oestrone sulphate assay.This test is reliable provided the animal is overthe age of three and is not a donkey.

SURGERY TO LOCATE AND REMOVETHE RETAINED TESTIS(ES)

The surgery should be performed with horse undergeneral anaesthesia, which can be maintained forhowever long is necessary to find the retained tes-tis. Although a flank approach has been used, shouldthe abdomen need to be opened a ventral, parapreputial approach is preferred.

With the horse in dorsal recumbency, prepare thescrotal region and ventral abdominal wall to theside of the prepuce on the missing side. Draw thepenis forward to avoid it being mistaken for testisduring inguinal exploration. Examine the scrotalarea for scars and the inguinal canal for testis ortail of epididymis. However certain you are thatnothing is palpable in the canal, always search itsurgically. If you subsequently are finding it diffi-cult to find an abdominally retained testis, you willknow for certain it is not in the inguinal canal andis there to be found somewhere in the abdomen.

Even if a testis is palpable in the canal, it is prefer-able not to try to bring it up to, and fix it to thescrotum before making the skin incisions. Insteadincise the skin parallel to the median raphe overthe scrotum and having incised the first layer of con-

9


9

nective tissue, discard the knife and continue the dis-section bluntly using the index finger on each handto split the tissues along the line of your incision.This will automatically expose the inguinal canaland will avoid damage to the large veins which arepresent in the area. Exploration of the inguinal ca-nal will reveal:-

1. an inguinally retained testisor

2. the remains of the vaginal sac after previouscastration which will instantly be recognised bythe presence of cremaster muscle. Transectionwill reveal the vas deferens in cross section

or

3. a small processus vaginalis containing tail ofepididymis but not testis. It is essential that youdo not mistake this for the testis. People occa-sionally do, and each year, we remove a ‘third’testis from the abdomen of a horse from whichthe referring veterinary surgeon has reputedly re-moved two testes. If you open the vaginal, sacyou will easily identify the coiled tubules of thetail of the epididymis from which will pass twowhite tubular structures – the vas deferens, andpart of the body of the epididymis.

The third white structure is the proper ligamentof the testis. There is no vascular component(Fig. 4). Gentle traction on the tail of the epid-idymis may enable the testis to be drawn throughthe deep inguinal ring into the canal from whereit can be removed. If not, leave a pair of fixationforceps attached to the epididymal tail to helplocate the testis during the abdominal explora-tion

or

4. a small processus vaginalis deep in the inguinalcanal containing only the remains of gubernacu-lum. (Adams 196 ) has described a techniqueusing bitch whelping forceps to grip the guber-

naculum and draw the testis into the canal.or 5. nothing may be found.

REMOVAL OF THE ABDOMINALTESTIS

Although the time honoured method was to con-tinue dissection of the inguinal canal and pushfirstly two fingers, or if necessary, the wholehand through the fascia at the deep inguinal ring,to enable the caudal abdomen to be searchedfor the testis, subsequent herniation of smallintestine was sometimes a complication. Al-ternative, safer techniques, may be employed.

i The vaginal process may be identified by fol-lowing the rudimentary scrotal ligament (in-guinal extension of the gubernaculum testis) intothe inguinal canal. It descends into the inguinalcanal along the medial or lateral margin of thecranial third of the superficial inguinal ring.Traction on the scrotal ligament may be usedto exteriorise the vaginal process, which, oncelocated, is opened with scissors. Gentle trac-tion is applied to the ligament of the tail of theepididymis, or the proper ligament of the testisuntil the testis is retrieved from the inguinalcanal. Dilation of the vaginal ring with one ortwo fingers is usually necessary to allowexteriorisation of the testis. Primary closureis accomplished by absorbable suture in thedeep fascia and subcutaneous tissues.

ii Para inguinal approachIf the vaginal process cannot be identified bythe above non-invasive technique, an alterna-tive is a para inguinal approach. The main ad-vantages are the ease of closure and avoidingdisruption of the vaginal ring.

Following exposure and exploration of the su-perficial inguinal ring, a 4-6 cm incision ismade in the aponeurosis of the external abdomi-nal oblique muscle, 2cm medial and parallel

10


10

to the superficial inguinal ring. The underlyinginternal oblique muscle is separated in the di-rection of its fibres and the peritoneum is en-tered bluntly using fingers. One or two fingersare introduced into the abdomen through the in-cision and the vaginal ring is palpated just cau-dal and lateral to the incision to locate the duc-tus deferens or epididymis, either of which maybe followed to the testis. The testis isexteriorised by gentle traction on the proper liga-ment. If the epididymis or its associated struc-tures are not readily palpable the incision maybe extended to accommodate the surgeon’s hand.Once located, the testis is exteriorised andemasculated routinely. The aponeurosis of theexternal abdominal oblique muscle is closedusing No. 2 polyglactin in a continuous pattern.

iii Spura pubic Paramedian ApproachAn oblique para preputial incision is made alongthe direction of the fibres of the rectus musclewhich is converging on the midline. How farcaudally the incision is made is sometimes lim-ited by a thick pad of fat in the area. Incision ofthe skin and cutaneous muscle will reveal thethick yellow tunic of the rectus muscle. Oncethis is incised, the rectus muscle itself is ex-posed. After an initial superficial incision, themuscle can be split using two fingers. This hasthe advantage of exposing the vessels whichtraverse the line of the incision before they rup-ture. They can then be ligated before complet-ing the incision. The thin internal rectal sheathis the next layer to be incised. Deep to this is avariable amount of retroperitoneal fat and peri-toneum. A small incision through the internalsheath will allow the peritoneum to be nicked,and tented by insertion of a finger. The remain-der of the internal rectal sheath and the perito-neum can then be safely cut with blunt endedscissors.

A careful search is then commenced for the tes-tis. Because in the abdominally retained testis

the seminiferous tubules are poorly developed,the testis has a soft flabby feel which makes itdifficult to distinguish from small intestine. Mostweigh about 50g and are most frequently closeto the deep inguinal ring. This is certainly trueof the partially retained testis. Here, traction onthe fixation forceps applied previously to theepididymal tail will help the testis to be identi-fied. If the testis is not found immediately, itmay be to the side of the rectum or bladder. Inthese cases identify the vas deferens in thegenito-vesicular fold. It is recognisable as aknitting-needle like diameter structure which canbe traced to the tail of the epididymis allowingthe testis to be identified and withdrawn throughthe abdominal incision. In most cases, sufficientof its attachments can be exposed to enable aligature of 1 vicryl to be applied to the vascularcomponent of the cord before removing the tes-tis with an emasculator. In those cases whichcannot be exposed so well, transecting the cau-dal attachment with an emasculator will allowthe testis to be rotated upwards thus enablingdirect traction to the vascular component of thecord and thereby exposure of a greater length.

If both testes are retained in the abdomen, theycan be removed via the same incision. A verysmall proportion of abdominally retained testsare terratomatous. This congenital developmen-tal abnormality of the testis can take one of twoforms. The less common form is a solid masswhich when transacted after removal revealsembryological remnants of cartilage, hair andteeth. More commonly, the testis comprises alarge cyst-like structure, which is easily mistakenin the early stages of the exploration for blad-der. The testis retains the vascular pattern on itssurface, but the vessels are much further apartdue to the great distension of its wall. Much ofthe large volume of fluid it contains can be re-moved by suction if available or simply througha 16 gauge needle, thereby significantly reduc-ing its size and enabling it to be removed via a

11


11

standard sized incision. No problem is experi-enced in ligating the vascular component be-cause the weight of the testis has stretched theattachments. Closure of the incision is achievedin three layers. Simple interrupted sutures of 1or 2 vicryl are used to close the peritoneum,internal sheath, rectus muscle and external sheath.Closure is made more simple by commencingclosure at each and leaving the middle until last.Additional sutures may be placed in the exter-nal rectus sheath which is the strongest layer.The subcutaneous tissue and cutaneous muscleare closed using a simple continuous suture of 0vicryl. Closure of the skin with a continuousintradermal suture of the same material avoidsthe need to remove skin sutures.

Only after the retained testis has been located and

removed is the fully descended testis, if present,

removed.

Laparoscopic Cryptochidectomy

Recent developments in laparoscopic techniquesand equipment now offer an alternative method oflocating and removing an abdominal testis. Thesurgery may be performed under general anaesthe-sia or in the standing, sedated horse.

Food is with held for 36-48 hours before surgeryto improve visualisation of intraabdominal struc-tures and minimising the risk of damage to viscera.For recumbent laparoscopy with the horse in dor-sal recumbency, facilities must be available to raisethe hind quarters into the Trendelenburg position.Positive pressure anaesthesia should be used toadequately ventilate the patient during abdominalinsufflation. The inguinal canals are searched toensure that the testis is not located outside the ab-dominal cavity. A 1.0cm stab incision is madethrough the linea alba just cranial to the umbilicus.The abdomen is insufflated with CO2 to 10-20 mm

Hg. The trocar is introduced into the original inci-sion. The laparoscope (30°) is then introduced intothe canula and connected to a fibre optic light sourceand video camera. The pelvis is now raised 30°-45° to displace the viscera cranially. Both vaginalrings are examined. In horses with complete ab-dominal retention the testis and associated struc-tures are seen within the abdomen and the vaginalring may appear as only a small depression. In anincomplete abdominal retention, the head of theepididymis may be seen near the vaginal ring, withthe remainder of the epididymis entering the ring.

Once the testis is located, an 18 gauge, 7.5cm needleis used to determine an optimum instrument portal.This is created, as previously described, for pas-sage of grasping forceps. The testis is grasped andeither ligated within the abdominal cavity, orexteriorised and emasculated. The instrument por-tal incision may have to be enlarged.

Standing laparoscopy is performed with sedationand infiltration of local anaesthetic at thelaparoscopic and instruments portals. The laparo-scope is inserted in a caudal direction slightly dor-sal to the crus of the internal oblique muscle. Theabdomen is insufflated and the vaginal ring exposed.Once localised, the testis must be anaesthetised byinfiltrating local anaesthetic into the parenchymausing a 20-30cm needle. The testis is removedthrough a separate incision closer to the inguinalring.

Prognosis and Complications

The prognosis for horses undergoingcryptochidectomy is usually excellent. Wound in-fection is probably the most common complication.Incomplete castration most often occurs when in-experienced surgeons attempt to castrate a horsewith incomplete abdominal retention and mistakethe tail of the epididymis for the complete testis.

12


12

Piroplasmosis under control?

JP Nurton and AJ GuthrieEquine Research Centre,

Faculty of Veterinary ScienceUniversity of PretoriaOnderstepoort 0110

South Africa.

The international trade of horses over the past fewyears has increased remarkably. Many South Afri-can horses are being brought and raced overseas,particularly in Singapore, Hong Kong, UAE andMalaysia. Some of these countries do not allow theimportation of horses with Theileri equi or Babe-sia caballi antibodies. Horses that have been in-fected by either of these protozoa may become car-riers, potential sources of infection, and could besource of outbreaks of the disease in previouslypiroplasmosis free countries.

Although sterilization of pirolpasmosis infectionsin horses is possible, the total effectivness of thesetreatments is not known and the treatments may posea risk to the horses. It would be safer to attempt tokeep the animals piroplasmosis free by controllingthe ticks that transmit the protozoa. Simple tick con-trol programs could ensure foals becoming piro-plasmosis free yearlings and hence piroplasmosisfree race horses competing internationally.

ObjectivesThe aim of this study was to institute a tick controlprogram on several Thoroughbred stud farms toprevent the spread of either T. equi or B. caballi toa particular foal crop and to keep these horses piro-plasmosis negative until they are yearlings.

Materials and Methods

Four Thoroughbred stud farms in South Africa wereincluded in the study. During January 2002 serumsamples were collected from each foal that had beenborn in 2001 and from each of their dams. Thesesame foals were re-bled in April, July, Septemberand January 2003. All serum samples were testedfor T. equi and B. caballi antibodies by the indi-rect fluorescent antibody test (IFAT). During theyear each farm undertook to carry out a weekly ap-plication of acaricides to their 2001 foal crop.

The same study was repeated during 2003 on thefoals born in 2002. A fifth stud was included inthis. Once again each farm undertook to applyacaricides each week to their 2001 foal crop.

The total number of foals that became infected witheither T. equi or B. caballi during the year werecompared, as well as the infectivity rates on eachfarm.

ResultsTwo of the farms included in the study had alreadyinstituted a tick control program in 2000 followinga high percentage of infected yearlings. This initialcontrol and the program from the two years of thisstudy meant a great reduction in the number of posi-tive horses.

During the first year of the study most of the foalsthat were piroplasmosis positive were already in-fected by the first bleed and thus the infectivity ratesfor the rest of the year were very low. Most of thefoals that were positive from the outset of the trialwere from dams that were piroplasmosis positive.

During the second year of the study, there was amarked reduction in the number of foals that werepiroplasmosis positive and the infectivity rates werelow. On two of the farms in particular there was agreat reduction (more than 50%) in the number ofhorses that were piroplasmosis positive in the sec-

13


13

ond year compared to the first year.

In neither years of the study did any of the farmsreport piroplasmosis outbreaks.

Conclusions

As most of the infected horses were already in-fected at the January sampling and these were frominfected mares, it is possible these foals becameinfected in utero. These animals, if infected andhave parasites, will still need to be in a tick con-trol program to prevent transmission to other horseson the farm.

The infectivity rate results show that the weeklyapplication of acaricides does kill the ticks thuspreventing the transmission of the piroplasmosisantigen. The tick control program should be startedas soon as possible after birth and maintained whilethe horse is on the farm.

It has been seen that piroplasmosis negative horsessold at the National Yearling Sales in 2003 weresold on average for approximately R25 000.00more than piroplasmosis positive horses and thiscould be due to their export potential. A simpletick control program on a farm would mean piro-plasmosis negative horses, which would be moreprofitable to the farm and their horses would beopen to the international market.

14


14

Complications ofCastration

Barrie EdwardsUniversity of Liverpool

Castration is the most common operation performedin horses. Complications are uncommon, but assome can be life threatening, it is important that weare aware of predisposing factors so that every ef-fort can be made to avoid them.

All horses about to undergo castration should beexamined preoperatively for the presence of two,fully descended testes, the absence of any sugges-tion of hernia and signs of systemic illness.

The surgeon has several options to consider re-garding restraint, anaesthetic protocol and surgicaltechnique. His/her choice will be governed by fac-tors such as: -

· Surgical training.· Early experience and success.· Regional tradition.· Size and temperament of the horse.· Descent of the testes.· Experience of lay assistants.· Facilities available.· Owner preference.· Commercial / insured value of the horse.· Cost of surgery.

The surgery may be carried out in the standing horse,or with the horse cast, which these days entails gen-eral anaesthesia. Each has its advantages and dis-advantages, but there is no evidence to suggest thateither is more risky.

The advantages of standing castration include elimi-

nation of risks associated with general anaesthe-sia, shorter procedure; less assistance required andlower costs. The disadvantages are that the proce-dure can be more difficult and hazardous even withimproved modern sedative drugs. It is unsuitablefor very small ponies, and very fractious, unhandledhorses. It is more difficult to maintaining asepsisand ligatures should not be used. It is not suitablewhere there is any risk of herniation where closedcastration is essential.

Closed castration relates to the state of the vagi-nal tunic on completion of the operation. Althoughit has been interpreted as application of the emas-culator to the neck of the unopened vaginal sac, Iprefer to define it as closure of the sac with liga-ture.

Closed castration should be carried out under gen-eral anaesthesia. The parietal tunic is dissectedfree as high up the inguinal canal as possible. Afigure of 8 ligature of 1 metric synthetic absorb-able suture material is applied as far proximal aspossible followed by application of an emascula-tor distal to it. Alternatively the vaginal sac maybe opened and the caudal ‘non vascular’ part of thecord cut with an emasculator, leaving the testes at-tached only by the vascular cord which is ligated.The vaginal tunic is twisted into a pedicle, ligatedand the excess removed with an emasculator.

Closed castration eliminates the risk of postopera-tive haemorrhage and herniation. Its disadvantagesare the cost and the logistics and risks of generalanaesthesia. A number of steps can be taken toreduce the risk of complications. The horse shouldbe kept in a clean, dry environment and rested for24 hours prior to surgery.

Tetanus prophylaxis is necessary. Antibiotics arenot usually necessary, but if used should be admin-istered prior to surgery. Knowing the potential com-plications and the factors which predispose to theirdevelopment is useful. A thorough precastration

15


15

examination, good, well-maintained equipment andstrict attention to good surgical principles will helpto minimise complications.

Most serious, life-threatening complications occurwithin the first 12-24 hours of surgery, so the ownerneeds to keep the horse under close observationduring this period. Other complications may bedelayed days, weeks or even months.

Castration Complications· Excessive haemorrhage· Prolapse of omentum· Evisceration· Scrotal and preputial oedema· Infection· Hydrocoele· Bacterial peritonitis· Anaesthetic accidents· Penile damage· Continued stallion-like behaviour

1. Haemorrhage

The source of bleeding may be the dartos, skin veinsor most significantly the spermatic artery. The lat-ter is usually the result of an improperly applied orpoorly maintained emasculator. If you can countthe drips, haemorrhage will usually subside within5 to 10 minutes. A continuous loss of bright redblood is cause for concern.

Observe and keep the horse calm to prevent rise inblood pressure.

The options open to arrest the haemorrhage are:

(1)Pack the scrotum and inguinal canal with gauze.Remember if bleeding is not arrested, this willnot be evident for a while until the packing be-comes saturated with blood. If successful, leavethe packing in place for 24-48 hours.

(2)Locate the bleeding vessel with carmalt forcepsby ‘fishing’ in the inguinal canal. If successful,attempt to ligate the vessel. If this is not suc-cessful, leave the clamp in place. Tie the handleswith suture material to secure. Leaving the su-ture material projecting for the skin incision willact as a reminder to remove the forceps after 48hours.

(3)If the vessel cannot be located in the standinganimal, the horse should be anaesthetised, andrestrained in dorsal recumbancy, the scrotal areacarefully cleaned and the skin edges separated.The margins of the incision in the vaginal tunicshould be identified and fixed with Allis for-ceps. This will enable a pair of carmalt for-ceps to be inserted up the inguinal canal to lo-cate the spermatic artery which can then be se-curely ligated.

Less satisfactory methods include: -· Administration of acepromazine to reduce blood

pressure.· Intravenous formalin.· Locally applied adrenaline.

2 + 3 Prolapse of Omentum or Evis-ceration

This may occur during castration or, in the majorityof cases, within a few hours of surgery. On rareoccasions, it can occur several days after surgery.

Predisposing factors include a large deep inguinalring and increased intra-abdominal pressure.

Prolapse of greater omentum from the skin inci-sions in the scrotum is no cause for alarm. How-ever, prolapse of small intestine is a life threaten-ing complication which demands rapid, decisiveaction. When the call from the owner is received,it is essential that a description is obtained of theprotruding tissue, so that it can be determined

16


16

whether it is intestine or omentum. If it is intestine,the owner is instructed to support it with a cleansheet to minimise contamination and trauma fromthe horse’s hind feet. On arrival at the premises,the horse should be sedated, the intestine washedand gently returned to the scrotum and inguinal ca-nal, and the skin sutured prior to transfer to a surgi-cal facility. Retaining the intestine within the scro-tum during the journey does not arrest ischaemicdamage, but does prevent irreparable traumatic in-jury. Under general anaesthetia, devitalised intes-tine is resected and the vaginal sac occluded bysuture.

Prolapsed Omentum can be recognised by itslace-like appearance once the ‘cord’ it forms out-side the scrotum is teased out. Gentle traction willallow a small amount of uncontaminated omentumto be exposed and transacted. Traction on the skinincision may allow the omentum to retract into theinguinal canal. However, there is a tendency forfurther prolapse and the possibility of extension ofinfection up the inguinal canal. I prefer toanaesthetise the horse in dorsal recumbency, re-move the contaminated prolapsed omentum and re-turn the remainder to the abdominal cavity by twist-ing the vaginal sac into a pedicle. A transfixingligature of the sac anchored to the superficial in-guinal ring will prevent further prolapse.

4. Scrotal and Preputial Oedema

Some oedema is common after castration. The veinsand lymphatics draining the prepuce and caudalventral abdomen pass up the inguinal canal. Pres-sure on these resulting from swelling of the emas-culated cord leads to preputial oedema but this sub-sides as the swelling in the inguinal canal de-creases. The oedema gravitates along the ventralabdominal wall, the last traces of which will bedetectable in the stenal region 7-10 days after cas-tration. This ‘normal’ post castration oedema willbe much more pronounced in stallions than in foals

because of the greater degree of traumatic inflam-mation. Routine walking exercise after castrationhelps to dispose the oedema.

Post castration oedema becomes of significancewhen scrotal swelling persists or increases. Thiswill be accompanied by persistent preputial oedemaand oedema extending along the ventral abdomen.Such findings indicate continuing and increasingpressure on the veins and lymphatics due to accu-mulation of fluid in the scrotum or progressive en-largement of the cord due to infection. As the firststep, opening up the scrotal incision will releaseany fluid which has accumulated and establishdrainage. In the absence of cord infection, this isusually successful in resolving the oedema.

5. Post-castration Wound Infection

Infection may result from contamination during orafter castration. Uneventful healing after castra-tion usually attends good drainage and controlledexercise and second intention healing is usuallycomplete within 14-21 days. Infection remains con-fined to the scrotal cavity as long as the scrotalincision remains open and draining.

The types of infection include: -· Septicaemia.· Acute streptococcal infection.· Chronic staphylococcal infection of the cord· Peritonitis· Clostridial infection· Tetanus· Malignant oedema

(a) Acute Infection

Acute infection, usually with streptococcuszooepidemicus become evident during the secondpostoperative week. Depression, pyrexia,localised heat and pain precede abscessation. Ex-cessive swelling of the scrotum and prepuce ispresent and the horse is reluctant to move. There

17


17

may or may not be a purulent discharge from thescrotum. The scrotal incision should be reopenedallowing any purulent material to escape and anyinfected haematoma to be removed. Maintainingdrainage and administration of penicillin will usu-ally bring about resolution, but if the infection in-volves the remains of the cord, prompt surgical ex-cision is necessary if extension of the infection alongthe components of the cord is to be avoided. Thismost commonly occurs along the vas deferens lead-ing to intrapelvic abcessation lateral to the blad-der. This should be checked for by rectal palpa-tion.

With horse under general anaesthesia and placedin dorsal recumbancy, the skin on the affectedside(s) is incised laterally and cranially from thescrotal area towards the superficial inguinal ring.A line of separation is identified between the thick-ened inflamed cord and the skin. Once the infectedportion of the cord has been freed, healthy vaginalsac and external cremaster muscle will be exposed.The healthy cord is transacted as high up the in-guinal canal as possible with an emasculator to in-sure that no residual infection remains. Post op-eratively, drainage is maintained via the scrotal in-cision. Cases in which infection has extended be-yond the deep inguinal ring carry a very poor prog-nosis.

(b) Chronic Staphylococcal Infection of the Cord– Scirrhous Cord

This complication, which is predisposed to by leav-ing the parietal vaginal tunic long and by the use ofnon-absorbable ligatures does not become appar-ent for several months or even years after castra-tion. Scirrhous cord comprises a chronic low-gradeinfection of the cord with staphylococcus aureus,leading to microabscessation surrounded by densefibrous tissue. Unlike streptococcal cord infection,there are no systemic signs and the firm swelling iscold and painless. Consequently, it goes unnoticedand unsuspected until one of the microabscesses

discharges on to the skin surface and is noticed dur-ing routine grooming. Alternatively, the scrotalmass is identified during a pre-purchase examina-tion. By the time the lesion is identified, it is thesize of a large orange, but can be considerably big-ger. Treatment involves surgical removal, much asdescribed for the acutely infected cord, but becauseof the chronic nature of the lesion dissection of theinfected cord from the surrounding tissues is moredifficult and the surgery becomes an exercise inhaemostasis. Once healthy cord is reached, sepa-ration is easier. The cord is transected with anemasculator as high up as possible. Even thoughthe surgery may be performed years after the cas-tration operation, infection will not have extendedinto the abdominal cavity.

Postoperatively, the scrotal incision is kept openuntil all evidence of drainage has closed.

(c) Peritonitis

Sub clinical, non-septic peritonitis follows castra-tion in many horses and nucleated cell counts > 10x 109/l are routinely present in the peritoneal fluidfor 5 days after uncomplicated castration. In con-trast, septic peritonitis is very uncommon becausethe funicular part of the vaginal process is col-lapsed as it traverses the abdominal wall and me-sothelial cells are phagocytic.

6. Hydrocoele (“Cystic Ends”)

Soft fluctuating swellings identifiable in the scrotumat variable times after castration. They cause thehorse no problems but owners may be concernedabout the possibility of hernia. This can beeliminated by palpation and ultrasonography. Theproblem is purely cosmetic and can be left untreated.However, if the owner is concerned about thecosmetic effects the affected cord or cords can bedissected free under general anaesthesia andremoved.

18


18

7. Penile Trauma

Although very uncommon, trauma has been reporteddue to mistaking the penile shelf for an inguinallylocated testis, or can be secondary to sedation withacepromazine.

8. Continued Stallion – like behaviour

20-30% of castrated horses have been reported toshow stallion-like sexual interest in mares. 5%show stallion-like aggressive behaviour towardspeople.

No difference has been established between horsescastrated before or after puberty.

Limiting social interaction with other horses andimposing stricter discipline will usually be suc-cessful.

When continuing stallion-like behaviour is due toimproper castration of a partial abdominally re-tained testis, the testis must be located and removed.

19


19

ANATOMY

NeoplasiaA number of neoplasms have been reported to af-fect the equine penis, including papillomas, squa-mous cell carcinoma, melanomas, sarcoids, mas-tocytomas and haemangiomas. Of these, squamouscell carcinoma is by far the most common.

Squamous Cell Carcinoma of the penis is seenalmost exclusively in aged geldings, but can occurin younger horses and has been reported in stal-lions. Although it has been suggested that lack ofpigment can predispose to the condition as it can atother sites on the body, the infrequency with whichthe penis is exposed to direct sunlight makes thisvery unlikely. It is more likely that penile SCC isrelated to possible carcinogens in smegma, whichaccumulates on the integument and particularly inthe suburethral fossa of geldings. In stallions, thisis removed during natural service and routine wash-ing of the penis and sheath at studs. SCC occursmost frequently on the glans, particularly in the re-gion of the urethral fossa. The preputial ring, whichis in contact with the glans when the penis is withinthe sheath, is the next most common site, but le-sions can occur at any site. Small depigmented,proliferative lesions may be a precancerous state.

Most commonly SCC appear as a friable, prolif-erative, cauliflower like lesions, which are remark-ably slow growing and very slow to metastasise toregional lymph nodes and elsewhere in the body.As they enlarge, the lesions tend to ulcerate andbecome secondarily infected and in the summer

months may become flyblown. The secondary in-fection may lead to lymphadenopathy of the inguinallymph nodes.

Much less frequently, the tumour takes on an ag-gressive scirrhous form. Here there may be littleevidence of proliferation and ulceration, but theglans and varying lengths of the body of the penisare very firm on palpation, giving a ‘wooden’ feel.This form of the tumour infiltrates very rapidly,particularly around the urethra and quicklymetastasises to the regional lymph nodes.

The age and the sex of the horse and the character-istic appearance of the tumour usually makes diag-nosis straightforward. Sedating the gelding to bringabout relaxation and protrusion of the penis allowsa small piece of the tumour to be removed for his-tological confirmation.

Treatment

Several options exist depending on the location,size and degree of infiltration of the tumour.

Small lesions confined to the integument may belocally excised or frozen.

Segmental prosthectomy or ‘reefing’ is frequentlyemployed to remove superficial, non-infiltrativelesions on the preputial ring. Two circumferentialincisions are made in the integument to include theSCC lesions, leaving a reasonable margin of healthytissue. The band of integument is carefully dis-sected from the underlying tissue. Haemostasis isachieved with forcipressure or thermocautery. Thecut edges are then carefully approximated with ab-sorbable sutures. Reefing is often used in conjunc-tion with partial phallectomy.

Partial Phallectomy is indicated when the lesionaffecting the glans or distal free part of the penishas infiltrated to deeper tissues. The technique Iprefer is that first described by Vinsot, in which

Equine PenileConditions


20


20

the penis is transected just distal to the urethros-tomy, which has to be created. With the horse un-der general anaesthesia and in dorsal recumbency,the penis is withdrawn and catheterised with a ure-thral catheter. A bandage is tied tightly around thepenis, just distal to the entrance to the sheath, toact as a tourniquet. The site for transection of thepenis is chosen and marked, allowing as muchhealthy penis as possible proximal to the SCC le-sion. A urethrostomy is created on the ventral as-pect of the penis proximal to the mark (Fig ). Atriangular piece of integument with the base 2 cmproximal to the intended site of transection, is re-moved. The urethra is readily identified by pal-pating the catheter in its lumen and is opened byincising through corpus spongiosum and the ure-thral mucosa. The mucosa is cut transversely for 1cm on either side at the base allowing it to be re-flected and carefully sutured along the three sidesof the triangle. The interrupted sutures of 2/0 syn-thetic absorbable material, which pass through theintegument, corpus spongiosum and the mucosa, areplaced quite close together to control haemorrhage.

On completion of the urethrostomy, the urethral cath-eter is removed prior to transecting the penis. Su-turing the stump is facilitated by transecting the penisin a wedge fashion. The large vessels on the dor-sal aspect can be readily identified, by looseningthe tourniquet if necessary, and ligated. The stumpis closed with interrupted sutures of 1 metric syn-thetic absorbable material which include the in-tegument and the tunica albuginea dorsal and ven-tral to the corpus cavernosus. A small amount ofbleeding may be expected, but this quickly abates.The resected portion of the penis is submitted forhistological investigation to ensure there is a mar-gin of normal tissue. Healing is uneventful andmost horses live on for several years with, in myexperience, no tendency for stenosis to occur atthe urethrostomy. In most horses, the urethrostomyand transection can be carried out on the free partof the penis distal to the preputial attachment, butmany have to be performed a little more proxi-

mally if the SCC is more extensive.

When the tumour is of the aggressive squamousform, there is a considerable likelihood of rapidrecurrence following partial phallectomy. In thesecases and those with proximal lesions or lesionsaffecting the preputial orifice en bloc resection isthe only means of ensuring, within reason, that alltumour tissue is removed

En Bloc Penile Resection The skin incision com-mences a few centimetres cranial to the entrance tothe sheath, extended caudally to encircle it beforecontinuing along the midline. A combination of di-athermy and blunt dissection is used to dissect thesubcutaneous and areolar tissue starting craniallyand continuing around each side of the prepuce,down to the deep fascia of the abdominal muscula-ture. Care is taken to avoid injury to the pudendalvessels in this region. Caudally the incision is con-tinued in the midline down to the body of the penis.Any vessels on the dorsal aspect of the penis whichneed to be cut in order to free it as far distally asnecessary to transpose it are ligated beforehand. Aurethrostomy is created just proximal to the intendedsite of resection. After transection of the penis 2cm distal to the urethrostomy, the stump is closedwith interrupted sutures. The superficial inguinallymph nodes are removed.

The penis is now freed proximally by blunt dissec-tion enabling the distal portion of the penis to beretroflexed through 180º. A 5cm vertical subischialincision is made at a pre-marked site 20cm distalto the anus. A 3cm portion of the penis is gentlymanipulated through the incision, the base of theurethrostomy now being orientated towards the hindlimbs. The stump of the penis is secured usingsimple interrupted sutures placed through the tunicaalbuginea and the adjacent skin in such as way thatit projects slightly beyond the skin thereby divert-ing urine away from the perineium.

Penrose drains are inserted in the subcutaneous

21


21

space left by the en bloc resection prior to closureof the subcutaneous tissue and skin. Healing is un-eventful.

PARAPHIMOSIS

Paraphimosis, or the inability of the horse to re-tract the prolapsed penis into the sheath, most com-monly occurs from preputial oedema caused bygenital trauma. It may also result from gross oedemaof the sheath following castration, and paralysisassociated with priapism, debilitation and caudaequina neuritis.

PENILE TRAUMA

It is not uncommon for stallions to be kicked on theerect penis during attempts at serving a mare. Geld-ings may sustain similar injuries. The trauma rap-idly leads to gross oedematous swelling of the pre-puce and sometimes penile haematoma. The swell-ing is most severe on the dorsal aspect and resultsin caudal deviation of the penis. In addition to thisinflammatory swelling, constriction at the entranceto the sheath and gravity further contribute to theoverall oedema. Despite the marked deviation andthe swelling, there is no significant obstruction tothe urethra, but it is always advisable to confirmthis by stimulating the horse to urinate by placing itin a clean box or administering a diuretic. It is notadvisable to pass a catheter because this may irri-tate or damage the urethral mucosa.

If the horse is presented very soon after the injuryhas been sustained, before the swelling has becometoo severe, reducing the size by manual compres-sion to disperse the oedema, may allow the penisto be returned to the sheath. Some advocate gen-eral anaesthesia and the use of an Esmarch ban-dage applied from the glans penis proximally toreduce the swelling. If the penis can be returned tothe sheath, the opening into the sheath should beclosed with suture or towel clips. Retaining thepenis within the sheath removes the constrictive

and gravitational factors allowing further reduc-tion in the swelling to take place.

However, in most cases I have seen, the swellingis so severe that any attempt at replacing the penisis futile. In these cases cold hosing the penis for10-15 minutes at a time helps to reduce blood sup-ply and minimise any further inflammatory swell-ing. The penis should be cleaned and dried and anon-water miscible coating of petroleum jelly lib-erally applied particularly in the clefts to affordprotection to the integument.

The one contributory factor to the swelling whichcan be managed effectively at this stage is gravita-tional oedema. Several different methods of achiev-ing this have been reported. I find the most effec-tive is to insert the swollen penis into a pair oftights from which the legs have been removed andwhich are attached by lengths of bandage to a surc-ingle in front and a crupper behind. This elevatesand supports the penis and the material allows urineto escape thereby minimising excoriation of the in-tegument.

This support is removed daily and the surfacecleaned and dried. Manual compression allowssome of the oedema to be dispersed. Petroleumjelly and a fresh support are applied. Over thenext 2-3 weeks, there is a progressive reduction ofthe swelling. The integument over the most pro-nounced area of swelling often splits allowingoedema fluid to escape and resulting in a signifi-cant reduction in swelling. If a haematoma ispresent this can be drained by needle suction onceit is certain that bleeding has stopped.

By three weeks after the injury the penis can bereturned to the sheath manually and often the horseis able to do this of his own accord. However, ifthere are ulcerated areas, it tends to prolapse thepenis most of the time. Although permanent pa-ralysis of the penis has been reported after suchinjuries, in my experience the vast majority are able

22


22

to withdraw the penis normally once the ulcerationhas resolved.

In those that remain permanently paralysed, the op-tions are retraction of the penis using the Boltz tech-nique, sometimes in conjunction with partialphallectomy. If these techniques are to be em-ployed, a stallion must first be castrated and suffi-cient time allowed for any postoperative swellingto subside.

PRIAPISM

Priapism is persistent penile erection without sexualarousal. It is uncommon, but when it does occur ina valuable breeding stallion, it is economically sig-nificant because impotence is the usual outcome.

In horses it occurs primarily following adminis-tration of phenothiazine-derivative tranquilizersparticularly acepromazine. It is usually stallionswhich are affected, but the problem has been seenin geldings. Because of the recognised link be-tween priapism and acepromazine, the conditionis rarely seen these days. I have however encoun-tered priapism in horses at the termination of colicsurgery. Although the penis is erect, it can usuallybe returned to the sheath, and if retained there withsutures or towel clips, detumescence takes placewithin a relatively short period of time.

Priapism occurs when the corpus cavernosus pe-nis (CCP) fails to detumesce due to disturbancesin arterial inflow or venous outflow. It is suggestedthat phenothiazine-derivative tranquillisers causepriapism by blocking alpha sympathetic impulseswhich mediate detumescence. Vascular stasis oc-curs in the CCP. Venous outflow becomes ob-structed by sickled erythrocytes leading to trabe-cula oedema and irreversible occlusion of the col-lecting veins.

The arterial supply is still patent early on, but even-tually is irreversibly occluded by clots and fibro-

sis. The trabeculae become fibrotic and inelastic.Prolonged erection may be compounded by injuryto the pudendal nerves presumably from tension orcompression against the ischium.

Non-surgical treatment

The penis is massaged, protected with an emollient dressing and supported as previously de-scribed. Diuretics and corticosteroids may help.

Surgery

If the initial management is unsuccessful; after 8-12 hours, the CCP should be irrigated withheparinised lactated ringers solutions. Severallitres are injected into the CCP through a 14 gaugeneedle inserted just proximal to the glans. The fluidis allowed to exit through 2 x 12 gauge needles inthe CCP 10-15cm caudal to the scrotum. This pro-cedure is carried out under general anaesthesia andirrigation is continued until fresh blood appears.

HABRONEMIASIS

Cutaneous habronemiasis or ‘summer sore’ is agranulomatous, slightly pruritic disease caused bycutaneous migration of the larvae of the equine stom-ach worm Habronema. The condition is seen dur-ing the spring and summer when flies are preva-lent.

The larvae stimulate an acute granulomarous reac-tion characterised by exuberant granulation tissuecontaining numerous small yellow caseous gran-ules. The preputial ring and urethral process areprediction sites.

Treatment comprises administration of Ivermectinand, if necessary, elliptical or circumferential re-section of the fibrotic tissue.

23


23

How to do anendoscopic

evaluation of theupper respiratorytract in the resting

horsePC Page, Department of Companion

Animal Clinical Studies, Faculty ofVeterinary Science, Private Bag X04,

Onderstepoort, 0110, RSA, (012) 529-8200, (012) 529 8308 (Fax),

[email protected]

IntroductionEndoscopic evaluation of the respiratory tract atrest is one of the primary diagnostic techniquesavailable to the equine private practitioner for de-tection of respiratory disease, the objective beingto evaluate the structure and function of the rel-evant structures. Resting endoscopy does havesome limitation however, in that the detection of anabnormality in the resting horse does not necessar-ily indicate a clinical problem. Conversely, the ab-sence of a respiratory tract abnormality at rest doesnot exclude the possibility of airway dysfunction atexercise. For this reason the resting endoscopicfindings should always be interpreted in conjunc-tion with a detailed history and thorough clinicalexamination and, if indicated, further diagnostictechniques such as high-speed treadmill endoscopyshould be utilised in order to reach a definitivediagnosis.

Requirements

Generally 3 people are required for the examina-tion; one restrains the horse, another passes the en-doscope, and the third person directs the endoscopemovement during the examination. With the use ofshorter endoscopes it is possible for one person toinsert and “drive” the endoscope alone. Usuallyonly a twitch is required for restraint. Having acompetent handler holding the horses’ head is para-mount; the examiner is usually focussed on the en-doscopic images and is therefore at risk should thehorse suddenly jump forward. Restraining the horsein a padded crush provides extra protection for thestaff and equipment involved. It is preferable notto use sedation to facilitate examination for assess-ment of functional abnormalities; xylazine sedationhas been reported to affect the subjective assess-ment of laryngeal cartilage movement.

Equipment options range from the simple fibreopticendoscope to colour chip video endoscopes, witha large array of image recording equipment andendoscopic accessories available. To reach themiddle trachea an endoscope with a 1 metre longinsertion tube is required; to evaluate the gutturalpouches the external diameter of the insertion tubeshould be less than 11 millimetres.

The fibreoptic endoscope system is based on lightand image transmission through optical glass fibresarranged in a light-guide bundle and an image-guidebundle, and various lenses. Two video imaging sys-tems are available, one employing a fibreoptic en-doscope system with an external video camera at-tached to the endoscope eyepiece and the otherutilising a video image endoscope. The video im-age endoscope does not contain an image-guideglass fibre bundle; instead it contains a chargedcouple device (CCD) microchip in the insertiontip of the endoscope. The CCD chip has a photo-sensitive surface, which converts light from theimage into electric charges. The video processorconverts the electrical signal from the CCD back

24


24

into a colour image, which is displayed on the moni-tor. The main advantages of the video endoscopesystem is that it provides images of much betterquality than does the conventional fibreoptic sys-tem and that several observers can view the ex-amination at once.

Method of examination

It is recommended that a routine of examination befollowed to avoid missing a structural or functionalabnormality. An example of such a routine is asfollows:

Pass the endoscope in a positive manner for thefirst 10 cm via the ventral meatus- insert to nasopharynx- evaluate structures in nasopharynx including epi-

glottis, soft palate, pharyngeal recess, gutturalpouch ostia, larynx

- perform nasal occlusion and induce swallow-ing to assess function in nasopharynx

- pass into trachea- evaluate trachea (and perform trans-endoscopic

aspirate of secretions if indicated)- retract back to nasopharynx ’! pass endoscope

into guttural pouch- evaluate guttural pouch- retract to caudal end of nasal septum- evaluate ethmoid labyrinth- evaluate sinus drainage angle ’! retract and

evaluate nasal passages and septum as with-drawing endoscope

- pass endoscope via opposite nostril to nasophar-ynx

- evaluate nasopharynx- pass endoscope into guttural pouch- evaluate guttural pouch- retract to caudal end of nasal septum- evaluate ethmoid labyrinth- evaluate sinus drainage angle- retract and evaluate nasal passages and septum

as withdrawing endoscope

Structures evaluated during resting endoscopy:

NasopharynxThe nasopharynx is a muscular tube that connectsthe nasal cavity to the larynx. The surface is nor-mally covered with a small amount of clear, waterymucous, with no remnant food particles. Swallow-ing, which can be induced by instilling a smallamount of water via the air/ flush channel of theendoscope or by touching the epiglottis with the tipof the endoscope or a blunt probe, is associatedwith rhythmic constriction of the nasopharynx anddilation of the guttural pouch openings. Nasal oc-clusion with the endoscope in place results in anincreased negative pressure in the nasopharynx,enabling pharyngeal constriction and dilation to berecorded. The nasopharynx should be examined forinflammation, exudate, foreign material or cicatrixformation.

EpiglottisThe normal epiglottis has fine surface blood ves-sels and a scalloped edge. The surface may be dis-torted by inflammation or obscured by epiglotticentrapment. Subepiglottic cysts may be seen directlyor may only cause a bulge of the soft palate. A hy-poplastic epiglottis appears relatively small andflaccid, and blends into the contour of the soft pal-ate.

Soft palateThe epiglottis normally obscures the most caudalaspect of the soft palate. Submucosal palatine cystsmay be seen distorting the soft palate or area ven-tral to the epiglottis. If dorsal displacement of thesoft palate (DDSP) occurs the caudal free borderof the soft palate may be inspected for any ulcer-ation or cleft. If DDSP is suspected as a cause ofrespiratory noise and poor performance, high-speedtreadmill endoscopy may be required to provide adefinitive diagnosis after due consideration of thehistory and clinical findings. Many normal horseswill spontaneously show DDSP after the endoscopeis withdrawn from the trachea.

25


25

Pharyngeal recessThe dorsal pharyngeal recess should be evaluatedfor degree of pharyngeal lymphoid hyperplasia(Table 1). This system of grading pharyngeal lym-phoid hyperplasia is more reliable than one thatevaluates the degree of hypertrophy over the roofof the pharynx.

Guttural pouchesThe nasopharyngeal openings of the guttural pouchesshould be evaluated for blood, exudate or defor-mity. The guttural pouches can be entered by firstpassing a blunt stylet (inserted via the biopsy chan-nel of the endoscope) through the guttural pouchopening, rotating the endoscope so that the openingof the biopsy channel is 180º away from the pha-ryngeal wall, and then advancing the endoscopethrough the open guttural pouch ostium using thestylet as a guide. The stylet is withdrawn into theendoscope once the pouch is entered. The gutturalpouch is divided into a larger medial and smallerlateral compartment by the stylohyoid bone. Thecaudal portion of the stylohyoid bone articulateswith the petrous temporal bone at the base of theskull. Vital structures associated with the pouchesare the internal carotid artery, the external carotidartery, the maxillary vein, cranial nerves VII, IX,X, XI, and XII, the sympathetic trunk and the cra-nial cervical ganglion. The retropharyngeal lymphnodes may be seen protruding through the walls ofthe pouches if they are enlarged. The pouchesshould be assessed for inflammation, empyema orchondroids, fungal plaques, gross haemorrhage andmass lesions. Temporary resolution of gutturalpouch tympany is obtained by passing the endo-scope into the affected pouch.

Palatopharyngeal archRostral displacement of the palatopharyngeal archhas been associated with some cases of fourth bran-chial arch defect syndrome. This syndrome ischaracterised by maldevelopment of the thyroidcartilage, cricothyroid articulation, andcricothyroideus and cricopharyngeus muscles. Ad-

ditional endoscopic findings include apparent right(or left) laryngeal hemiplegia.

LarynxThe rima glottis should be evaluated for asymme-try and the arytenoids should be assessed for rangeand symmetry of movement. Apparent asymmetryof the laryngeal structures may be noted due to theeccentric position of the endoscope in the nasophar-ynx (perspective distortion); i.e. when the endo-scope is passed via the right nostril, the rightarytenoid appears less abducted than the left, andvice versa. Endoscopic evaluation of the larynxshould therefore be performed via either nostril inturn. Various grading systems have been describedfor recurrent laryngeal neuropathy (Table 2, Table3). High-speed treadmill endoscopy is indicatedwhere doubt exists as to the significance of the le-sion. The vocal cords should be examined for signsof previous ventriculectomy orventriculochordectomy. The arytenoids should beinspected for gross thickening and granulomatousprojections associated with arytenoid chondropa-thy.

TracheaThe trachea should be evaluated for shape, inflam-mation, secretions, haemorrhage, or mass lesions.Trans-endoscopic aspiration of secretions can beperformed via a catheter inserted through the bi-opsy channel of the endoscope if indicated.

EthmoidEndoturbinate II and endoturbinates III - IV are thevisible structures of the ethmoid labyrinth thatproject rostrally into the caudal part of the nasalcavity. Numerous passages, the ethmoidal meatusesare present between the endoturbinates. This areashould be examined for any abnormal discharge,haemorrhage, or mass lesion.

Sinus drainage angleThe communication between the maxillary sinusand the nasal cavity is hidden in the caudal part of

26


26

the middle meatus. The sinus drainage angle areashould be examined for any abnormal discharge,haemorrhage, or gross obstruction.

Nasal passagesThe conchae and meatuses should be evaluated forany mucosal lesion, abnormal discharge,haemorrhage, gross obstruction, masses, or foreignbody.

References

1. Baker GJ 1987 Diseases of the pharynx. InRobinson NE (ed) Current Therapy in EquineMedicine (2nd edn). WB Saunders, Philadelphia:

2. Ducharme NG, Hackett RP, Fubini SL, ErbHN 1991 The reliability of endoscopic examination in assessment of arytenoid cartilagemovement in horses. Part II. Influence of sideof examination, reexamination and sedation.Veterinary Surgery 20: 180 - 184

3. Lane JG 1993 Recurrent laryngeal neuropathy (RLN): current attitudes to aetiology, diagnosis and treatment. Bain-Fallon MemorialLecture Proceedings, Canberra, Australia,June 1993

4. Lumsden JM, Stick JA, Caron JJ, NickelsFA, Brown CM, Godber LM, Derksen FJ 1995Upper airway function in performance horses:videoendoscopy during high-speed treadmillexercise. The Compendium 17: 1134 - 1143

5. Parente EJ 1996 Diagnostic techniques forupper airway diseases. In Robinson NE (ed)Current Therapy in Equine Medicine (4th

edn). WB Saunders, Philadelphia: 401 – 403.

6. Rakestraw PC, Hackett RP, Ducharme NG,Nielan GJ, Erb HN 1991 Arytenoid cartilage

movement in resting and exercising horses. Veterinary Surgery 20: 122 - 127

7. Roy MF, Lavoie JP 2003 Tools for the diagnosis of equine respiratory disorders. InVassallo J (ed) The Veterinary Clinics ofNorth America: Equine Practice. WBSaunders, Philadelphia: 1 – 17

8. Traub-Dargatz JL, Brown CM (eds) EquineEndoscopy (2 nd edn). Mosby, St. Louis

27


27

Table 1. Grading system for pharyngeal lymphoid hyperplasia (Baker 1987)

Grade Appearance of dorsal pharyngeal recess

1 Hypertrophy limited to <180º (insignificant).

2 Hypertrophy extends the full circumference of the dorsal pharyngeal recess (insignificant

in horses d” 3 years old.

3 The pharyngeal hypertrophy makes midline contact (significant in all horses).

4 Hypertrophic masses extend from the dorsal pharyngeal recess (significant in all horses).

Table 2. Grading system for laryngeal movement (Lane 1993)

Grade Movement 1 All movements, both adductory and abductory, are synchronized at rest and after exercise. Any appearance of asymmetry arises as an artefact of the position of the endoscope and when the right and left nostrils are used in turn the perspective distortion is cancelled. This being the case a ‘mirror’ effect operates such that when the endoscopy is performed via the right nasal chamber, the right arytenoid may appear less abducted and vice versa. 2 All major movements are symmetrical with a full range of abduction and adduction. Transient asynchrony, flutter, or delayed or biphasic abduction may be seen especially of the left arytenoid. 3 Although the left arytenoid is still capable of full abduction, activity is generally reduced on the left when compared to the right with periods of prolonged asymmetry, particularly during quiet movements. Full bilateral abduction can be stimulated transiently by partial asphyxiation using nasal closure, but it is not sustained. 4 The left arytenoid is no longer capable of full abduction and during adduction compensation by the right arytenoid crossing the midline may be evident. Asymmetry is marked, but some residual movements are present. 5 True hemiplegia i.e. there is a complete absence of active movement on the affected side and no response to the slap test will be provoked.

Table 3. Grading system for laryngeal movement (Rakestraw 1991)

Grade Movement 1 Symmetrical, synchronous abduction and adduction of the left and right laryngeal cartilages. 2 Some asynchronous movement (hesitation, flutter or abductor weakness) of the left arytenoid cartilage during any phase of respiration; full abduction of the left arytenoid cartilage can be maintained by swallowing or nasal occlusion. 3 Asynchronous movement (hesitation, flutter or abductor weakness) of the left arytenoid cartilage during any phase of respiration; full abduction of the left arytenoid cartilage cannot be induced and maintained by swallowing or nasal occlusion. 4 There is no substantial movement of the left arytenoid cartilage during any phase of respiration.

28


28

Summary- Most endoscopy is performed on horses which

are at rest any yet there are no races for horsesstanding still - endoscopy is often used to pre-dict events which onlycur when the subject isgalloping at racing speed

- Highspeed treadmill endoscopy (HSTE) pro-vides the best means to make a definitive diag-nosis of dynamic obstruction of the upper res-piratory tract in equine athletes

- Other aspects of respiratory and cardiac func-tion can be assessed simultaneously

- HSTE is safe provided that careful screeningand training programmes are used

- Malfunctions of the soft palate are the most fre-quently diagnosed dynamic disorders of theequine upper airways

- The findings of HSTE are frequently at odds with

the conclusions reached by endoscopy in thehorse at rest.

- Dynamic obstructions are often complex and donot involve single structures or causes

An inability to breathe freely provokes obviousperformance-limitations for the athletic horse andthe presenting signs in afflicted animals include re-duced stamina through an inability to sustain aero-bic muscle function and audible respiratory noisesthrough increased turbulence within the upper res-piratory tract. The minute volume of normal horsesat rest is of the order of 250L but this is increasedto as much as 2500L during fast exercise.

The pressure gradients required to move such largevolumes of air can be as much as 40cm water andthese act across the walls of the airway so that con-siderable “collapsing forces” come into play dur-ing inspiration. In the nasal passages and the tra-chea the semi-rigid structure of the lining of the air-way helps to resist this effect but the obvious areasof weakness lie at the nares and in the pharynx andlarynx.. At rest 70-85% of the total airway resis-tance arises at these points but through musculareffort this is reduced to approximately 50% duringforced breathing. For example, the action of thenaso-labialis muscles dilates the nares, the pharyn-geal and palatal musculature helps to maintain thepatency of the musculo-membranous tube of the na-sopharynx and the crico-arytenoideus dorsalismuscles abduct the cartilages of the larynx. Obvi-ously there will be occasions when a structural de-formity leads to compromised airflow, for examplewith epiglottal entrapment, sub-epiglottal cysts andarytenoid chondropathy, but it is a failure to with-stand the collapsing forces of respiration which isresponsible whenever horses show signs of dynamicobstructive dyspnoea.

Earlier comments were made regarding the limita-tions of endoscopic examinations made during quietbreathing, i.e. when the patient is standing in thestable or has recently returned from exercise. In fact,

Understanding thedynamics of urt

obstructions in equineathletes – what lessonscan be learned from

the highspeedtreadmill?

J. Geoffrey Lane BVetMed DESTS FRCVS

Department of Clinical VeterinaryScience, University of Bristol, LangfordHouse, Langford, Bristol, BS40 5DU

29


29

for the majority of equine clinicians in practice suchexaminations form the lynch-pin for diagnosis inhorses showing signs suggestive of dynamic URTobstruction, but how dependable are the findings?The best means to achieve a definitive diagnosis isto assess the patient while it is exercising vigor-ously.

The advent of highspeed treadmills and modern in-strumentation enables the simultaneous recordingof endoscopy of horses exercising at speeds up to16 m/sec. as well as respiratory sounds, volumeflow loops, end-tidal oxygen and carbon dioxide,minute volume, and oxygen consumption on a breathby breath basis.

Horses take to treadmill exercise surprisingly welland the technique is very safe provided that a rig-orous screening and familiarisation training rou-tine is adopted. At the University of Bristol over700 clinical cases have been investigated on thetreadmill with an excellent safety record. On ar-rival all horses are carefully screened for lame-ness so that no horse with current orthopaedic dis-ease is admitted to the treadmill trainingprogramme. A small number are also rejected onthe grounds of temperamental unsuitability.

Endoscopy of the URT is performed at rest and withthe history and palpation findings a tentative diag-nosis is made – this is compared later with the truediagnosis when the patient is tested at speed. Agradual process of introduction and training onthe treadmill takes place in three sessions over a48 hour period by which time horses are ready fora full test to the limit of their ability. Some centresuse a test routine which is dictated by the speed atwhich maximum heart rate is reached. At Bristol astep test is used which starts at 6.5 m./sec for 90secs before the speed is increased to 8 m./sec fol-lowed by increments of 1 m./sec every minute untilthe horse fails to keep up with the treadmill – thepoint of fatigue. All tests are conducted on a 10%slope and most horses reach the point of fatigue

between 11 and 12 m./sec but exceptional athletesmay reach 13 m./sec. The overall procedure oftreadmill testing is noisy and trainers who askwhether a ‘noise’ was heard from the horse duringthe test would otherwise be disappointed if it werenot for the simultaneous recording from a micro-phone placed in the face mask which also accom-modates sensors to measure other respiratory pa-rameters such as flow rates of the inspired and ex-pired air as well as its content.

The data from five hundred and fifty horses un-dergoing highspeed treadmill endoscopy (HSTE)have now been reviewed and the diagnosesreached were as follows: No upper respiratory tract abnormalityseen 123

Dorsal displacement of the soft palate(DDSP) 179

Palatal instability (PI) 145

Dynamic arytenoid cartilage collapse(ACC) 57

Vocal cord collapse (VCC) without ACC 16

Axial deviation of the aryepiglottal fold(ADAEF) alone 15

ADAEF with other forms of dynamiccollapse 55

Fourth branchial arch defects 7

Right sided ACC / VCC 3 Epiglottal entrapment 2

Epiglottal retroversion 2

Posturally dependent laryngeal collapse 1

30


30

The finding that malfunction of the soft palate con-stitutes the most frequent definitive diagnosis (324out of 550 horses) is consistent with previous re-ports (Morris and Seeherman, 1991; Kannegieterand Dore, 1995). This should come as no surpriseas it is now widely agreed that a diagnosis of DDSPcannot be made from endoscopic findings at rest.The report from the jockey is far more reliable!

Current opinion is that DDSP results from weak-ness of the palatal musculature and an inability onthe part of the horse to maintain an efficient oro-pharyngeal seal between the ventral aspect of thepalate and the dorsal aspect of the tongue. Onceair enters the oro-pharynx the palate becomesdestabilised like a wet sail and eventually sponta-neously moves to a position dorsal to the epiglot-tis.

There is some evidence that DDSP arises follow-ing upper respiratory tract infections and it is con-jectured that the innervation to the palatal muscles– the pharyngeal branch of the vagus – is damagedby infection where it passes through the auditorytube diverticulum and lies immediately under therespiratory epithelium. In treadmill terms a pre-dictable sequence of events occurs leading up toDDSP.

This commences with billowing movements by themore rostral portion of the soft palate correspond-ing to separation of the oro-pharyngeal seal, fol-lowed by flattening of the epiglottis against the cau-dal soft palate representing the opposition betweenthe contraction of the hyo-epiglotticus muscle andthe elevation of the palate by the air ventral to it.Eventually the free border of the palate slips fromunder the epiglottis and vibrates causing obstruc-tion particularly during expiration and there is animmediate dramatic reduction in ventilation.

One aspect of the study of the horses referred tothe University of Bristol’s Equine Sports Medi-cine Centre was to compare the RLN gradings of

horses examined at rest on arrival with the diagno-sis achieved by endoscopy on the treadmill - 459horses were reviewed for this aspect of the study.(Franklin, 2002).

82 Grade 1 at rest yielded 1 Arytenoid cartilagecollapse (ACC) ontreadmill

3Vocal cord collapse

(VCC)

256 Grade 2 at rest yielded 11 ACC

4 VCC


9 VCC


0 VCC

6 Grade 5 at rest yielded 6 ACC10 Others

Thus, in a population of horses which were referredfor the investigation of poor performance, often witha history of abnormal respiratory noise, only 29 /82 (35%) animals with Grade 3 RLN at rest wereconfirmed to show dynamic collapse of the leftarytenoid cartilage and/or vocal fold during tread-mill exercise. Four horses out of 23 (17.4%) with aGrade 4 score at rest and would have been expectedto show dynamic collapse on the left side of thelarynx showed consistent near-symmetrical abduc-tion throughout HSTE and were spared unneces-sary laryngeal surgery. These results also show thatthere were isolated cases (19 / 338 – 5.6%) wherehorses showing ‘normal’ laryngeal motility – Grades1 and 2 - during quiet breathing showed dynamicarytenoid or cord collapse under exercise condi-tions. In all cases there was palpable wasting ofthe laryngeal musculature on the left side and thepatients made progressive ‘roaring’ noises at exer-cise.

31


31

To the unaided human ear the inspiratory noisesproduced by horses afflicted with axial deviationof the ary-epiglottal folds (ADAEF) is not distin-guishable from the ‘roaring’ or ‘whistling’ associ-ated with RLN. In this series of 550 horses therewere 15 horses with ADAEF and no other concur-rent form of dynamic collapse in the URT, 44 whereit was associated with palatal malfunction, 7 wherethere was concurrent dynamic collapse of thearytenoid or vocal fold and 4 where it was the ma-jor source of airway obstruction in cases of fourthbranchial arch defect. The cause of ADAEF is notknown. The tissue which shows dynamic collapseis not muscular and represents the lateral exten-sions of the glosso-epiglottic mucosa. Thus, simplestretching of the mucosa seems to be responsiblealthough it is unclear why some horses showADAEF and others exhibit epiglottal entrapment.

There is a tendency in clinical practice to makesimple single diagnoses but HSTE has shown thatdynamic collapse in the equine upper respiratorytract is often complex with multiple sources of ob-struction. On the other hand the traditional assump-tion that RLN and DDSP often go together holdslittle water. Only 17 of the 73 (23.3%) horses withcollapse of the arytenoid cartilage and / or vocalfold showed concurrent palatal malfunction – DDSPor PI.

HSTE has led to an improved understanding of thedynamics of previously recognised disorders suchas recurrent laryngeal neuropathy, epiglottal entrap-ment and dorsal displacement of the soft palate.However, it has also led to a broadened repertoireof diagnoses so that dynamic obstructions of theURT which cannot begin to be identified duringquiet breathing can now be recognised. Terms suchas dynamic collapse of the pharyngeal walls or axialdeviation of the ary-epiglottal folds (ADAEF), ret-roversion of the epiglottis, posturally dependent la-ryngeal collapse and dynamic rostral displacementof the palatal arch can now be added to the equineclinician’s vocabulary, and no doubt there will be

more to come!

An understanding of the aetiopathogenesis of pala-tal instability and dorsal displacement of the softpalate is far from complete. A combination of analy-sis of pharyngeal dynamics in naturally occurringcases of DDSP and PI during HSTE and experi-mental surgery suggests that weakness of the pala-tal musculature and a failure to maintain an effec-tive oro-pharyngeal seal is responsible. The epig-lottis appears to be an innocent party in the onset ofDDSP and surgical techniques which interfere withthe epiglottis are irrational.

The role of palate resection surgery (staphylectomy)is also dubious other than as a means to reduce thevolume of tissue contributing to the overall expira-tory obstructive effect of the disorder. The use oftechniques which increase the tension in the oralaspect of the soft palate by partial thickness resec-tion (Ahern procedure), cautery or the injection ofsclerosis chemicals has become fashionable. Thesemay improve the stability of contact between theunderside of the palate and the upper surface of thetongue but they only involve a thick layer of glan-dular tissue.

No technique has been devised which will makethe muscles of the palate stronger and this being thecase all are doomed to have a have a “success”rate of about 60%. One group of patients worthyof specific comment consists of those which “quitout” abruptly in races and on the treadmill developPI. It has been suggested that these horses have ex-perienced DDSP in the past and are pre-emptingthe partial asphyxiation which accompanies it bystopping once the initial stage of palatal weaken-ing has been sensed.

Clearly not all horses which show poor or deterio-rating performance and/or which make untowardrespiratory noises at exercise can or should be re-ferred for HSTE. The selection of horses for thistechnique should include those patients where the

32


32

noises heard at exercise cannot be explained bythe findings of palpation or endoscopy; horseswhich fade abruptly in races without abnormal res-piratory sounds; horses where previous airway sur-gery has been unsuccessful; and horses which havebeen subjected to nerve-muscle pedicle graft sur-gery to ameliorate RLN and where the outcomecannot satisfactorily be evaluated during quietbreathing.

References

Franklin, S.H. (2002) Studies of dorsal displace-ment of the soft palate in Thoroughbred racehorses.PhD Thesis, University of Bristol.

Kannegeiter, N.J. and Dore, M.L. (1995) Endos-copy of the upper respiratory tract during tread-mill exercise: a clinical study of 100 horses. Aus.vet.J. 72, 101 – 107

Morris, E.A. and Seeherman, H.J. (1991) Clinicalevaluation of poor performance in the racehorse:the results of 275 evaluations. Equine vet. J. 23,169 - 174

33


33

Control ofVeterinary Drugs

R Sykes, Department of Pharmacologyand Toxicology, Faculty of Veterinary

Science, University of Pretoria, PrivateBag X04, Onderstepoort, 0110.

The need for control of drugs:• Protect patient and public• International requirement of trade• Promote availability of new drugs

The purpose of control• Ensure availability of effective and safe drugs• Regulate supply and use of drugs• Control manufacture and quality• Monitor adverse reactions

Definition of Stock Remedy Act 36:Any substance or mixture of substances, intendedor offered to be used in connection with “animals’for the diagnosis, prevention, treatment or cure ofany disease, infection or other unhealthy condition,or for the maintenance or improvement of health,growth, production or working capacity, butexcluding any substance in so far as it is controlledunder the Medicines and Related SubstancesControl Act 1965, (Act 101 of 1965).

Definition of Veterinary Medicines Act101:“Any substance or mixture of substances, other thana stock remedy or farm feed registered in terms ofAct 36, used or purporting to be suitable for use ormanufacture or sold for use in connection withvertebrates, for the treatment, diagnosis, preventionor cure of any disease, infection or other unhealthycondition, or for the maintenance or improvementof health, growth, production or working capacity,

or for curing, correcting or modifying and somaticor organic function, or for correcting of modifyingbehaviour.”

In addition, the conditions of supply and use ofveterinary medicines, selling and administration,supplying and drug control will be discussed.

34


34

35


35

36


36

Standing surgery of theequine paranasalsinses – when and

where should we makeholes in horses’ heads?

J.Geoffrey LaneBVetMed DESTS FRCVS

University of Bristol, Department ofClinical Veterinary Science,

Langford House, Langford, BRISTOLBS 40 5DU, United Kingdom

INTRODUCTIONThe clinical signs associated with diseases of theparanasal sinuses of the horse include nasal dis-charge, which may be mucoid, purulent,haemorrhagic or a combination of these, facialswelling and obstructive dyspnoea. Expansive le-sions in this area may produce facial swellings orobstruct nasal breathing and on occasions will dis-place orbital tissues resulting in exophthalmos. Itis exceptional for a sinus disorder to extend cau-dally into the cranium to provoke central nervoussigns. Nevertheless, the discomfort associated withsinu-nasal disorders may be responsible forbehavioural changes in some. The intranasal struc-tures are richly vascular and it is not surprisingthat trauma and destructive conditions frequentlylead to epistaxis.

The purpose of this contribution will be to com-ment on three more recent developments which areapplicable in clinical practice: (1) *** the diag-nostic value of direct sinus endoscopy, (2) *** thetechnique of frontal flap surgery performed on thestanding horse and (3) *** intralesional treatmentof progressive ethmoidal haematomas.

ANATOMICAL CONSIDERATIONSThe paranasal sinuses of the horse are extensiveair-filled spaces lined by mucoperiosteum. Thehuman nasal mucosae produce in excess of 0.5 litresof mucus daily and thus it is reasonable to suggestthat the paranasal sinus lining of the horse secretesseveral times this volume. The normal removal ofmucus is a dynamic process depending onmucociliary flow to the drainage ostia which donot lie at the lowest points in the sinuses. Once thenasal meati are reached mucus is lost by a combi-nation of evaporation and further mucociliary flowtowards the nasopharynx. The aetiopathogenesisof primary sinusitis in horses hinges on stagnationof mucus in the sinus cavities through inhibition ofdynamic clearance. Other sinu-nasal disorders suchas space-occupying conditions produce secondaryempyema by physical obstruction of the drainageostia.

The five paired paranasal sinuses of the horse are:

1) Frontal/conchofrontal2) Caudal maxillary3) Rostral maxillary4) Ethmoidal5) Sphenopalatine

The frontal sinus is divided into conchofrontal(CFS) and frontal (FS) portions. Drainage takesplace through the fronto-maxillary foramen into thecaudal maxillary sinus (CMS). The ethmoidal andsphenopalatine sinuses also drain via the CMS intothe middle nasal meatus. The rostral maxillary si-nus (RMS) has an independent drainage ostium,again into the middle nasal meatus. The RMS isdivided into a lateral bony and a medial turbinateportion within the ventral conchus (ventral conchalsinus, VCS). These are separated by the infra-or-bital canal and a sheet of bone joining it ventrallyto the roots of the cheek teeth. It can be seen that inthe young horse the lateral bony compartment islargely occupied by the roots of the cheek teeth andthat, regardless of age, the VCS is not easily acces-

37


37

sible for surgery or for direct endoscopy other thanvia the floor of the CFS. A thin-walled bulla ofthis compartment extends caudally into the CMSand can be appreciated on radiographs.The roots of cheek teeth 4, 5 and 6 lie within themaxillary sinuses: these are most prominent in younghorses and recede towards the floor of the sinuseswith age. The roots of CT3 form the rostral wall ofthe RMS. Surgical dental extraction proceduresmust take account of vital structures such as thenasolacrimal canal, infra-orbital canal and the an-gular atery and vein .

OBJECTIVES OF MANAGEMENTThe management of sinus diseases of the horse de-pends upon a decision-making process with clearlydefined objectives: to identify and eliminate thecause of disease, and to restore function.

1) Identification of the primary sinusdisorder:The principle diagnostic procedures to investigatesinu-nasal conditions comprise external assessment,radiography, endoscopy via the nostrils, direct en-doscopy through the sinus wall, exploratory sur-gery and biopsy. An accurate case history is in-valuable and particular note should be made of pos-sible contact with infectious respiratory diseaseand of the duration and nature of any nasal dis-charge. It is unusual for sinusitis to be bilateraland it is logical that the discharge will be largelyunilateral whenever its origin lies rostral to the cau-dal limit of the midline septum. Even when a horseis presented with unilateral epistaxis enquiriesshould be made regarding possible associationswith exercise to eliminate a diagnosis of EIPH.Epistaxis due to guttural pouch mycosis may beacute and, even if episodic, the course of the his-tory is unlikely to exceed 3 weeks. Progressive eth-moidal haematoma (PEH) is a more likely expla-nation when episodes of epistaxis span a longerperiod, especially if the blood is not fresh. A foetidnasal discharge points to suppuration but this couldarise from a wide range of chronic sinus lesions.

Horses involved in steeplechasing, hurdling, showjumping or eventing may become unreliable jump-ers in the face of sinusitis, presumably reflecting apainful jarring sensation on landing.

A External assessmentThe facial area should be inspected for evidenceof deformity of the supporting bones through swell-ing or trauma. Percussion of the walls of theparanasal sinuses is an unreliable technique but in-creased resonance may be perceived when thewalls become thin or dullness may develop whenthe sinuses are completely filled by fluid or softtissue. The airflow at each nostril should bechecked to assess obstruction of the nasal meati.The clinical crowns of the cheek teeth are exam-ined for the presence of fracture, displacement orimpaction of degenerate ingesta. The patency ofthe nasolacrimal duct can be checked bycatheterisation and infusion of saline solution fromeither end.

B RadiographyThe excellent contrast which exists between air,bone and teeth makes the sinu-nasal region a goodtarget for diagnostic radiographs.

C EndoscopyThe endoscopic examination of the nasal area isperformed in two ways. First, by conventional pas-sage of the instrument into the nasal meati and, sec-ond, by direct inspection of the sinus contents withthe endoscope passed through a small trephine hole.It is not exceptional for major abnormalities to beidentified by direct endoscopy into the sinuses whenconventional examinations per nasum have revealedlittle untoward. All endoscopy of this region isbest performed on the standing horse because ori-entation is straightforward and the nasal tissues ofthe recumbent animal become discoloured and en-gorged.

Endoscopy via the nose may reveal changes suchas narrowing of the nasal meati; distension of the

38


38

ventral or dorsal conchi reflecting filling of the ven-tral conchal and concho-frontal sinuses respectively;the presence of a soft tissue mass such as an ethmoi-dal haematoma; discharge streaming from the sinusdrainage ostium; and mycotic plaques on the surfaceof the conchal mucosa.

*** Direct sinus endoscopy (DSE)

It is generally not possible to pass an endoscopethrough the drainage ostia of the paranasal sinusesunless there has been distortion by surgery or chronicdisease. Thus, it is perfectly possible for sinus dis-orders to remain undetected by endoscopy per nasumand for an incomplete diagnosis to be made unlessthe contents of these airspaces are inspected directly.

Indications for direct sinus endoscopyThe sinus compartments which lend themselves bestto DSE are the caudal maxillary (CMS), the true fron-tal (FS) and the concho-frontal (CFS) sinuses. Theseare inter-connected via the fronto-maxillary foramenand, coincidentally, share a common drainage os-tium to the middle nasal meatus.

The presence of blood, pus or mucopus emergingfrom the caudal area of the middle meatus estab-lishes the sinuses as the source of a nasal dischargeand yet there may be no other evidence of disease toidentify by endoscopy of the nasal structures. Forexample, in cases of ethmoidal haematoma or myco-sis confined to the sinuses. PEHs may arise from thenasal aspect of the ethmoturbinates, in which casethey will be available for diagnosis by endoscopyper nasum, or on the sinus surfaces, in which casethey will not. A complete diagnostic evaluation forPEH requires that four sites are checked, i.e. en-doscopy via left and right nares, and left and rightDSE even when the clinical signs are unilateral.Mycotic infections of the nasal region produce de-structive changes but may be confined to the liningof the sinuses. Surprisingly, the changes on radio-graphs are often minimal and endoscopy via the narescan be unrevealing unless the mycotic plaques have

destroyed through the conchi to the nasal surfaces.Thus, DSE is indicated for those horses which showa persistent, unilateral, low-grade, malodorous na-sal discharge with non-specific findings on radio-graphs.

Technique and equipment for DSEAlthough there are reports of the use of rigidendoscopes, i.e. arthroscopes, for DSE and a vari-ety of entry points have been suggested, the authorhas found that flexible equipment passed into theCMS provides a simple and effective approach. Aflexible gastroscope with an external diameter of7.5 - 9.0 mm is suitable but, of course, a trephinewith a slightly larger diameter is also needed.

A linear rather than circular incision is used so thatit can be closed with sutures if there are negativefindings within the sinuses, but a treatment cathetercan still be placed if required. The incision is madeover the CMS, bisecting the angle between the bonymargin of the orbit and the facial crest. The perios-teum is cleared in the usual way. Care is requiredto make sure that the bony edges are smooth forfear of damage to the outer covering of the endo-scope. Strict asepsis may not be possible but thedistal section of the endoscope should be thoroughlycleaned and surgical spirit is applied immediatelybefore introduction into the sinus.

Endoscopic findings during DSEThe normal landmarks which are readily identifi-able include the roots and reserve crowns of thefifth and sixth cheek teeth in the foreground ven-trally; the infra-orbital canal running horizontallyabove the tooth roots; the bulla of the RMS ros-trally; the wide fronto-maxillary foramen in the mid-dorsal field and through this the leaves of theethmoturbinates. The FS and CFS can be inspectedby advancing the endoscope through the fronto-max-illary foramen.

DSE is not normally required in cases of primarysinusitis, but inflammation of the mucosal lining and

39


39

the pooling of a mucus-based discharge ventrallywould confirm such a diagnosis. Dental periapicalsuppuration produces such gross proliferativechanges around the tooth roots that the view forDSE is likely to be obscured and a specific diag-nosis may not be possible. Ethmoidal haematomasare usually obvious although the colour of the le-sions is very variable.

Care should be taken to inspect the dorsal aspectof the ethmoids in the FS where small lesions maybe overlooked. Large lesions on the nasal surfacesof the ethmoids may distort the medial walls of thesinuses. Again, there is no diagnostic subtlety re-garding mycotic infections - these lesions produceobvious plaques from which material can be takenfor culture and typing. Less common lesions whichmay be seen by DSE include sinus cysts and neo-plasms - both conditions are more likely to be di-agnosed on the basis of radiographs and explor-atory surgery. However, in horses with suspectedneoplasia DSE offers a means to obtain represen-tative tissue samples for pathological interpreta-tion.

The rostral maxillary sinus (RMS) is not easilyamenable to DSE because of the position of theinfra-orbital canal as well as the reserve crownsand roots of the cheek teeth. Also, there are mini-mal indications to inspect the contents of this com-partment. The exception might be chronic empy-ema but frankly this is far better dealt with usingthe standing frontal flap technique described be-low.

2 Return of a normal drainage systemor creation of alternative drainagethrough a sinu-nasal fistula:Non-surgical methods to manage sinusitis includeantibiotics, mucolytics, steam inhalations, volatileinhalations and continued exercise. The objectiveis the return of normal mucociliary clearancemechanism. Simple trephination has similar inten-tions with the addition of irrigation, possibly in-

cluding topical antibiotic agents, to clear stagnantmucus and eliminate secondary infection.

In the face of chronic sinusitis, sinus cyst and PEHthe natural drainage system may be physically ob-structed. Fistulae can be made by removal of amedial section of the floor of the CFS or medialwall of the VCS so that there is free communica-tion between the sinus cavities and the nasal meati.Fistulation surgery can be highly haemorrhagic andshould not be attempted in the standing patient.

3 Adequate visibility for accuratediagnosis and surgeryThe miserable visibility conveyed by a traditionaltrephine hole can be greatly enhanced by directendoscopy as described above. However,frontonasal or maxillary flap surgery is requiredfor more extensive excisional procedures and toinspect the contents of the RMS.

*** Standing facial flap (SFF) surgery

Good access to the concho-frontal, frontal and max-illary sinus compartments can be achieved througha laterally based frontal flap approach performedwith the horse standing, under sedation and localanaesthesia and, at the very least, is a valuable ex-ploratory technique. SFF surgery is particularlysuitable to manage empyema of the RMS in horsesof all ages. The bulla of the RMS may bulge cau-dally into the CMS when it is inflated by pus andthis is easily punctured and partly excised. Thereis less haemorrhage with the standing approachbecause the postural change of anaesthesia isavoided and orientation is simple. The SFF ap-proach might also be used to ablate those ethmoidhaematomas which prove inaccessible by DSE andsome sinus cysts may also be removed by this ap-proach.

Technique for standing sinus flap surgery

The frontal area is clipped and prepared for clean

40


40

surgery in the normal manner and at the same timethe site for CMS trephination is also prepared forthe later placement of an irrigation catheter. Heavycontinuous sedation is provided using a detomidineand butorphanol combination administered in anintra-venous drip. Local anaesthetic is infiltratedbetween the skin and periosteum over the surgicalsite which is located over the CFS, avoiding theline of the naso-lachrymal duct. An incision is madethrough the skin and periosteum together and thisshould be fashioned at least 3 mm. wider than theintended bone incision. A 5.0 cm. trephine is idealto make the bone window but if this is not avail-able a series of smaller overlapping holes can beused in the style of Olympic-rings. On entry intothe CFS topic local anaesthetic is sprayed onto thelining.

Landmarks such as the ethmoidal turbinates, theinfra-orbital canal and RMS bulla are identified.The bulla can be punctured with the point of a fin-ger and as much of this structure as possible isresected with scissors and rongeurs. Haemorrhageshould be no more than slight but trauma to the me-dial wall of the exposed VCS should be avoided.Inspection of the sinus contents is followed by ab-lation of localised lesions, lavage of inspissatedpus and the placement of an irrigation catheter. Theskin/periosteum incision is closed in a single layerwith a combination of sutures and staples. Althoughthe disc of trephined bone is rejected, the cosmeticresults are generally good.

ResultsIn a series of 60 cases (Quinn and Lane, 2004, inpress) the overall rate of resolution of sinus disor-ders following SFF surgery has been comparableto the results achieved by more radical surgery per-formed under general anaesthesia. The findings con-firmed by this technique included empyema of theRMS (22 cases – 14 with inspissated pus),generalised chronic sinus empyema (10), mycoticsinusitis (8), PEH (6), sinus cyst (4), dental apicalinfection (4), neoplasia (3), ethmoidal abscessation

(1), bone sequestration post-trauma (1) and an un-specified osseous reaction (1). Secondary surgeryunder anaesthesia was required in only 6 horses,generally to create a sinu-nasal fistula when drain-age via the natural ostium continued to be ineffec-tive.

Facial flap surgery under anaesthesia

Fronto-nasal or maxillary flap surgery under gen-eral anaesthesia is required for more extensive andhaemorrhagic procedures such as the removal ofsinus cysts, large PEHs and selected tumours as wellas for fistulation techniques. Fistulae can be madebetween the sinus cavities and the nasal meati butthis may provoke major haemorrhage and cannotbe performed safely with the horse standing. In sur-gical practice the fistulae described provide con-venient routes by which to lead sock-and-bandagepressure packs to the nostrils (see below).

4 Control of HaemorrhageSinus surgery is bloody surgery - haemorrhage in ahighly vascular area is exaggerated by the posturalchange in an anaesthetised horse. Care must be takento provide circulatory support by aggressive intra-venous fluid administration although whole bloodreplacement is rarely necessary. Hypotensive an-aesthetic agents are not desirable when prolongedsurgery renders horses vulnerable torhabdomyolysis of the dependent limbs.

Temporary bilateral carotid occlusion can reducehaemorrhage and improve visibility during the in-traluminal stages of sinus flap surgery and comprisesthe pre-placement of snares around each commoncarotid artery which are drawn tight only for the15-20 minutes required to complete the intranasalstages of the surgery. However, the advantages ofslight haemorrhage reduction must be weighedagainst the disadvantages of prolonging the surgeryand also the risk during placement and removal ofthe snares of insult to the recurrent laryngeal nerveswhich run within the carotid fascia .

41


41

Pressure packing within the sinus cavities and na-sal chambers is essential to control haemorrhageon completion of the surgery and during the initialrecovery period, i.e. 48-72 hours. Sock-and-ban-dage packing consists of lengths of cotton bandage

packed into tubular stockinet socks. These are pre-pared ahead of surgery and 1-4 may be needed foreach operation. The open end of the stockinet isled to the nostril through a fistula created betweenthe sinus cavity and the nasal meati. On the third orfourth day after surgery the bandage is withdrawnand a day later the stockinet is removed.

5 Facilities for topical post-operativetreatment and monitoring of progressThe implantation of a Foley balloon catheter, typi-cally into the CMS, offers a convenient route forpost-surgical irrigation and medication. It must beappreciated that blood clots and devitalised tissueare inevitably left after all sinus surgery and op-portunist infections, frequently mycoses, are likelyto become established. Balloon catheters are rec-ommended as a routine to permit physical displace-ment of debris by irrigation and for topical medi-cation which should include an antimycotic agent -a portable pressurised garden spray is a practicalmeans of administration which is well tolerated bythe patients.

6. Early return to exerciseIn spite of the radical nature of some sinus surgicalprocedures an early return to exercise is to becommended as an integral part of treatment. Forcednasal ventilation increases the evaporation ofresidual discharges when stagnation mightotherwise encourage post-operative infections tobecome established.

7 Pleasing cosmetic resultThe cosmetic results of trephination and facial flapsurgery are both satisfactory as no more than a slightdepression at the operation site should result fromeither. However, it has been conceded above that

when a replaced bone flap heals without compli-cation, the cosmetic result is marginally superior.Occasionally after all sinus surgery proliferativesuture periostitis is seen, presumably as a result of

vibrations in the suture lines during trephinationor sawing.

Specific indications for sinus surgery inhorses:

1 Dental ExtractionThe traditional means to extract the cheek teeth isby repulsion and for maxillary CT 4 - 6 this meanstrephination through the paranasal sinuses. Check-ing the oro-antral fistula and sinus content is animportant part of nursing and thus the trephine holesshould be prevented from closure until the floor ofthe sinus has healed and secondary infection hasresolved. Dental extraction is one indication forsinus surgery where trephination is preferred andfacial flaps should be avoided. Once a flap hasbeen closed there is no access to the alveolus forinspection or curettage unless the flap is re-opened.

2 Acute SinusitisThe normal progress in the treatment of sinusitis isto use medical regimes initially. When these failand the diagnosis of sinusitis is confirmed byendoscopy and radiography and dental disease hasbeen ruled out, the treatment should progress to thenext level with trephination into the CMS in thecorner between the facial crest and orbital margin.This is performed with the horse standing underlocal anaesthesia. A Foley balloon catheter is placedfor direct irrigation and medication and the horseshould continue in moderate exercise.

3 Chronic SinusitisFailure of simple irrigation is seen as continuednasal discharge, possibly malodorous and arisesthrough necrosis of the sinus lining, inspissation ofpus and occlusion of the natural drainage ostia.Comprehensive radiographic and endoscopic in-

42


42

vestigation aims to eliminate other disease pro-cesses and if none is found standing facial flap sur-gery is indicated. Chronic primary sinusitis mustbe differentiated from sinusitis secondary to den-tal periapical suppuration.

4 Removal of Sinus CystsThey are expansive lesions, usually in the CMS orCFS, with a distinct wall and characteristicallycontain vivid yellow fluid. At facial flap surgerythey can be peeled away from the inside of the si-nuses. In the event of incomplete ablation smallareas of residual cyst tissue do not appear to causecomplications and the condition carries a goodprognosis.

5 *** Treatment of progressive ethmoidal haematomasProgressive ethmoidal haematoma (PEH) is a mul-tifocal disease of unknown aetiology which pro-duces expanding, discrete, soft tissue masses filledwith clotted blood which are attached to the sur-faces of the ethmoturbinates. Intermittent splittingof the overlying mucous membrane produces thespontaneous leakage of dark blood which is seenat the nostril. Although one mass may be larger thanthe others and account for the presenting clinicalsigns which may include obstructive dyspnoea aswell as epistaxis, it is rare for lesions to be soli-tary. Thus, most published surgical series on thetreatment of PEH report a significant recurrencerate but whether the secondary lesions are recur-rences at the original site or new lesions altogetheris far from certain. PEH is probably best viewedas a lifelong affliction for susceptible horses re-quiring tactical treatment as and when required.Thus, there has recently been a move away fromsurgical resection of PEH, unless the lesions arevery large, to ablation by intra-lesional injectionof necrotising agents. At least 14 years agoGottschallk was using of euflavin for this purposein South Africa but more recently 10% formalinhas become the agent of choice. The treatments areperformed trans-endoscopically using a bevelledcatheter passed through the biopsy channel and are

applied directly via the nose or in combination withDSE. Most lesions require more than one treatmentso that horses are re-examined and treated at monthlyintervals until clear of lesions. Even so it is quitelikely that episodes of recurrence will arise indefi-nitely.Complications are unusual.

6 Primary mycotic rhinitis and sinusitisAlthough mycotic opportunism is common after sur-gery or secondary to other suppurative conditionssuch as dental periapical abscessation horses areencountered where these infections arise on the sinu-nasal tissues without obvious underlying disease.Topical medication with the benzimidazole agentenilconazole has proved to be effective in theauthor’s experience and primary mycosis carriesan excellent prognosis. A Foley balloon catheter isplaced into the CMS in the usual manner and thesinus cavity acts as a reservoir for the medicationwhich is infused twice daily. Prolonged treatmentmay be needed.

7 TraumaFractures of the walls of the paranasal sinuses arecommon injuries to horses through kicks, falls, etc.They are generally comminuted and sometimes com-pound. The direct trauma causing the fractures pro-duces a depression of the fragments involved.Haemorrhage, emphysema, sequestration, second-ary sinusitis and disruption of the nasolacrimal ductare potential sequels. Each case must be individu-ally assessed and treatment ranges from conserva-tive antibiotic cover to aggressive surgery to con-trol haemorrhage, to remove detached bone frag-ments and to elevate depressed plates of bone intotheir normal alignment. A balloon catheter for irri-gation/medication should be considered when se-vere haemorrhage has been sustained and for allcases where the sinuses have been contaminated incompound fractures.

43


43

Angular Limb Deformities


GENERAL POINTSAngular limb deformities (ALD. refer to any de-viation of the limb from the normal axis. The de-viation may be either medial or lateral from theNormal sagittal axis of the limb.

Valgus:Lateral deviation of the distal part of the limb.Varus:medial deviation of the distal portion of the limb.

The potential locations are:metaphyseal growth plate (physis.epiphysiscuboidal bones of the carpus or tarsusmetaphysismetacarpal/metatarsal II and IV

The most common location is the metaphysealgrowth plate of the distal radius. Growth is asym-metric across the physis, occurring at a differentrate medial and lateral.

The joints affected in order of frequency are thecarpus, tarsus and metacarpophalangeal /metatarsophalyngeal.

The differential diagnoses are soft tissue laxity ofthe carpal or tarsal joints and fractures involvingthe joint.

AETIOLOGYThe factors which cause angular limb deformitiesto occur can be listed as follows:

1. Perinatal Factors:• Incomplete ossification of cuboidal bones. Os-

sification of the carpal and tarsal bones occurslate in gestation – 270 – 300 days. The bonesare normally rounded on radiographs.

• In dysmature foals ossification lags behind.There is more cartilage than bone. Physiologi-cal loading leads to deformation, and ossifica-tion leads to permanent distortion e.g. tarsal bonecollapse.

• Intrauterine posture.• Endocrine problems – hypothyroidism, vitamin

A?, copper deficiency, cuboidal bone collapse.• Flaccidity of the periarticular structures leads

to dynamic deformity, which is reducible. How-ever, if the foal is allowed persistent or exces-sive exercise, uneven loading of the osseusstructures may lead to permanent deformation

2. Developmental Factors:• Over or under balanced nutrition• Asymmetric forces on the physis or epiphysis• Excessive exercise with trauma to the growth

plate.• Overload of the limb due to contralateral lame-

ness.

As we consider this problem we must also con-sider the normal propensity for correction of thesedeformities, since many foals will correct an an-gular deformity with treatment as simple as re-stricted exercise or corrective trimming of the feet.

The physeal growth curve or the ability of thephyseal growth to respond to the forces places uponit is the likely explanation for the natural correc-tion seen in some individuals. Physeal cells thatare loaded more heavily, respond by growing faster.Those cells which are subjected to a lower load,grow more slowly. The above-described responseis the normal or physiological state when the loadis applied in an intermittent manner. In cases ofdeformity where the angulation is so severe, thatthe increase in load is constant (pathologic load-

44


44

ing. then the acceleration in growth does not occur.Relating the above to the real life situation, it wouldappear that this mechanism is active in the mildlyto moderately affected foal that corrects the defor-mity with conservative treatment. In the more se-vere cases, the physis in unable to adapt to the in-creased load, necessitating intervention in the formof surgical correction.

It is important to know when growth stops inthe physis.

In the Distal metacarpal physis growth is rapidbetween 4-6 weeks of age and had ceased by12 weeks.In the distal radial physis growth is rapid andceases by 15 months.The tibial physis closes by 12 months and themetatarsal physis by 7 weeks.

This means that if the physis closes, further cor-rection is impossible and may even be harmful.Fetlock deformities must be dealt with early andearly recognition is essential, medical approach isless effective.

Carpal and tarsal deformities can be managedmedically to start with. However, severe defor-mities have no chance to correct without interven-tion.

SignalmentAngular limb deformities are seen in neonates andnursing foals 0 – 4 months.

Clinical SignsThere will be visible varus or valgus deformity.The carpus, tarsus and fetlock joints are most com-monly affected. There may be a potential incitingcause such as an injury to the same or oppositelimb.DIAGNOSIS1. Physical examinationCarry out a visual assessment to define the loca-

tion/locations, e.g. carpal valgus and fetlock varus.Look for evidence of soft tissue laxity and injury orpain in the opposite limb, which results in exces-sive weight bearing.

2. Radiography: Allows determination of location and type of de-formity. In order to determine the degree of angu-lation, it is essential that most if not all the radiusand metacarpus are included. Because of concur-rent slight outward rotation of the limb, each forlimbshould be radiographed separately. Weight bear-ing and stressed viewsa. Dorso-palmar to assess angulation.b. Draw lines through the centre of the proxi

mal and distal long bones.The point of intersection will give the location.The location helps to determine treatment andprognosis.

c. Individual joint measurement.d. Lateral-medial: to assess the cuboidal

bones.

3. Potential locations of deformity are:-a. Joint area – physis, epiphysis, cuboidal bones,

splint bones.b. metaphysis or diaphysis (rare).

TreatmentThe treatment selected will be determinedby:-· Foal’s age.· Joint affected.· Severity of deformity

fracture Harris, Salter,

physis of closure premature

· Remaining growth potential (closure of the growthplate).

1.Conservative treatment: young animals withmild deformities.a. < 2 – 3 weeks fetlock

< 4 – 6 weeks carpus/tarsus.b. Stall rest with minimal exercise.c. Reduce food intake of mare.(d.Corrective trimming

45


45

Valgus – lower lateral wall and extend mdialwallVarus – lower the medial wall, extend la-teral wall.Corrective shoeing – glue on shoes.

2.Splinting or tube castingOnly used to treat soft tissue laxity.a. One must be able to manually straighten valgus

or varus deformity.b. Tube cast from elbow/stifle to just above the

fetlock.c. Splints may be easier to manage despite the need

for frequent bandage changes.d. Must bear weight to maintain strength in the ten-

dons.

3. Surgical Treatment

a. Growth Acceleration: Periosteal Transectionand Elevation.The mechanism of increased growth rate on the sideof surgery is unknown, but is thought to result frominflammation and increased blood supply, or tophysical release of tension on the periosteum. Theaim is to increase the growth rate on the shorterside of the limb. The surgery is simple and lowrisk.

I. Location – shorter side of the limb metaphysealside of the growth plate.i. Carpal valgus

distal lateral radius between the common andlateral digital extensor tendon

ii. Carpal varusmost medial part of the distal radius.

iii. Tarsal valgusdistal lateral tibia between the lateral and longdigital extensor tendons.

iv. Tarsal varusmost medial part of the tibia.

v. Fetlock varus or valgusDistal MCM/MTMlateal (valgus.

medial (varus.

II. Timing - While growth potential remains inthe growth plate.< 35 – 60 days distal MCIII / MTIII< 60 – 120 days distal radius and ulnaAfter this period of time some correction may beachieved with either or both of the surgical proce-dures; however, the prognosis given to the ownersmust be guarded for significant correction of thelimb deviation

III. Procedure – hemicircumferential periostealtransaction (periosteal strip.i. Vertical incision of skin and subcutaneous tis-

sue.ii. Inverted ‘T’ incision in the periosteum. The aim

is to elevate 180° circumference with the ‘crossof the ‘T’ +/- transection of the distal attach-ment of the vestigial ulna.

iii. elevation of the periosteum.iv. closure of subcutaneous tissue and skinv. light dressing.

IV Aftercare – restricted exercise until the limbstraightens.

V Advantages – simple, short, minimally invasivetechnique which will not over-correct. The proce-dure can be repeated.

(b.Growth Retardation: Transphyseal BudgingThe mechanism of growth retardation is physicalimpairment of growth on the longer side of the limb.

I. Location – the longer side of the limb across thephysis (from the metaphyseal to epiphyseal sides.i. Carpal valgus distal medial radiusii. Carpal varus

lateral distal radius between thecommon and lateral digitalextensor tendons.

iii. Tarsal valgus distal medial tibia.

46


46

iv. Tarsal varus most lateral part of the tibiabetween the lateral and longdigital extensor tendons.

v. Fetlock varus or valgusDistal MCIII/MTIIImedial (valgus.lateral (varus.

II. Timing - Use after the majority of growthpotential has been lost.

50 – 60 days - fetlock60 – 120 - carpus.

in foals with severe deformities.

III. Procedurei. Vertical or curvilinear incision over the area

of the physis or lateral.ii. Incise skin and subcutaneous tissue.iii. Locate physis with a hypodermic needle.iv. Place one screw in the metaphysis 1.5cm

proximal to the physis.v. Place a second screw in the epiphysis; be-

ware of joint and physis.vi. A figure of 8 wire is placed around the screws,

the ends are turned down and the screws tight-ened.

vii. Close the subcutaneous tissue and skin.viii. Radiographs should be taken intraoperatively.

Alternatively a transphyseal bridge can also be cre-ated using two large stainless steel staples or byusing a small plate across the physis

IV. Aftercare –prophylactic antibioticsstall restlimited exercise until the limb straightens.

The screws (staples or plate. are removed assoon as the limb is straight.

V. Advantages - The procedure can be performedwith minimal growth potential, i.e. if past maxi-mum growth potential or with severe angular de-

formity.

VI.Disadvantages – The procedure is moderatelyinvasive. A second surgery is required to removethe implants. It is possible to overcorrect ifprogress is not monitored carefully.

VII. Prognosis for Angular Limb DeformitiesGood: When treated early and the problem involvesphysis or epiphysis.Fair to Poor

with severe angulationwith multiple site involvementwith crushed carpal boneswith secondary degenerative joint diseasewith metaphyseal deformity

c. OsteotomyOsteotomy is usually reserved for severe deformi-ties of the metaphysis or diaphysis. The procedurewould usually be used for salvage purposes, as ath-letic ability is likely to be limited. This is a veryinvasive procedure with the potential complicationsbeing similar to those experienced with long bonefractures. These procedures must be very carefullyplanned to maximise the chances of a good outcome.

FURTHER READINGAuer J A, Martens R J, Morres E L (1982.Angular deformities in foals.Pt I Congenital Factors. Comp. Contin. Educ. Pract.Vet. 4 (8. 330-338.Pt II (1983. Developmental factors. Comp. Contin.Educ. Pract. Vet 5 (1. 27-35Bramley L R (1999.The science and art of angular limb deformity cor-rection. Equine Vet. J. 31: 182-183.Brauer T S, Booth T S, Riedsel E (1999.Physeal growth retardation leads to correction ofintracarpal angular deviations as well as physealvalgus deformity. Equine Vet. J. 31 193-196.Metlwraith C W, Turner A S (1987.Equine Surgery: Advanced Techniques. Lea andFebiger, Philadelphia 120-132.

47


47

48


48

The Surgical Management of

the EquineColic Case –

General PointsBarrie Edwards,

University of Liverpool

Colic surgery is a team effort and the chances ofsuccess are greatest when the optimum number ofpeople and back up facilities are available.

As stated previously, the patient in abdominal cri-sis is either in shock or predisposed to it and ide-ally should not undergo laparotomy until all itsphysiological parameters are within normal limitsand the gastrointestinal tract has been decom-pressed. However, this is rarely a practical propo-sition. A balance between restoration of blood vol-ume and complete rehydration must be found be-cause if the whole of the calculated fluid deficit isgiven before anaesthesia, a substantial proportionwill diffuse into the lumen of the intestine beforethe obstruction can be relieved. This will not onlybe lost from the circulation but it will also makethe surgery more difficult. It is therefore advisableto administer as much balanced electrolyte solu-tion as possible during preparation for surgery andthen to restore the remainder during the operationonce the obstruction is relieved. This approach issatisfactory for horses with relatively mild defi-ciencies in circulating blood volume. However,acute restoration of the circulation in horses in se-vere shock is best achieved using hypertonic sa-line; 4ml/kg of 7.5% saline given rapidly before

induction of anaesthesia draws fluid into the circu-lation as well as increasing cardiac contractilityand output. The effect can be dramatic and lastswell into the surgical period during which isotonicsolutions are administered as usual.

It is generally agreed that the prognosis depends toa large extent on the duration of the operation whichshould be performed as expeditiously as possiblewithout sacrificing a good surgical technique.Whenever possible, the ventral abdomen should beclipped beforehand to reduce to a minimum the in-terval between induction and the first incision. Thisis particularly important in those horses with se-vere abdominal distension, where rapid decompres-sion of the large intestine is essential if the patientis not to succumb to respiratory embarrassmentcaused by pressure on the diaphragm. The passageof a nasogastric tube and evacuation of fluid stom-ach contents prior to induction reduces the risk ofgastric rupture, regurgitation and aspiration of fluid.

Premedication and anaesthesia

The anaesthetist frequently has to contend with theresidual effects of a variety of drugs (e.g. seda-tives, narcotics and spasmolytics) which have beenadministered between the onset of colic and refer-ral for surgery. Colic patients are often quiet anddepressed, but when sedation is required, the al-pha-2 agents are the drugs of choice. Xylazine maybe preferable to detomidine as it is shorter acting,but small doses of detomidine (5-10 mg/kg) mayalso be used.

Induction and MaintenanceThe objective should be to achieve:· smooth induction so that the horse sinks quietly

to the ground· A similarly smooth recovery a relatively short

time after completion of surgery

A variety of drugs and dose rates may be used de-

49


49

pending on the preference and experience of theanaesthetist and the state of the patient. Whicheverinduction technique is chosen, it is important it isone with which the anaesthetist is fully familiar andit must be remembered that in toxic patients thedoses required of any depressant drug will be con-siderably reduced.

The main requirements of anaesthetic maintenanceare similar to any procedure except there is muchgreater emphasis on fluid replacement.· Progress should be assessed by regular moni-

toring of PCV and plasma protein· Arterial blood pressure, mucous membrane

colour and capillary refill time (CRT) providevaluable information as to the efficiency of thecirculation.

· Cardiac support with the inotropes dopamine ordobutamine is widely accepted as effectivetherapy whenever hypotension is evident.

Respiratory depression may be a problem in thehorse with colic, but the relative merits of positivepressure ventilation and spontaneous respirationmust be balanced for each individual concerned.

Blood gas analysis, if available, will enable theexistence and degree of acidosis or alkalosispresent to be determined. In the absence of meansof blood gas measurement, it is reassuring that oncefluid therapy, kidney function and hepatic circula-tion are restored, the body rapidly adjusts its acid/base deficit.

Recovery from AnaesthesiaIf colic surgery has been successful in resolvingthe problem, the horse is usually remarkably calmin the recovery period.

Laparotomy (Celiotomy) Technique

The ventral midline approach is used now almostuniversally for colic surgery.· The incision allows easy, rapid access to the

abdominal cavity with the minimum ofhaemorrhage

· Great latitude of access and exposure of the vis-cera is possible, an important factor when weconsider the frequency with which laparotomiesare performed without the exact site of the ob-struction being known.

· Adequate draping is necessary to protect the sur-gical field.

· The abdomen and legs of the patient are cov-ered with a large cotton drape and the area ad-jacent to the incision is further protected withwaterproof, plastic sheeting.

The initial incision is made accurately in the mid-line extending cranially from the umbilicus for16cm. This can be extended if necessary.

In order that a lesion does not go undetected in this,the largest and most complex of the body compart-ments, it is imperative that a routine, systematicexploration be employed.· Much of the search is conducted virtually at

arm’s length; correlating palpable findings withthe surgeon’s knowledge of anatomical relation-ships. An accurate command of both normal andpathological anatomy is a considerable advan-tage.

· On incising the peritoneum the colour and char-acter of any effusions, the distribution pattern ofdistended bowel and any discerniblediscolouration of visceral or peritoneal surfacesshould be noted.

· If gas- or fluid-filled bowel is ballooning out ofthe abdomen, some decompression of the ali-mentary tract will be necessary before explora-tion can commence. In addition to facilitatingexploration, decompression reduces intra-ab-dominal pressure, encourages peristalsis andsimplifies closure of the abdomen.

· Decompression of the caecum, which can bepartially exteriorised, can be quickly achievedusing 16 gauge needle attached to a suction line.

· Removal of gas from the large intestine is fre-

50


50

quently necessary in situ by needle suction be-fore any attempt can be made to exteriorise it.

· Lifting distended, sometimes friable, large co-lon must be done very carefully to avoid rup-ture.

· Evacuation of its contents is carried out by plac-ing the pelvic flexure between the horse’s hindlegs, preferably on a colon tray, and performingan enterotomy in the terminal part of the left ven-tral colon. Dry contents are flushed from thelumen using a hose introduced up the left dorsaland ventral parts in turn via the enterotomy in-cision.

· Decompression of the small intestine can beachieved by stripping its contents into the cae-cum.

· When most of the small intestine is severely dis-tended, decompression must be carried out insections commencing distally. This means thatthe distal jejunum and ileum will be handledseveral times.

Gentle handling and ample lubrication with warmHartmann’s solution will minimise trauma andthe risk of ileus. The caecum can be evacuatedof the large volume of fluid it contains via anenterotomy incision at its apex.

· The initial gentle sweep of the abdominal cav-ity serves to check the sites of commonly oc-curring obstructions.

· Palpation is aimed at detecting firm masses,fluid distension and impaction or tympany of thelarge intestine. Abrupt changes in direction ofintestine, tight mesenteric bands around or acrossintestine, or immobility of normally mobile por-tions of intestine indicate an area of involve-ment.

· If palpation fails to disclose the problem, thebowel must be exteriorised to facilitate visualexamination.

· Normal small intestine can easily be exteriorisedexcept for the proximal

1 metre and the terminal 15-20cm.· The apex and part of the body of the caecum can

be lifted out, as can the left ventral and dorsallarge colon, and parts of the right dorsal and ven-tral colon.

· The proximal 60-70cm of the small colon andthe rectum are inaccessible.

· Location of the obstruction can be achievedquickly and with less trauma to the intestine ifthe manipulation is commenced at the distalempty portion of the bowel and continues proxi-mally. The terminal reference point of the seg-ment of bowel which appears to be involvedshould be located, namely the ileum for the smallintestine and the pelvic flexure or proximal smallcolon for the large intestine.

Examination of the Small Intestine

· The ileum can be located by exteriorising thecaecum and turning it backwards to reveal thedorsal band which bears the ileocaecal fold. Ifthis fold is traced downwards to the lesser cur-vature of the caecum, it will lead to the ileumwhich is instantly recognised by the ileocaecalfold on its mesenteric border.

· If it cannot be exteriorised, the ileum must beinvolved in the obstruction.

· Compared to the remainder of the small intes-tine, the ileum is involved in a wide variety ofobstructive conditions to a disproportionate de-gree and in these patients the cause of the ob-struction will be quickly identified.

· If the ileum is not involved, the empty flaccidintestine is traced proximally until the obstruc-tion and distended bowel proximal to it arereached.

· Each length of bowel examined is returned tothe abdomen as the adjacent bowel is lifted out,and a rough check is kept of the length exam-ined.

· Eventually, in the absence of obstruction, the nextpart of the small intestine which cannotexteriorised will be the duodenum.

51


51

Examination of the Large Colon

· Obstruction of the large intestine can usually beanticipated prior to laparotomy on the basis ofthe physical examination.

· Segments of large intestine are more easily dif-ferentiated on the basis of their appearance andposition than are those of the small intestine.

· By taking note of the pattern and extent of thedistension of the various parts, and taking intoaccount the common causes and sites of obstruc-tion, the location of the problem can be deducedwithout too much expenditure of time or energy.

· The caecum again serves as a landmark for theinitial exploration. If its base and ventral longi-tudinal band cannot be palpated, a caecocaecalor caecocolic intussusception should be sus-pected.

· If the caecum can be exteriorised, the caecocolicfold is found and followed to the right ventralcolon. This can then be traced cranially to thesternal flexure and then caudally to the pelvicflexure which is another easily recognisable partof the large colon. From there it can be fol-lowed back to the diaphragmatic flexure and onto the transverse colon cranial to the root of themesentery. The transverse colon which is shortin length and fixed in position constitutes anabrupt constriction of the lumen and change indirection.

Evaluation of Gut Viability

The surgery necessary to relieve obstruction mayvary from simply incising a constricting band oftissue to resecting several metres of intestine. Thedecision as to the necessity for resection and thelength of bowel which needs to be removed oftendepends on a subjective assessment of bowel func-tion.

· Any intestine or abnormal colour, decreasedmotility or thickened appearance must be con-

sidered suspect.· After correction of obstructions causing second-

ary vascular embarrassment, observation of thebowel for 5-10 minutes for the return of colour,peristalsis and pulsation of vessels will aid indeciding for or against resection.

· The junction between viable and compromisedbowel may be difficult to discern especially af-ter displacement has been corrected and a sig-nificant improvement in the appearance of thebowel has taken place. Making a small incisionin questionable bowel to determine how easilyit bleeds and the appearance of the mucosa isfully justified.

Such clinical assessment of viability is not uni-formly reliable and its accuracy has been put aslow as 36%. The use of these criteria become morebeneficial with experience. It has been shown ex-perimentally that following release of jejunal liga-tures applied 50 minutes earlier, progressive de-generation continued even though there was grossevidence of perfusion and muscular activity soonafter release. A number of alternative techniqueshave been investigated.

· The most popular clinically applicable methodsof evaluating intestinal viability measure tissueperfusion by some direct or indirect method.Unfortunately, ischaemic damage can occur atthe cellular level in spite of apparently adequateperfusion and can be impossible to discern in-tra-operatively.

· Intravenous fluorescein and Doppler ultrasoundhave been the most reported methods of detect-ing local perfusion of segments of bowel. Ex-perience is needed to use either method.

· Fluorescein dye injected IV (6.6-11 mg/kg) israpidly distributed to all perfused tissues. Theserosal surfaces become yellow/green within 60seconds and emit a yellow fluorescence whenilluminated with long wave ultraviolet light. Itis important to compare the segment being evalu-ated with unaffected small intestine or colon.

52


52

When reduced fluorescence is generalised, littlecredence can be placed upon the procedure.

· The Doppler probe senses the passage of bloodthrough vessels within the wall of the intestine.Signals from arterial flow in any form are con-sidered to indicate viable bowel, with clinicaland experimental evidence indicating a highdegree of accuracy. One limitation is that theprobe has to be placed in the exact area to beevaluated. When compared to sodium fluores-cein fluorescence, the Doppler is generally nobetter in detecting non-viable segments.

· Surface oximetry measures the oxygen tension(mmHg) where the oxygen probe contacts thetissue surface. The PO2 on the surface of thebowel (Ps02) depends upon diffusion distancefrom the nearest vessel, local O2consumption,arterial Pa02 and local blood flow. Measure-ment of Ps02 gives a qualitative estimate of tis-sue oxygenation beneath the 3 mm electrode.Applied to ischaemic bowel, values are com-pared to normal bowel and to Pa02.

In summary, evaluation of bowel viability remainsa perplexing surgical dilemma and at present thereis no reliable method available. False interpreta-tion of intestinal viability can result in continuedshock, ileus, peritonitis and death or, less dramati-cally, but equally disappointing, in adhesion for-mation and secondary obstruction. Therefore, inequivocal cases, the surgeon should choose to re-sect suspect bowel rather than risk leaving com-promised bowel in situ.

Resection of Small Intestine

A physiological limit of small intestine resectionhas been identified in the horse. Ponies in which50% of the small intestine had been resected main-tained their pre-surgical weight. These findingscorrelate well with clinical experience which sug-gests that in all but exceptional cases 8 metres is

the maximum length which should be removed.

Resection and anastomosis.

· Resection and anastomosis of the jejunum in thehorse is simplified by the long mesentery, theclearly visible blood vessels for ligation and theintestinal calibre which allows ample inversion.

· It is widely accepted that, when technically fea-sible, an end-to-end anastomosis is the simplestand most physiologically compatible method.

· Whenever possible the fluid-filled ischaemicbowel should be isolated with intestinal clampsbefore manipulation is begun. If not containedin this way, toxic fluids will reflux into normalintestine and be absorbed, resulting in rapidphysiological deterioration of the patient. Fail-ing that, the gut should be clamped as soon as itis freed.

· A suitable site for resection can subsequently bechosen proximal and distal to the strangulatedbowel.

· The mesenteric vessels to the compromisedbowel are double ligated, the ends of the proxi-mal ligature being left long.

· The distal end of the gut is transected and themesentery incised between the ligatures.

· As each vessel is cut, the long ends of the indi-vidual proximal ligatures are tied together. Thisgreatly reduces the length of the gap in the me-sentery to be closed when anastomosis has beencompleted. This is particularly helpful when along length of intestine has been resected.

· With the infarcted gut now mobilised in this way,the distal end can be carefully lifted beyond theabdomen and drained into a suitable receptacleby removing the distal clamp.• Removing the proximal clamp allows

decompression of much of the distendedbowel proximal to the ischaemic portion.

Open end-to-end anastomosis using one of a num-ber of inversion suture patterns is still the most com-

53


53

monly employed method of intestinal anastomosisin the horse, but other methods have been evalu-ated experimentally and clinically. The author pre-fers a two layer closure comprising a simple con-tinuous suture for the muscosa and a continuousCushing seromuscular suture or alternatively a singlelayer closure using interrupted Lembert sutures.Synthetic absorbable suture material (e.g.polyglactin or polyglycolic acid) is used in bothtypes of anastomosis.

Closure of the Mesentery

· After the anastomosis has been checked for pa-tency and leakage, the remaining gap from thestump of the mesentery to the mesenteric borderof the intestine is closed with a continuous su-ture.

· In order to prevent adhesion formation to theextensive stump of the mesentery in which someischaemic tissue remains distal to the ligature,after resection of a long length of bowel, it canbe enveloped in two folds of adjacent mesen-tery, one drawn from each side.

· The intestinal segment and the mesentery arerinsed clean of blood using warm polyionic col-lusion before being carefully replaced in theabdomen.

Anastomosis of Intestinal Segments ofDifferent Diameters

· Dilatation of the proximal segment necessitatesjoining intestine of unequal diameters. Whilethis can be overcome by cutting the smaller di-ameter segment obliquely, a side-to-side anas-tomosis is preferable and is essential whenchronic obstruction of small intestine due to pro-gressive constriction, of its lumen by neoplasiaor ileoileal intussusception results in gross hy-pertrophy of the proximal bowel.

· Side-to-side anastomosis is used routinely bysome for all jejunal anastomoses.

· It is also used for jejuno-and ileo-caecostomy

for bypassing obstructions and anastomosingadjoining segments of large colon.

Resection of the ileum

· The ileum is involved in obstruction disease al-most as frequently as the remaining 21 metresor so of the small intestine. Many of these ob-structions result in strangulation of bowel ne-cessitating resection and anastomosis which, dueto the inaccessibility of the terminal ileum via aventral midline incision, can be technically dif-ficult.

· Ileocaecal and jejunocaecal anastomoseswhereby the nature ileocaecal junction is by-passed have proved very successful in overcom-ing the problems of restricted access and lim-ited blood supply.

· A right-angled clamp is applied as low downthe ileum as possible. After the contents havebeen stripped proximally for 20 cm, an intesti-nal crushing clamp is applied and the ileum istransacted just distal to this clamp.

· Oedema and friability frequently make closureof the ileal stump difficult. A double row ofinversion sutures is inserted.

· To avoid leaving potentially necrotic ileum insitu, it is necessary to progressively invaginateit into the caecum, using a continuous Cushingsuture. Alternatively, the ileum may be occludedusing an automated stapler as close the caecumas possible and then transacted.

· The jejunum is clamped and transected at a suit-able site proximal to the ischaemic bowel.

· After closure of the jejunal end with a doublelayer inversion suture, the jejunum is placedbetween the dorsal and medial bands of the cae-cum with its closed end pointing toward the baseof the caecum.

· A side-to-side anastomosis is now performedcreating an opening 8-10 cm long using a con-ventional suture pattern or alternatively staplingequipment may be used (Figure 2).

· On completion of the anastomosis the mesen-

54


54

teric defect is closed by suturing the cut edge ofthe jejunal mesentery to that of the ileum and tothe ileocaecal fold

A modification of this technique in which the il-eum is anastomosed side-to-side to the caecumwithout resection can be used to bypass non-stran-gulating obstructions caused by hypertrophy or ileo-ileal intussusception.

Automated Mechanical StaplingTechniques

· The use of stapling equipment in equine intesti-nal surgery is now becoming widespread. Thevarious instruments have been developed forintestinal anastomosis in order to reduce sur-gery time and thereby increase the chances ofsurvival of critically ill patients.

· The very fine stainless steel staples, which closeto form a perfect B, preserve the blood supplyto the tissues involved in the anastomosis andtherefore avoid ischaemia.

· The linear staplers, which have 30mm, 60mmand 100mm cartridges, insert staples in a doublestaggered row. The 4.8mm size of staple is rec-ommended for equine use. The application ofthese linear staplers include closure of intes-tine during resection of small or large intestine.As the instrument does not cut automatically, thismust subsequently be performed with a scalpel.

· The gastrointestinal anastomosis instrument(GIA) inserts staples arranged in two doublestaggered rows 3.5mm apart. A knife-blade cutsbetween them creating a side-to-side anastomo-sis. It is used for jejuno- and ileo-caecostomy,gastro-jejunostomy and large colon anastomoses.

· Care should always be taken not to use staplingequipment if tissues are oedematous or thick-

ened because of the risk of disruption and leak-age.

Resection of Large Intestine

Generally resection of large intestine in the horseis performed very much less frequently than resec-tion of the small intestine for two reasons.

· Firstly, many of the obstructions comprise dis-placement with no or only minimal interferencewith blood supply, or simple obstruction of thelumen, for example by enteroliths, which can berelieved by means of a simple enterotomy.

· Secondly, when a strangulating obstruction ispresent, the length of bowel involved may be sogreat that resection and anastomosis is not con-sidered feasible because of technical difficul-ties or because of likely postoperative nutritionalor metabolic problems.

CaecumPartial resection of the caecum is indicated when itshows infarctive changes due to intussusception orthromboembolism. A small amount of healthy cae-cum beyond the infracted zone is included in theresection which is usually performed at the level ofthe attachment of the caecocolic fold. The medialand lateral caecal arteries and veins are double li-gated in their course along the medial and lateralbands. The diseased portion is excised and clo-sure carried out in the layers using a Cushing su-ture.

Total resection of the caecum together with an ileo-colostomy requires an approach through a lateralright flank laparotomy in which the 17th and 18thribs are resected.

Large colonClinical and experimental investigations haveshown that horses tolerate resection of between 60and 75 % of the large colon remarkably well.

55


55

Many of the technical difficulties can be overcomeby the use of automated stapling equipment but ifthe infarction due to torsion or thrombo-embolismis restricted to the left colon, resection can be car-ried out successfully using conventional techniques.

A side-to-side anastomosis is created between ad-jacent parts of the dorsal and ventral colons proxi-mal to the infarcted portion. Delaying resectionuntil after this procedure has been carried out helpsto prevent the bowel retracting into the abdomen.

Small ColonFollowing resection of infarcted small colon, con-tinuity is restored by end-to-end anastomosis usingsimple interrupted Lembert sutures.

The large amount of fat in the mesocolon makesidentification of the vessels more difficult than thejejunal mesenteric vessels. Particular care mustalso be taken when placing sutures at the mesen-teric border to ensure a water-tight seal.

After ligation of the vessels and resection, thestumps are closed with a two layer continuous in-verting Cushing suture.

Closure of the Midline Incision

Midline incisions heal more slowly than paramed-ian or flank incisions because of the relative lackof vasculature of the linea alba, but reconstructioncan be accomplished quickly and easily with onlyminimal risk of herniation and evisceration. A widevariety of suture techniques and materials have beendescribed.

· The peritoneum is thin and tears easily but pro-viding adequate decompression of bowel hasbeen carried out, it can be sutured using a con-tinuous suture of polyglactin. However, experi-mental and clinical experience has shown thatno detrimental effects result when the peritoneum

is left unsutured.· Closure of the linea alba with a continuous su-

ture of 5 metric polyglactin doubled has provedreliable and effective in a large number ofhorses.

· However, in very large horses, or when per-forming colic surgery in heavily pregnant mareswhich may conceivable abort, 5 polyester fibresuture is preferred.

· The suture bites should be 1 cm from the mar-gins of the incision and the edges approximatedwithout undue tension.

· Thorough decompression of the intestine greatlyfacilitates closure.

· In extremely large or muscular horses, the far-and-near suture pattern has much to recommendit.

· The subcutaneous tissue is closed with a con-tinuous suture of polyglactin and the skin with acontinuous mattress suture of nylon or stapled.

· Although the use of continuous suture patternsand absorbable materials would appear, theo-retically at least, to be risky, it has proved to bea reliable method and has the advantage of sig-nificant saving in time and a reduction of sinusformation.

56


56

AlimentarySystem colic

G.B. Edwards

Colic is not a specific disease or even a diagnosis,it is only a symptom and represents a challenge ofdiagnosis. It simply indicates that the horse haspain, usually but not invariably in its abdomen andusually related to its gastrointestinal tract.

There are numerous body movements and postureswhich are associated with colic:-

· In response to mild pain the horse may occa-sionally paw the ground, turn its head to itsflanks, stretch out or lie down for longer thannormal.

· When moderate pain is present, the horse mayshow pawing, cramping with attempts to liedown, kicking at its abdomen, laying down andattempting to roll and turning its head to its flank.The horse is constantly moving about.

· If pain is severe, sweating, dropping to theground, violent rolling and continuous movementor pawing are the signs usually displayed.

Such behaviour is not confined to horses with ali-mentary colic and many of the signs described maybe shown by horses which have one of a number ofpainful conditions unrelated to the gastrointestinaltract (i.e. ‘false colic’).

False Colics

· A mare with uterine torsion in the last trimesterof pregnancy will exhibit signs of moderate painassociated with tension on the uterine broad liga-ments brought about by rotation of the uterus.

· A horse with acute exertional rhabdomyolysismay suddenly stop during exercise, drop to theground, sweat and kick out.

· Severe impairment of blood supply to the hindlimbs caused by aorto-iliac thrombosis can simi-larly cause a horse to exhibit signs normally as-sociated with severe colic.

Severe bladder distension due to urethral obstruc-tion by a calculus, pleuritis, liver disease andlaminitis can also simulate gastrointestinal colic.

Incidence and Mortality of GastrointestinalColic

The incidence of colic in a normal population isreported to range from 10-36% per year. Of theseapproximately 80% will be mild episodes where aspecific diagnosis is not made. Another 10% arelikely to be cases of impaction, flatulence or en-teritis which are diagnosed but which are treatedsuccessfully. Between 6-8% will have a seriousobstruction that, unless corrected surgically, willlead to the death of the horse.In most cases no specific diagnosis is made. Thebreakdown of disease is approximately as follows:

Mild idiopathic colic 83% Impaction 7% Gas colic/spasmodic 4% Gastric rupture 2% Enteritis 1% Strangulation 3%

An intelligent approach to the management of colicrequires an understanding of the causes and mecha-nisms of gastrointestinal pain and the pathophysi-ological changes which occur as the result of intes-tinal obstruction.

The majority of colic cases are associated with dis-ruption of normal gut motility brought about by avariety of factors such as diet, management and para-sites. Certain anatomical features of the equine ali-

57


57

mentary tract, particularly the large colon, also pre-dispose to obstruction.

Several factors can contribute to the pain associatedwith alimentary (true) colic:-

· An increase in intramural tension is probablythe most common cause and may be broughtabout by distension associated with excessivefermentation or accumulation of fluid and/or gasoral to obstructions caused by impaction, dis-placements or strangulation obstructions.

· Spasm of intestine associated with hypermotilityand disruption of the normal co-ordinated con-tractions of bowel is another frequent cause.

· Pain due to tension on mesentery may well ac-company intestinal displacement, torsions, her-nias and intussusceptions.

· Ischaemia of gut brought about by vascular oc-clusion due to a variety of strangulation obstruc-tions to which the horse’s intestine is prone, re-sults in the rapid onset of severe pain due tohypoxia which later abates when the gut becomesnecrotic.

· Mucosal inflammation and irritation present inconditions such as acute salmonellosis resultsin mild colic.

The pain associated with these factors is desig-nated visceral pain and is manifested by the clini-cal signs described earlier.

The pain which follows rupture of the stomach orintestine causing widespread peritonitis due to es-cape of ingesta is classed as parietal pain. Inmarked contrast to horses with visceral pain, thosewith severe parietal pain show great reluctance tomove and obvious boarding of the abdominal wall.

Depending on the cause of the problem one or moreof these factors may be contributing to the pain inindividual colic cases. For example, in horses withspasmodic colic, hypermotility and uncoordinatedcontractions are the sole cause, whereas in the early

stages of a strangulation obstruction, ischaemia,hypermotility, distension and mesenteric tensionmay all be contributing to the pain exhibited.

Colic can conveniently be classified into thefollowing types: -· Spasmodic· Impactive· Flatulent· Obstructive· Enteritis

Colic cases with a mild uncomplicated disease pro-cess fall predominantly into the first three catego-ries while those with serious life-threatening con-ditions usually have obstructive lesions.

The earlier these various disorders are recognisedand specific therapy instituted, the better theprognosis for recovery.

The aims of therapy are:-· to relieve pain· to restore normal propulsive motility of the

gut· correction and maintenance of hydration and

electrolyte/ acid-base balance treatment ofendotoxaemia

Relief of Pain

Relief of visceral pain in horses with severe colicis essential on humane grounds and to minimise therisk of injury to the horse and attending personnelduring evaluation and therapy.

The most satisfactory method of pain relief is cor-rection of the cause of increased intraluminal ten-sion resulting from distension or spasm. Howeverthis may take time and it is frequently necessary toachieve temporary relief of severe pain chemothera-peutically to allow a thorough clinical examinationwithout risk of injury.

58


58

The primary treatments are decompression of thestomach and intestines, and administration of anal-gesics.

Decompression

Nasogastric intubation can help relieve gastric tym-pany or remove gastrointestinal reflux due to a smallintestinal obstruction or ileus. In all cases severalattempts should be made at starting a siphon bysuction or filling the tube with water and then low-ering the end of the tube below the level of thestomach.

The other site at which gaseous pressure can berelieved by decompression is the caecum. A 5-6inch 14-16 gauge needle is inserted via the rightparalumbar fossa midway between the last rib andthe ventral prominence of the tuber coxae.

Systemic Analgesics

Systemic analgesics are the most common way tocontrol colic.

Non-steroidal Anti-inflammatoryDrugs (NSAIDs)

NSAIDs are amongst the most useful.

Approach to Diagnosis in Colic Cases

The majority of colic cases, probably in excess of90%, respond to medical therapy.

The primary aim of the initial examination is todistinguish horses with a mild or uncomplicateddisease process from those with a potentially life-threatening disorder requiring further monitoring,surgery or possibly euthanasia.

In cases of a serious nature, any attempt at a diag-nosis is often made under stress and with less thanfavourable conditions, but in mild cases there will

be adequate time to examine and initiate therapywithout placing the patient at risk. However, evenwhen a horse has mild colic, the veterinarian shouldcomplete a thorough examination and not be caughtin a trap of letting the response to treatment guidethe decision making.

The ideal goal of the systematic examination is anaetiological diagnosis and it could include the fol-lowing:-· History· Observation· Clinical examination· Laboratory investigations

The cause of the colic and the length of time it willhave been in existence will largely determinewhether a diagnosis can be made at the initial ex-amination or requires the procedure to be repeatedat two-hourly intervals. It is important that the re-sults are carefully documented. By comparing find-ings recorded at different times, the veterinarian isable to discern important trends in the disease.

History

The most important factor of the history is the timewhich has elapsed since the onset of clinical signs.This may be known precisely but often can only beestimated; for example, in the case of horses foundin colic at the owners’ first inspection of the day,having been seen normal for the last time the previ-ous evening. It is essential that a reasonably accu-rate assessment of the likely duration is made inorder that the significance of the clinical findingscan be evaluated.

General History· Housed or at grass· Feed· Use· Daily routine· Parasite control· Past medical history

59


59

Recent History

· When last fed· Consumption of feed and water· Any recent changes in feeding, bedding or

routine· Recent worming· Pregnancy· Recent exercise

Details relating to the present colicepisode

· Degree and any changes in pain· When last defaecated· Sweating or other signs

Clinical Examination

Observation

While the history is being taken, the horse may beinspected in its stall and its behaviour noted:-

· Nature and degree of colicking signscurrently being shown.

· Skin abrasions over the eyes and tuber coxaeas evidence of rolling and other violentbehaviour prompted by severe pain.

· The state of the stall.· Other signs such as abdominal distension,

sweating or muscular tremors.

The veterinarian should now proceed to a system-atic clinical examination of the horse to include:-

1. Cardiovascular system· Rate and quality of pulse· Appearance of mucus membranes

2. Examination of abdomen· Abdominal distension· Auscultation and palpation· Rectal examination

· Paracentesis abdominis· Nasogastric intubation

3. State of peripheral perfusion andhydration· Capillary refill time· Packed cell volume· Total proteinIf the colic is so severe that an orderly examina-tion is impossible without risk to the horse orthe veterinarian, heavy sedation preferably withxylazine is necessary. In the majority of casesthe pain is sufficiently mild to allow most of theexamination to be performed without recourseto the use of drugs which might modify the heartrate or gut motility. However on completion ofexamination of the cardiovascular system andauscultation of the abdomen, the administrationof a sedative will greatly facilitate rectal exami-nation which is a vital part of the examinationand other procedures such as nasogastric intuba-tion and paracentesis which may be performed.

Examination of Cardiovascular System

Heart rate and Pulse Character

· The heart rate and pulse character are impor-tant criteria in assessing the colic patient.

· Pain and the activity as a consequence of painhave only relatively minor effect on the heartrate which is influenced much more byhaemoconcentration and diminished venous re-turn, and toxins absorbed from the intestine.

· There will be a close relationship betweenthe pulse rate and the nature and duration ofthe colic.

· The heart rate will be only slightly raised af-ter 48 hours in horses with pelvic flexure im-paction.

· In contrast strangulation obstruction is usuallyaccompanied by a non-fluctuating elevationin heart rate which increases progressivelyas toxic shock develops

60


60

Mucus Membranes

· The colour of the mucus membranes is of valuein assessing the severity of the disturbance andthe prognosis.

· Reddening of the oral mucus membranes reflectsdeveloping haemoconcentration and at a laterstage when the patient is in shock, vasodilationadds to the reddening process.

· Patients with cyanotic mucus membranes inevi-tably die.

Examination of the Abdomen

Abdominal Distension

· The abdomen should be thoroughly auscultatedfor several minutes along the caudal edge of therib cage from paralumbar fossa to ventral ab-domen on right and left side.

· The sounds normally heard are fluid gurglingmixed with gas.

· Increased sounds are heard in horses with spas-modic colic and during resolution of ileus intympanic or simple cases of colic.

· In the remainder of colic cases the propulsivesounds will be reduced.

· In cases of severe intestinal disease such asstrangulation, all sounds will be absent withina very few hours of the obstruction occurring.

· Sounds will be reduced or even absent after theadministration of drugs such as xylazine ordeomidine.

· The primary cimportance of auscultation is inmonitoring the progress of the disease rather thanarriving at a diagnosis.

· Palpation of the abdominal wall in the adulthorse is of little value other than identifying‘boarding’ in response to generalised peritoni-tis due to rupture of the stomach or intestine.

Rectal Examination

· Rectal examination is the single most importantpart of the clinical examination of the horse withcolic and should be carried out in all cases when-ever possible but must be approached with re-spect for both its value and the risk involved.

· Adequate restraint is essential to prevent dam-age to the horse or examiner. Sedation withxylazine will aid a thorough examination of thecaudal 40% of the abdomen which is withinreach.

· Several large intestinal obstructions can be di-agnosed by this means including pelvic flexureimpaction, caecal and large colon tympany,nephrosplenic entrapment of large colon, largecolon volvulus and caecal impaction.

· Although rectal examination enables a specificdiagnosis of very few obstructions of the smallintestine such as inguinal hernia and ileal im-paction, seldom does it provide no useful find-ings. Small intestinal obstructions or adynamicileus produce distended loops of bowel lyingside by side. The presence of distended smallintestine almost always indicates a problem re-quiring surgical correction.

Paracentesis Abdominis

· Examination of the peritoneal fluid reflects thechanges that occur in the tissues and organswithin the abdominal cavity and on the perito-neal surface. In colic cases it assists in deter-mining the type of disease and the severity of thelesion.

· The simplest method is to insert a 19 gauge 1.5inch needle through a prepared site on the ven-tral midline of the abdomen at its most depen-dent point. Entry of the needle into the perito-neal cavity is indicated by the flow of varyingamounts of fluid, which is collected in a tubewith or without anticoagulant.

· The fluid obtained is evaluated by gross visualexamination, total protein determination and, ifnecessary, microscopic examination.

· Normal peritoneal fluid is pale yellow and clear.

61


61

· As the fluid changes with specific diseases, itcan become more turbid due to increases in pro-tein, red blood cells and white blood cells. Nor-mal fluid will be obtained in horses with non-strangulating obstructions or strangulation ob-structions within an hour or two of the obstruc-tion occurring or where the infarcted bowel isnot in direct contact with the peritoneal cavity,e.g. diaphragmatic hernia.

Nasogastric Intubation

· In addition to being of diagnostic value, decom-pression of the stomach produces immediate al-leviation of pain and reduces the risk of rupture.

· Gastric reflux of more than 2 litres is consid-ered to be significant and usually indicates aprimary disorder located in the small intestineor stomach.

· Normal gastric fluid has a pH of 3-6 but fol-lowing intestinal obstruction pH will be 6-8 dueto the buffering effect of fluid from the smallintestine.

· It is most important in horses suspected of hav-ing gastric dilatation that continued efforts aremade at decompression even though the initialattempt(s) at starting a siphon are unsuccessful.

State of Peripheral Perfusion andHydration

Capillary Refill TimePacked Cell Volume (PCV) and Total Protein

· PCV on its own is an unreliable indicator of thepatient’s intravascular hydration because of thewide range of normality.

· Progressively increasing PCV on repeated ex-aminations and values over 50% are consideredsignificant.

· In the absence of a means of spinning down bloodsamples, they can be left to settle out.

· Since changes in PCV rather than a single valueare of significance in assessing colic cases,

simple visual comparison is sufficient· When PCV is considered along with total pro-

tein (normal 65-75 g/l) it provides a very usefulmeans of assessing intravascular hydration.Raised PCV + TP represent intravascular dehy-dration.

Classification into Categories

Although at first sight this may appear a formidablelist of procedures, with experience, the clinicalexaminations can be carried out in 15-20 minutes.At the initial examination it should be possible toclassify the problem into one of the following threecategories:-

1. A benign problem requiring medicaltherapy, e.g. pelvic flexure impaction diagnosedby rectal palpation.ActionAdminister the appropriate treatment and makearrangements to monitor progress.

2. A problem requiring surgical correction.Action Arrange for immediate transfer to a sur-gical facility or, if not feasible, immediate eu-thanasia.

3. A problem which may require surgery or eutha-nasia but for which the evidence at this point isnot conclusive.Action

· Administer an analgesic· Ensure the horse is in a safe environment· Arrange to re-examine in 2 hours’ time· In conjunction with palpation of the extremities

this provides a direct means of assessing thestate of peripheral tissue perfusion while pro-viding indirect information on the degree of hy-dration and vascular tone.

· The application of digit pressure on the oralmucus membranes just above the incisor teeth isthe simplest way of assessing CRT.

· Adequate peripheral perfusion, hydration and

62


62

vascular tone are indicated by a normal refill of1-2 seconds, and warm extremities.

An increase to 3 seconds or more and coolextremities indicate inadequate peripheralperfusion and excessive vascular tone orvasoconstriction.

At the second visit the same examination proce-dures are carried out and the results comparedwith those 2 hours earlier. The horse may be found:-· to still be inconclusive, in wich case the horse

should be re-examined 2 hours later

Recognising the Case Which Requires Surgeryor Euthanasia

Surgical intervention is indicated:-

1. When the exact cause of the colic can be diag-nosed and the obstructing lesion requires sur-gery for its correction.

2. When there is no exact diagnosis but there issufficient evidence to indicate that surgery isthe only means of saving the animal’s life.

3. When animals with recurrent colic over a pe-riod of days or weeks are suspected of havingpartial obstruction due to adhesions, neoplasiaetc.

A careful history taking and full clinicalexamination are essential.

History and Signalment

Several components of the history and signalmenthelp the surgeon to decide whether or not surgeryis indicated. For instance, age and sex-related con-ditions must be kept in mind when examining theanimal. Obstructive conditions involving the dis-tal colon/rectum and defects in the urinary tract oc-cur commonly in neonatal foals. Ileal or ileocaecalintussusceptions tend to occur in horses less than

18 months of age and colonic torsions are most com-mon in mares which have foaled within the previ-ous 90 days. Intestinal strangulation obstruction (in-carceration, volvulus and 360º colonic torsion)tends to have a relatively shorter clinical coursethan does a simple obstruction or displacement. In-guinal hernias in stallions are frequently associatedwith a history of exercise or breeding of a mare.Because of the strength of the association of certainconditions with a horse’s age, it is important thatthe age of the animal be kept in mind during theexamination. To further emphasise this point, epi-ploic foramen entrapments and caecal impactionsgenerally occur in horses older than 8 years andpedunculated lipomas usually cause problems inhorses over 15 years of age.

The most important feature of the history is the lengthof time the horse has been in colic. The stage atwhich the horse is first examined by the veterinar-ian will vary from case to case and will govern theclinical findings. In some instances the precise du-ration of the colic is known while in others the horseis found in colic by the owner in the morning hav-ing last been seen normal the previous evening.

However, it is usually possible to determine ap-proximately when the colic began from the evidenceavailable, e.g. if the horse is showing severe painand has eaten most, if not all, its hay, it is likely thecolic began only a few hours earlier, whereas if theobstruction developed late the previous evening ahorse with a strangulating lesion may have pro-gressed beyond the stage of violent pain and be ex-hibiting the severe depression associated withendotoxaemia. However evidence of trauma aboutthe eyes and over the tuber coxae, together withmarks on the wall of the box and severely disturbedbedding indicate that the horse had previously beenin severe pain.

Physical Examination

When evaluating a horse with colic, particular at-

63


63

tention must be paid to the cardiopulmonary andgastro-intestinal systems. Changes in the horse’svital signs are usually indicative of hypovolaemiaand/or endotoxaemia. Furthermore, these changesare indicative of the magnitude or duration of anintestinal obstruction or the severity of damage tothe intestinal mucosal barrier to enteric organisms.Careful evaluation of the animal’s vital signs withrespect to the duration of the colic episode and aknowledge of the patho-physiological sequelae ofintestinal obstruction, may provide the surgeon withan accurate appreciation of the underlying intesti-nal problem.

Pain

Persistent acute unrelenting pain which is unrespon-sive to analgesics is the most reliable parameterindicating the need for surgery. Obviously differ-ent types of surgical lesions will produce varyingdegrees of pain which, when combined with otherphysical examination findings, signalment and anaccurate history will aid in determining not onlythe need for surgery but may offer a clue as to thetype of disorder.

For example, horses with large colon torsions mostoften exhibit an extremely violent degree of painduring the initial period prior to devitalisation ofthe colon. Presented with a post partum mare ex-hibiting such severe pain the veterinarian shouldrefer her to a surgical facility immediately. Otherstrangulating lesions may cause only mild to mod-erate degrees of pain which is easily controlled byanalgesics. Disorders such as an epipoloic fora-men entrapment of small intestine may be maskedby analgesics until cardiovascular deterioration hasoccurred. Intermittent, moderately severe pain isusually associated with non-infarctive conditions,e.g. impactions and partially occlusive conditionssuch as ileal intussusceptions and large colon dis-placements.

In general a heart rate which has risen progres-

sively to 60 or more per minute within 4 to 6 hoursof the onset of colic gives cause for concern, par-ticularly if it remains high during quiet interludesand in the face of adequate analgesia. Such a pulsecontinuing to rise and weakening is indicative ofcirculatory damage and ischaemic gut.

The colour of the mucous membranes is of consid-erable value in assessing the severity of the distur-bance and the prognosis. Reddening of the mem-brane reflects developing haemoconcentration and,at a later stage, when the patient is in shock, va-sodilatation adds to the reddening process. A cap-illary refill in excess of 3 seconds is further evi-dence of impending circulatory collapse.

Rectal Examination

Rectal examination is the single most important partof the clinical work up of the horse with colic andshould be carried out whenever possible. The de-cision for surgery is usually based on the findingsat rectal examination carried out after reviewingthe pertinent aspects of the history, particularly theduration of colic, and the rest of the physical ex-amination.

In this way an attempt can be made to predict whatshould be felt and to compare the findings with thosepreconceived ideas. It must be emphasised thatcertain conditions requiring surgical interventionmay be diagnosed by rectal palpation before theanimal becomes severely ill or peritoneal fluid al-terations become evident. In such instances, theonly diagnosis and referral of these cases signifi-cantly improves the individual’s prognosis withsurgery and reduces the occurrence of postopera-tive complications.

Consequently rectal examination is of paramountimportance in identifying large intestinal problemsincluding displacements and torsion of the largecolon and caeco-caecal intussusception.

64


64

It is not surprising that specific obstructions of thesmall intestine are palpable less frequently becauseits long mesentery allows it to occupy any part ofthe abdominal cavity from the pelvis to the dia-phragm. Because only the caudal 40% of the ab-domen can be explored by rectal palpation, muchof the small intestine is out of reach of the exam-iner. However, the terminal ileum is relativelyfixed at the base of the caecum and lesions of thissegment, such as impaction and intussusception, arethe ones most commonly palpated.

In other types of small intestinal obstruction therectal findings vary from nothing abnormal in ahorse presented within 2 to 3 hours of an obstruc-tion developing, to tightly distended loops of gutextending back into the pelvic inlet in cases of 18hours or longer duration.

From 4 to 8 hours one or more fluid/gas filled loopsmay be palpated but these may not be immediatelyapparent and careful patient examination is oftennecessary to identify them. However their pres-ence is an indication of the need for surgery andtheir recognition at this early stage is rewarded bya much more favourable prognosis following sur-gery.

Passage of the Nasogastric Tube

A volume of gastric reflux in excess of 2 litres isconsidered to be significant and usually indicatesa primary small intestinal obstruction. However,in some cases of large colon obstruction, such asleft dorsal displacement, the proximal small intes-tine is compressed preventing normal gastric emp-tying. Two further conditions - acute grass sick-ness and anterior enteritis - are also characterisedby large volumes of gastric reflux and must be dif-ferentiated from cases with physical obstructionsof the small intestine. Based on the presence orabsence of gastric reflux and the time which haselapsed since the onset of colic, it is often pos-sible to predict the level at which the intestine is

obstructed. High obstruction leads to gastric dis-tension within a relatively short time whereas sev-eral hours must elapse following ileal obstructionbefore significant volumes of reflux are present.

Paracentesis abdominis

Although in most referred cases a peritoneal fluidsample has been taken and analysed, this evalua-tion is of secondary importance to the rectal exami-nation and does not have a significant influence onthe decision to operate. However, it does help toidentify horses with intestinal rupture of primaryperitonitis and to determine the morphological sta-tus of the bowel.

Sanguinous fluid is decisive evidence of infarctionwhereas reddish brown fluid containing large num-bers of white as well as red blood cells indicatesmore advanced changes and consequently a poorerprognosis.

From the point of view of the practising veterinarysurgeon and pertinent to the outcome of the indi-vidual case, every effort should be made to referhorses with colic of unknown cause before the peri-toneal fluid is altered. If marked small intestinaldistension is evident per rectum, paracentesis maybe contra-indicated because of the risk of lacera-tion of the bowel.

Auscultation of the abdomen

In general, normal or increase borborygmi are notconsistent with major tissue changes whereas sus-tained absence of intestinal sounds frequently ac-companies irreversible morphological changes.

Laboratory Tests

Although laboratory aids permit an accurate appre-ciation of the animal’s haematological/metabolicstatus, they seldom help the surgeon to decide whichhorse requires surgery. On the other hand, they can

65


65

be of considerable help in assessing prognosis.

If a diagnosis is not possible at the first visit, theexamination should be repeated at intervals of nomore than 2 hours and the findings compared withthose of the previous examination(s). This shouldenable the horse with an obstruction requiring sur-gical correction to be recognised early enough inits course to ensure a favourable prognosis. How-ever care should be taken during this time to avoidthe use of potent, prostaglandin synthetase inhibi-tors such as flunixin, which mask several of thesigns of developing toxaemia on which recognitionof the surgical case is based. The apparent re-sponse, often for several hours, of horses with in-testinal ischaemia, following treatment with suchcompounds frequently leads to a false delay in em-barking upon surgery.

Table 1 summarises the criteria for surgical in-tervention in order of importance. However, theyare only guidelines. Such is the great variationin the type of obstruction, the part and length ofthe gut involved and the degree of occlusion, thatsome cases will inevitably present problems in di-agnosis.

When evidence for and against surgery is evenlybalanced, intuition based on clinical experience isoften the deciding factor. I encourage veterinarysurgeons to refer cases for further examination and,if necessary, surgery, rather than wait until they arecertain of their diagnosis. This inevitably resultsin some horses and owners making what might beconsidered to be unnecessary journeys if furtherevaluation at the referral centre shows that surgeryis unnecessary but, more importantly, it reduces thenumber of horses which do not survive to make thereturn journey.

The key to success in colic surgery is being able tomake the decision to perform surgery as early aspossible. If this can be done, all parties includingthe owner of the horse, the referring veterinarian

and the surgeon will be pleased with the outcome.

Preparation of a Horse for Transport

If a horse is to be referred to a University hospitalor other centre and this involves a journey of anysignificant length, the following measures shouldbe taken:-

1. Decompress the stomach and, if necessary, leavethe nasogastric tube in place and tape it to thehead collar.

2. Administer an analgesic. If it is clear thatsurgery is necessary and a strangulationobstruction is suspected, flunixin is the drug ofchoice because in addition to relieving pain, itwill counter the effects of endotoxaemia.

3. If the horse is in shock, electrolytes may be givento improve the circulating blood volume whileawaiting the arrival of a horse box but departureto the surgical centre should not be delayed forthe purpose of administering the large volumesnecessary to make any significant impressionon the packed cell volume.

4. Administer a broad spectrum antibiotic.

5. Rug the horse up and bandage it limbs.

6. Provide a detailed report of the treatmentadministered prior to referral.

7. Provide the owner with accurate instructionshow to get to the hospital.

66


66

TABLE 1

1. Degree of painIn some cases of strangulation obstruction, particularly 360º large colon torsion, the pain from theoutset is so severe and unresponsive that immediate surgery or euthanasia is required.

2. Rectal findingsPositive rectal findings of obstructions such as volvulus, intussusception, marked small intestinaldistension, are indications for surgery regardless of the other clinical findings.

3. Heart rate and pulse quality• Strangulation obstructions are accompanied by a non-fluctuating elevation in heart rate which

increase progressively as toxic shock develops.• In general a pulse rate which has risen progressively to 60-70/minute 6 hours after the onset of

colic gives rise for concern particularly if it remains high during quiet interludes and in the faceof adequate analgesia.

1. Cardiovascular deteriorationProgressive deterioration evidenced by a PCV > 55 and injected mucous membranes despite fluidtherapy.

2. Absence of gut sounds

3. Nasogastric refluxPositive nasogastric reflux in excess of 2-3 litres in horses in which primary gastric dilatation can beruled out.

4.. Paracentesis abdominisPositive changes in peritoneal fluid viz. an increase in RBC, WBC and protein, indicate morphologicalchanges of the bowel.

5. Abdominal distensionProgressive Abdominal Distension which is becoming life-threatening.

67


67

Pathophysiology of Intestinal Obstruction

G.B. EdwardsUniversity of Liverpool

Any interference, be it mechanical or functional,constitutes obstruction of the intestine. Obstruc-tive diseases of the alimentary tract can be classi-fied into 3 general groups: Mechanical, vascularand neurogenic obstructions. Mechanical obstruc-tions, which are by far the most common, result incomplete or partial occlusion of the lumen. Pri-mary vascular obstructions due to thrombi or em-boli result in functional obstructions due to inabil-ity of the ischaemic musculature to contract but theseare usually limited to the large intestine and arerare in the SI. Neurogenic obstructions arecharacterised by interference with the nervous con-trol of mobility. This may be primary as in grasssickness, in which there is degeneration of auto-nomic ganglia and the intestinal intramural plex-uses, or secondary as in paralytic ileus due to peri-tonitis or associated with surgery of the alimentarytract.

Simple Obstruction

(a) Small intestinePhysical obstruction of the intestine usually occursby impacted food material, stricture or foreign body,thereby preventing the passage of the large volumeof fluid produced in the upper alimentary tract fromreaching the absorptive surfaces of the lower in-testine so that it becomes sequestrated or maybelost by nasogastric reflux. During one day this vol-ume almost equals the extracellular volume of thehorse (approximately 125 l), systemically the primeconcern in simple obstruction is depletion of plasma

volume and reduction in cardiac output together withacid-base disturbances. Gas production by bacte-rial action continues and is even enhanced by thestatic medium. With continued secretion of fluidsand the build up of gas, the intraluminal hydrostaticpressure (IHP) increases and distends the bowel.As stretch receptors in the distended intestinal wallare activated, the pain increases and becomes con-tinuous. Peristaltic waves diminish and then ceasealtogether as the intestinal lumen is progressivelyfilled, leaving an atonic rapidly distending tube.Once IHP increases above 15cm H2O, absorptionof water by the mucosa stops and instead waterbegins to flow from the mucosa into the lumen. Theincreasing pressure and the expanding volume offluid causes reflux into the stomach. The diameterof the small intestine increases in a proximal todistal direction. Approximately 23 l of fluid canaccumulate in the distal third whereas 17 l and 13 lcan accumulate respectively in the middle andproximal thirds. Therefore, in a horse with ilealimpaction, 53 litres are needed before fluid beginsto accumulate in the stomach. In a 500 kg horsesecreting 3-4 l of precaecal fluid per hour, gastricdilatation will occur after 12-18 hours.

If the obstruction is located in the proximal third ofthe small intestine, the prestenotic fluid will reachthe stomach after 3-6 hours whereas gastric dilata-tion will occur after 6-12 hours when the obstruc-tion is located in the middle portion (Huskamp1998).

During the initial four hours of ileal impaction, thewater reserve in the large colon is absorbed; theintravascular volume therefore initially remainswithin normal parameters. Once the water reservein the colon has been used up, PCV and TPP beginto increase steadily and in parallel, andhypovolaemia develops.

Increased vascular hydrostatic pressure in the bowelpromotes leakage of protein-rich plasma into theperitoneal fluid. Few leukocytes and no erythro-

68


68

cytes appear in the peritoneal fluid within the first12-24 hours but may become more numerous withthe progression of degenerative changes and vas-cular compromise of the intestinal wall. Damagemay be sufficient to allow absorption of endotox-ins and cause production of prostaglandins andleucotrienes which may further compromise thecardiovascular system. However, endotoxic shockplays only a very limited part in the fatal outcomeof unrelieved simple obstruction. Hypovolaemiaand altered blood electrolytes are the usual causesof vascular collapse.

The severity of clinical signs associated withsimple obstruction of the small intestine dependson the degree of obstruction (complete or incom-plete) and the level of obstruction (proximal or dis-tal). In general proximal obstructions have a moreacute onset, produce greater pain, generate a greatervolume of gastric fluid sequestration and have amore rapidly fatal cause than distal obstructions.In proximal obstructions large quantities of chlo-ride are lost, particularly if gastric reflux is re-moved by nasogastric tube, resulting in metabolicalkalosis. Later the metabolic disturbance becomesmore complicated by acidosis secondary tohypoperfusion. Clinical signs resulting from dis-tal small intestine obstructions develop moreslowly and are generally less severe due to com-pliance of the intestine and the ability to continuesome absorption until THP initiates secretion. Es-tablished cases of distal small intestinal obstruc-tions are characterised by metabolic acidosis withlow serum levels of HCO3.

(b) Large intestineSimple obstruction of the large intestine is usuallydue to impaction with foodmaterial, enteroliths orother intraluminal masses, or a change in positionof the colon, e.g. nephrosplenic entrapment, andmay be partial or complete.

In general the clinical signs or rate of systemic de-terioration are much lessdramatic in simple ob-

struction of the large intestine compared to simpleobstruction of the small intestine. Incomplete ob-struction allows the passage of small amounts ofingesta and gas. Dehydration is mild at first be-cause water still passes into the caecum where it isreadily absorbed.

If the obstruction becomes complete ingesta, andparticularly gas, accumulate much more rapidly.Distension becomes marked and may become sogreat as to exert pressure on the diaphragm and venacava resulting in impaired pulmonary function andvenous return to the heart. Prolonged and/or markeddistension of the caecum and colon may cause in-terference with mucosal perfusion leading todevitalisation and possibly fatal rupture.

Strangulating Obstruction

(a) Small intestineStrangulating obstructions of the small intestine in-clude incarcerations, intussusceptions and volvu-lus, and represent a common cause of acute abdomi-nal crisis. The same fluid retention which occursdue to simple obstruction is present but becausevascular compromise of the intestine is present fromthe outset, the pathophysiological changes associ-ated with strangulation obstruction are more acuteand severe. The vascular compromise may bevenous, or venous and arterial, but the typical le-sion will cause venous occlusion before arterialocclusion with consequent venous congestion.Within minutes of strangulation occurring the in-volved segment of bowel and its mesentery becomedeep red as veins and venules are distended withblood. If there is immediate concurrent arterialocclusion, as in some cases of obstruction by a pe-dunculated lipoma, the intestine becomes cyanoticbut not oedematous. More often, thicker walledarteries and anterioles resist compression for a whileand continue to pump blood into the distended veinsand venules. As the involved intestine is engorgedwith blood, vascular stasis develops and the seg-ment becomes red/black in colour. Almost imme-

69


69

diately, the vascular endothelium becomes morepermeable and plasma diffuses into the tissue.Within a few hours degeneration of vascular en-dothelium becomes so extensive that blood poursout of the distended vessels into the tissues (venousinfarction stage) and eventually into the lumen.Eighty per cent of the blood supply to the intestinegoes to the mucosa. The mucosal villi are extremelysensitive to hypoxia and within minutes of oxygendeprivation, ultrastructural morphological changesare evident. The epithelial cells slough in sheetsstarting at the tip of the villus and working towardsthe crypts. Within 4-5 hours the mucosal epithe-lium is completely necrotic. By 6-7 hours the de-generative effects of hypoxia have extended throughthe external muscular layer.

As soon as the mucosal barrier is damaged, gramnegative bacteria and endotoxins permeate thelamina propria and submucosa. Early in the devel-opment of the ischaemic lesions, the bacteria andendotoxins readily gain entry to the circulation viaviable tissue adjacent to the lesion. In addition, by6 hours or possibly earlier, as the musculous de-generates, bacteria and toxins leak through the se-rosa into the peritoneal cavity from which they arereadily absorbed. Release of endotoxin into thegeneral circulation results in damage to endothe-lial cells and platelets. Platelets are immediatelystimulated and release the patent vaso-constrictedsubstances, thromboxane and serotonin. Damageto the endothelium increases vascular permeabil-ity, prostacyclin is released and neutrophils arestimulated especially in the lungs and sites of in-testinal injury. The endotoxic shock is dose re-lated and is more severe and rapidly developingthe greater the length of bowel involved and theseverity of vascular occlusion.

The clinical picture is acute with severe pain whichis continuous and shows no, or only temporary, re-sponse to analgesics. The heart rate increases pro-gressively and pulse quality deteriorates. Mucusmembranes become congested and the capillary

refill time increases. The PCG and TPP rise pro-gressively and the respiratory rate increases in re-sponse to the developing metabolic acidosis. Atfirst the peritoneal fluid is slightly serosanguinouswith a mild increase in protein and leukocytes. Asthe strangulation process continues, all these sub-stances increase

dramatically and the fluid becomes flocculent andturbid. Toxic neutrophils indicate leakage of tox-ins and bacteria. The clinical course is rapid andmost horses with an untreated strangulation obstruc-tion of small intestine will die within 24-36 hoursof the onset of disease from irreversible septic shockand marked vascular collapse.

(b) Large intestineStrangulation obstructions of the large intestine in-clude intussusception ofthe caecum, volvulus of the large colon and incar-ceration of the small colon. The pathophysiologyis similar to that previously described for the smallintestine but there are points of variance.

The rate of systemic deterioration can vary mark-edly between caecocaecal intussusception in whichit is slow, and 360º large colon volvulus which isthe most rapidly fatal of all intestinal obstructionsin the horse. Such is the size of the submucosalspace in the large colon, venous occlusion can re-sult in the horse losing half its circulating bloodvolume into the wall of the gut within 4 hours of a360º volvulus occurring.

Hypovolaemia is rapidly profound and the mucousmembranes become pale and cyanotic. The degen-eration of the large surface area of bowel wall al-lows massive leakage of endotoxin and bacteriainto the peritoneal cavity and the effects ofendotoxaemia are added to those of hypovolaemia.Because of the short clinical course prior to death,rupture is not normally seen.

70


70

Radiolographic views suggested for pre-purchase examination.

Carstens A , Section Diagnostic Imaging,Department of Companion Animal Clinical

Studies, Faculty of Veterinary Science, PrivateBag X04, Onderstepoort, 0110, South Africa

Diagnostic quality radiographs are required to en-sure that correct diagnoses of many musculoskel-etal conditions of the horse in clinical practice aremade. In addition to this the correct views and theoptimal number of views per area are required.Horses undergoing pre-purchase examinations mayalso require radiographic evaluation and particu-larly when overseas purchasers or groups likeJockey Clubs are concerned, adhering to minimumrequirements for radiographs are often essential tothe buyer.

The purpose of this paper is to suggest the mini-mum standard views required to be taken for clini-cal diagnostic purposes, but also for the pre-pur-chase scenario. The views are required to opti-mize the evaluation of certain conditions that mayoccur in each joint. The views were selected usingthe references below, one of which is the JockeyClub of Hong Kong’s requirements for permanentimportation of racehorses.

1. Carpus: 5 views: DPa LMD30°LPaMO,D60°LPaMO

D45°MPaLOFlexed LM

Conditions that may be identified: chip fractures,

some slab fractures, degenerative joint disease,OCD lesions

2. Fetlock: 4 views: Front: DPaLMDLPaMODMPaLOFlexedLM

4 views: Hind: DPlDLPlMODMPlLOLM

Conditions that may be identified: chip fractures,degenerative joint disease, OCD lesions, synovialhyperplasia

3. Tarsus: 4 views: DPlD15°-35°LPlMOPl15°LDMOLM

Conditions that may be identified: degenerative jointdisease, OCD lesions

4. Stifle: 2 views: LMCdCrCdLCrMO

Conditions that may be identified: degenerative jointdisease, OCD lesions, subchondral cyst-like lesions

5. Phalanx3:2 views: D65°PrPaDiO(upright pedal)DPa weight-bearing(horizontal beam)LM

Conditions that may be identified: fractures, degen-erative joint disease, OCD lesions, subchondralcyst-like lesions, pedal osteitis, hoof imbalance

71


71

6. Navicular: 3 views D65°85°PrPaDiO(uprightpedal)LMPaPrPaDO(skyline)

Conditions that may be identified: fractures,degenerative joint disease, subchondral cyst-likelesions, navicular disease.

REFERENCES

1. Butler LA, et al (Eds) Clinical Radiology ofthe Horse. 2nd Ed. 2000. Blackwell ScienceLtd, London

2. Jockey Club of Hong Kong. Radiographicviews required for permanent importation ofracehorses into Hong Kong.

3. Morgan JP, et al. (Eds) Equine Radiography.1991. Iowa State University Press

4. Phillips TJ. The use of radiography in the pre-purchase examination. In Mair TS (Ed) ThePrepurchase examination. A BEVA manual1998 154-160.

5. Poulos PW. Radiologic evaluation of the horserelevant to purchase. VCOT. Examination forpurchase 1992 8: 319-328

6. Section Diagnostic Imaging, Faculty ofVeterinary Science, Onderstepoort, SouthAfrica - personal communication

7. Thrall DE (Ed) Veterinary DiagnosticRadiology. 4th Ed. 2002 W.B. Saunders Co,Philadelphia.

72


72

How to interpretyearling

radiographsH.J. Marais, Department of Compan-ion Animal Clinical Studies, Faculty of

Veterinary Science, University ofPretoria, Private Bag X04,

Onderstepoort, [email protected]

Radiography in pre-purchase examinations, year-ling sales and for export of has become standardpractice in recent years. Veterinarians are beingput under pressure from trainers and owners al-most everyday to make a decision on future racingperformance, when evaluating radiographs. It istherefore of utmost importance for the practitionerto know how to take good quality radiographs,which views to take and more important, how toevaluate and interpret any changes that is evidenton the radiographs. While another paper will lookat which radiographic views to take of the limbs,this presentation will deal exclusively with theprevalence and distribution of radiographic lesionsin the fetlocks, carpi, tarsi, stifles and forefeet ofthe horse, as well as the associations of these le-sions with racing performance. Due to the fact thatradiographs do not reproduce well, no radiographicpictures are included in the proceedings. It is how-ever strongly recommended to obtain the two ar-ticles below for reference.

Further reading:

1. A.J. Kane, R.D. Park, C.W McIllwraith.Equine Veterinary Journal (2003) 35 (4), p 350– 381.

2. 46th AAEP Proceedings 2000.

73


73

How toDo ultrasound of

the normalequine abdomen

L Sweers, Diagnostic Imaging Section,Onderstepoort Veterinary Academic

Hospital, Onderstepoort, South Africa

INTRODUCTIONThe transcutaneous ultrasonographic evaluation ofthe adult horse’s abdomen plays an important rolein the making of diagnostic decisions in patientspresenting with colic. It allows confirmation ofabnormalities found during rectal palpation andacquiring of additional information, which may pro-vide increased insight into the surgical or non-sur-gical nature of the condition. It is important thatthe clinician familiarise him- or herself with thenormal abdominal sonographic anatomy to be ableto identify and interpret pathologic changes.

EQUIPMENTThe frequency of transducer to use depends on thesize of the patient. The highest frequency trans-ducer that will allow the best resolution at the de-sired depth should be used. This is usuallyachieved by using a 2.5-5 MHz transducer on mostpatients, which will penetrate up to a depth of 30cm (but with poorer image quality at that depth). Inthinner and smaller patients even higher frequen-cies may be used. Linear and sector transducersmay be used. However, because the intercostalapproach is mostly used when scanning the abdo-men, a sector transducer with smaller footprint andwider far field is more user friendly.

PATIENT PREPARATIONClipping of the entire abdomen’s hair is impracti-cal in a horse and therefore the skin and hair shouldrather be thoroughly wetted with copious amountsof fluid (i.e. methylated spirits or alcohol). Whenusing an alcohol-based agent, the transducer shouldbe protected with a glove or condom after applica-tion of coupling gel to the transducer’s footprint.Coupling gel can also be used on the skin in addi-tion to the fluid for increased coupling.

BASICS WHEN SCANNING THEABDOMENThe transducer should always be held in a consis-tent fashion to help the sonographer get familiarwith the location of organs in relation to one an-other. With practice and by using a consistentmethod, the sonographer will be easily alerted ifsomething appears “out of place” or “not right”.This will lead to further investigation and recogni-tion of pathology. When using the intercostal ap-proach (thus with the transducer in a transverseplane), always ensure that the dorsal aspect of thepatient is kept to the left of the screen. When scan-ning along the ventral abdomen in a transverse plane,the patient’s right side should be kept to the left ofthe screen. When using a sagittal, parasagittal ordorsal plane of scanning, cranial is always kept tothe left of the screen. All organs and structuresshould always be scanned in at least two perpen-dicular planes, although it may be more difficultwhen scanning intercostally.

The image should be optimised when starting thescan by adjusting the power, gain, reject and time-gain compensation controls. This will be differentfor different types of ultrasound machines and willalso vary between operators. It is best to find themost optimal image for you and then try and keep itconstant. It is also important to note that obesepatients are always much more difficult to scan dueto poorer image quality. The sonographer shouldbe aware of and be able to recognise ultrasound

74


74

artifacts. These artifacts may be confusing (use-less) or useful in the interpretation of suspect pa-thology. A small amount of anechoic peritoneal fluidmay sometimes be found in normal horses.

SCANNING THE LIVERThe entire liver cannot be evaluated due to the dor-sally overlying lung. The left side of the liver,which is normally smaller than the right side, canusually be seen from the 6th to 9th intercostal spacesimmediately dorsal to the sternum. The cranial poleof the spleen is seen medial to the liver in the 8th to9th intercostal spaces on the left side of the abdo-men. The right liver is seen from the 6th to 15th

intercostal spaces, with the right dorsal colon me-dial to it. In the cranial to mid abdomen, the duode-num lies between the liver and right dorsal colon.The right kidney is seen caudal and lateral to thecaudate process of the right liver lobe.

Normal liver parenchyma is homogenous and ofmedium echogenicity (less than the spleen and morethan the renal cortex) with an easily recognisablebranching vascular pattern. The portal and hepaticveins are seen as tubular anechoic structures withinthe liver parenchyma with the portal veins havingmore echogenic walls. The hepatic veins maysometimes be traced into the caudal vena cava insmaller horses. The ventral margins of the livershould be smooth and sharp. Liver size is difficultto determine and relies on a relative estimation ofthe amount of liver imaged ventral to the lung mar-gin. In older animals, atrophy of the right liverlobe may make it more difficult to visualise.

SCANNING THE SPLEENThe spleen can be visualised along the left side ofthe abdomen, along the entire ventral border of thelung from the 7th intercostal space to the paralumbarfossa. Cranially, it lies medial to the liver andmay cross the ventral midline towards the rightside in some horses. Further caudally it lies im-mediately adjacent to the diaphragm and left body

wall. The left kidney lies medial to the splenic tailin the caudodorsal abdomen. The left dorsal colonis seen medial to the spleen. The left dorsal and/orventral colon may be seen at its ventral aspect.

The spleen is the most echogenic organ when com-pared to the liver and kidney cortices, with the pa-renchyma having a dense, even, homogenousechotexture. The splenic capsule is seen as a thinhyperechoic line. In the region of the 10th intercos-tal space, the splenic vein may be seen as an anechoictubular structure along the medial aspect of thespleen. This is an easily recognisable landmarkfor the location of the fundus of the stomach, whichlies immediately medial to the spleen. The spleen’smargins should normally be smooth and sharp.Sedatives often cause splenomegaly. It is impor-tant to note that splenic size is variable even in nor-mal horses.

SCANNING THE GASTRO-INTESTINAL TRACTLarge intestine may be visualised almost in everyabdominal region. The specific part of it being im-aged is usually difficult to determine and is mostlydependant on the location within the abdomen.Jejenum is not that readily seen and mostly only inthe ventral abdomen. The caecum is seen along theright dorsocaudal body wall. The stomach fundusmay be seen as a convex semicircular hyperechoicstructure on the left side of the abdomen, medial tothe spleen in the region of the splenic hilus and cau-dal to the left lateral lobe of the liver. The de-scending duodenum is seen on the right, coursingalong the caudal and medial liver margin towardsthe caudal pole of the kidney. It can be imagedconsistently between the 14th and 17th intercostalspaces immediately ventral to the right kidney anddorsal and dorsolateral to the caecal base. It nor-mally appears collapsed until some fluidy ingestamoves through it in a wave-like motion.

Ultrasonography is useful in assessing the lumenalcontent and diameter, wall thickness and layering,

75


75

location as well as intestinal motility and mobility.The lumenal echo and diameter is dependent on thetype and amount of content (i.e. gas, fluid, food ormucus). Five sonographic intestinal wall layerscan be visualised under optimal conditions (frominside to outside): a hyperechoic mucosal-lume-nal interface, hypoechoic mucosa, hyperechoic sub-mucosa, hypoechoic muscularis and hyperechoicserosa.

Wall thickness varies from 2-3.75 mm in normalsmall and large intestine. The ileum (only imagedwith transrectal ultrasound) may have a seven-lay-ered appearance as a result of an extra muscularlayer and its thickness may therefore be up to 4-5mm. The stomach wall may measure up to a thick-ness of 7.5 mm. The normal frequency of intestinalcontractions is as follows: small colon (0-3 perminute), large colon and caecum (2-6 per minute)and small intestine (6-15 per minute).

SCANNING THE KIDNEYS ANDBLADDERThe right kidney’s cranial pole is positioned in thecaudate lobe of the right liver (renal fossa) on theright side of the abdomen, with the entire kidneyfound from the 14th to 17th intercostal spaces at thelevel of the tuber coxa. It has a triangular curvilin-ear or heart shape and a prominent hilar notch. Theleft kidney is more difficult to image due to itsgreater depth and attenuation of the sound beam bythe laterally located spleen. It is located more cau-dal and ventral, from the 17th intercostal space tothe paralumbar fossa. It normally lies medial tothe spleen in the left caudal abdomen and has amore elongated (bean shape) when compared tothe right.

The kidneys have a distinct cortex (being finely ho-mogenous to slightly mottled and hypoechoic to thesurrounding tissues) and a less echogenic medulla.The cortico-medullary junction is sometimes lessdistinct than in small animals. The renal pelvis is

normally hyperechoic due to the presence of fat andfibrous tissue. The left kidney is 15-18 cm long,11-15 cm wide and 5-6 cm thick. The right kidneymeasures 13-15 cm long, 15-18 cm wide and 5 cmthick. The renal vessels and most proximal part ofthe right ureter are usually imaged at the renal hilusas tubular anechoic structures. The ureters (exceptthe most proximal part of the right ureter) are notnormally imaged.

The urinary bladder is located in the caudoventralabdomen at the pelvic brim. Its visualisation isdifficult due to its location, however when full, maysometimes be seen from a pre-pelvic, ventral ab-dominal transcutaneous approach. It is better tovisualise the bladder transrectally, assessing theechogenicity of the urine, wall thickness and ab-normal contents or calculi. The bladder should al-ways have a rounded to oval shape. Equine urineis normally echogenic as a result of normal crys-talluria and mucus. Urine entering the bladder inspurts from the urethra can sometimes be visual-ized, however is better imaged from a transrectalapproach. The bladder wall is normally hypo- tohyperechoic and measures up to 3-6 mm dependingon its degree of distension.

SUMMARYTranscutaneous ultrasound is a useful diag-nostic tool for evaluating abdominal diseaseor conditions in an adult horse. It is non-invasive and safe, but also extremely user-dependant. The clinician should strive togain knowledge in the normal anatomy andultrasonographic appearance of abdominalstructures as well as experience in transcu-taneous abdominal ultrasound scanning, tobe able to diagnose abdominal pathology.

76


76

Ultrasonographic pathology of the gastro-intestinal tract of the horseCarstens A, Section Diagnostic Imag-

ing, Department of Companion AnimalClinical Studies, Faculty of Veterinary

Science, Private Bag X04,Onderstepoort, 0110, South Africa.

Ultrasonographic examination of the gastro-intes-tinal tract has become an integral part in the diag-nostic evaluation of the horse with colic, chronicweight loss and conditions such as fever of unknownorigin. The visualization of the organs is limited bythe acoustic windows for the abdomen (transcuta-neous or rectal), and it must be kept in mind thatonly sections of the tract can be visualized. Theseareas may appear normal ultrasonographically, butan adjacent or deeper lying section that is not vis-ible by ultrasound may still be abnormal. The fol-lowing short descriptions of conditions of the gastro-intestinal tract can be diagnosedultrasonographically:

Stomach:Gastric distension: the ultrasonically visualizedstomach wall is usually less circular than normaland seen further caudally than normal up to the 15th

intercostal space. It can be gas-filled and/or filledwith anechoic to hypoechoic fluid.

Gastric impaction: the stomach is again usuallyless circular than normal, extending over more than5 intercostal spaces on the left. If severe, the dis-tension may be seen also on the right. Hyperechoicshadow-casting content is present.

Gastric squamous cell carcinoma: thisinhomogenous echogenic mass in the wall of thestomach is often seen to invade into adjacent or-gans. Peritoneal effusion may be present.

IntestinesPosition, motility, peristalsis, wall thickness andluminal content must be evaluated. An organ dis-placed from its normal position, with wall thick-ness of over 3mm that is hypo- to hyper- to amotile,with abnormal content and/or volume of content issuspect.

Enteritis / colitis: thickened walls, hyper-, hypo-,amotile, with usually fluid content. Duodenal dis-tension is seen with anterior enteritis as well assecondary to jejunal obstruction.

Impaction: colon or caecum may be visualized aslarge (20-30cm) relatively amotile viscous struc-tures with no visible haustra, filled with ahyperechoic luminal content.

Intussusceptions: are seen as concentric multi-lay-ered intestinal walls (target or bull’s eye lesion)which are usually thickened. Jejunal-jejunal intus-susception is usually found in the middle of the je-junum and is more commonly found in foals but canbe found in adults. Ileal –ileal intussusceptions canbe ultrasonographically scanned trans-rectally ascan ileo-caecal intussusceptions which can also beseen from the right flank area. Caeco-caecal intus-susceptions can be seen in the right ventral abdo-men and caeco-colic intussusceptions in the upperright quadrant of the abdomen.

Sand (gravel) colic / enterolithiasis can be evalu-ated ultrasonographically if the affected bowel isdisplaced ventrally by the weight of the sand / en-terolith and the bowel is adjacent to the body wall.An enterolith can be seen as a shadowcasting largehyperechoic line, often rounded. Sand can depressthe subperitoneal fat, resulting in little to no move-ment of the bowel and may be seen as hyperechoic

77


77

echoes casting shadows.

Nephrosplenic displacement: If the left kidney canbe visualized there is no bowel in the nephrosplenicspace. If it cannot be visualized, nephrosplenic en-trapment of the left colon is a differential diagnosisbut not a definite diagnosis.

Strangulating small intestines: oral to the stran-gulated area the intestine is often fluid-filled. Thestrangulated intestine usually has a thickenedoedematous wall with little motility.

Ileus: little or no peristaltic activity of the intes-tines is present. The bowel diameter is either nor-mal or increased and the wall thickness is usuallynormal

Herniation: abdominal wall, diaphragmatic, in-guinal and umbilical herniation of small and/or largeintestines may be seen with the intestines displacedinto abnormal positions. Depending on the insult tothe intestines various degrees of intestinal compro-mise may be seen. Intestinal motility may be mini-mal or absent.

Adhesions: may be seen as hyperechoic tissue be-tween intestines or, between the intestines and otherorgans or the abdominal wall. There will be de-creased to no motility of the intestines.

Abscesses: may be associated with any gastro-in-testinal organ and may also involve the mesentericroot and the abdominal wall. Abdominal abscessesoften have a loculated appearance but may alsoappear solid. Air-fluid interfaces can be seenultrasonographically and a surrounding capsule upto 10 cm has been reported.

Neoplasia: intestinal neoplasia may be visualizedif the affected intestine is adjacent to the abdomi-nal wall or palpable rectally. Lymphosarcoma isthe most common mass and has a relatively homog-enous ultrasonographic appearance. Intestinal ad-

enosarcoma, myxosarcoma, leiomyomas and benignpolyps have been reported..

78


78

Recent advances in understanding and preventing

founderRowe, J.B., University of New England,

Armidale, NSW 2351, [email protected]

Summary

It is becoming clear that the aeitiology of laminitisin horses fed grain or grazing lush green pasturesis essentially the same and has rapid fermentationof soluble carbohydrate in the caecum and colonas the primary factor. The challenge in managinglaminitis therefore focuses on controlling the in-take and pattern of carbohydrate digestion and/ormanipulating fermentation to prevent the accumu-lation of lactic acid and low pH that initiate thecascade of events leading to laminitis and second-ary complications. This paper summarises recentresearch to prevent the adverse effects of caecal/colonic fermentative acidosis by managing lacticacid-producing bacteria through selective antibi-otics or by vaccination against major lactic acidproducing bacteria of the equine hind gut.

The product Founderguard has been found to beextremely effective in reducing the risk of fermen-tative acidosis, laminitis and even some of the ad-verse behavioural changes that develop in horsesfed grain. Increasing interest in vaccination as analternative to using antibiotics led to a detailedstudy of the caecal and colonic bacteria respon-sible for lactic acid accumulation resulting fromrapid fermentation as a first step to producing vac-cines against these bacteria. These studies foundthat there are relatively few bacteria consistently

implicated in lactic acid accumulation and thatStreptococcus equinus and S. bovis are almost al-ways among the most aggressive lactic acid pro-ducers. Unfortunately experiments to investigateefficacy of vaccines have not demonstrated satis-factory efficacy. Our conclusion is that the productFounderguard, based on the antibioticvirginiamycin, remains the most effective methodof preventing fermentative acidosis associated withboth grain and pasture laminitis.

Introduction

Too much fermentable carbohydrate in the caecumand colon, whether associated with grain or lushpastures, essentially causes nutrition-related lamini-tis. Management and control of nutrition-relatedlaminitis depends on limiting the amount of ferment-able starch consumed, ensuring digestion in thesmall intestine or controlling acid production in thehind gut. Stated in this way the problem appears tobe relatively simple and therefore easy to manage.However, it is variability between horses, grainsand grain processing that makes as well as signifi-cant variation in the concentration of pasture car-bohydrates, that makes it such an unpredictable con-dition to manage and therefore prevent.

In addition to the unpredictable nature of its occur-rence, the permanent serious consequence of evena single event, makes laminitis one of the most im-portant aspects of equine management. Rotation isnot reversible and laminitis is therefore essentiallynon-treatable. Effective management relies on pre-vention. This paper reviews options for managingthe risks of hind gut fermentative acidosis andlaminitis.

Strategies for managing fermentativeacidosis

The major pathways involved in development ofacidosis and critical control points are summarisedin Figure 1.

79


79

Choice of grain Starch

or sugars

Lactic utilisation

Figure 1. Summary of the major pathways involvedin development of acidosis and control points wherethe condition can be managed or prevented.

Method of feeding

Lactic production

Buffers

LACTICVFA

*CHO*

**ph*

Once lactic acid starts to accumulate there is a verysignificant increase in acidity and decrease in pH.For this reason many of the successful strategies formanaging acidosis focus on reducing lactic acidproduction.

Feed composition and feeding

Choice of grain:

The amount of starch and its intestinal digestibilityare the critical factors. There are good reasons forthe traditional choice of oats as the starch is dilutedby significant levels of fibre and oil. In addition,oat starch tends to be more digestible in the smallintestine than other cereal grain. Grains such asmaize and sorghum tend to be the least digestible inthe small intestine and should be used with a degreeof caution. Recent research has found rye and cer-tain cultivars of triticale to contain starch that isefficiently digested in the small intestine (Bird etal. 1999). All methods of grain processing that in-volve heat treatment or cooking increase small in-testinal starch digestion and make grain safer forhorses. Steam flaking extrusion and micronisationare some of the most effective treatments. Apartfrom the cost of these treatments is the risk that over-consumption or incomplete digestion delivers highly

fermentable carbohydrate to the hind gut. Pro-cessed feeds while safer than unprocessed grainshould therefore still be used with caution. Thesecond consideration is the extent and rate of fer-mentation of undigested starch in the hind gut andis determined by intestinal digestibility, pattern offeeding as well as the fermentability of the carbo-hydrate. Frequent small meals are preferable tolarge amounts of grain in a single meal to ensureefficient digestion and also to minimize the amountof undigested starch entering the hind gut at anytime.

Pasture:

The major store of plant carbohydrates is in theform of fructans. During rapid growth and activephotosynthesis fructans can build up to over 20%of plant dry matter. Times of the year when fructansreach highest levels are in spring and autumn wherewarm clear days, suitable for photosynthesis, areoften combined with cold nights that limit respira-tion and the breakdown of fructans. Fructans arenot digested in the small intestine and pass throughto the colon and caecum where they are rapidlyfermented. Recently Pollitt and his colleagues havedemonstrated that laminitis can be induced by con-sumption of the fructan oligosaccharide, raftilose.The risk of excessive fructan intake involves acombination of fructan levels in the pasture, amountof pasture on offer, grazing pattern and rate of in-take. To some extent it can be managed by re-stricting grazing time and pasture management butit remains an extremely difficult aspect of horsemanagement and the risk is very real for all horsesgrazing lush pastures.

Microbiology

As indicated above, lactic acid accumulation isthe main contributor to fermentative acidosis. Thisis probably due to the rate that lactic acid can beproduced relative to the volatile fatty acids andsecondly the fact that lactic acid does not appear

80


80

Table 1: Effect of the antibiotics avoparcin and virginiamycin on pH, L-lactate and VFA duringthe incubation of mixed caecal/large colon digesta with buffer and cornstarch (15 mgml).

Antibiotic pH LactateTotal VFA Acet:Prop___________ ___________ ___________ ___________

(µg/ml) Mean SE Mean SE Mean SE Mean SEAvoparcin

0 5.34 0.042 46.8 2.93 97.5 6.56 2.9 0.182 6.14 0.054 8.9 1.04 102.6 1.92 2.9 0.058 6.33 0.006 11.0 0.42 82.1 4.92 3.3 0.06

32 6.43 0.012 15.1 0.57 89.8 2.33 3.6 0.16

Virginiamycin0 5.34 0.042 46.8 2.93 97.5 6.56 2.9 0.182 6.57 0.009 0.2 0.05 93.2 5.15 2.9 0.108 6.66 0.009 0.2 0.10 79.7 8.75 3.2 0.03

32 6.66 0.009 0.1 0.04 87.1 0.74 3.7 0.08

to be absorbed from the hind gut. Control of lactichas two options – restricting the production or in-creasing its conversion to VFA. Antibiotics andthe possibility of vaccination offer ways of reduc-ing activity of lactic acid producers whileprobiotics offer a possible way of increasing lac-tic acid conversion to VFA. While a number ofprobiotics have been investigated under experimen-tal conditions but logistics and cost preclude thisas a commercial option. Although there are a num-ber of lactic acid producing bacteria able to func-tion under anaerobic conditions in the hind gut thosethat are almost invariably associated with devel-opment of acidosis are Streptococcus bovis and S.equinus. S. bovis and probably S. equinus too,have the ability to switch from VFA production whenroughage is the main substrate to hom-lactate pro-duction in the presence of starch and sugar (Russell). This is an important adaptation. With roughageas the substrate, the amount of ATP per unit fer-mented is the limiting factor and VFA productionthe best option for growth. However, with starchor sugars available lactic acid production yieldsless ATP per mole of hexose but ATP productionand growth are far more rapid. S. bovis has a dou-

bling time of less than 30 minutes in presence ofstarch or glucose and quickly multiplies to play animportant role in total lactic acid production, aci-dosis and laminitis. S. bovis and S. equinus ap-pear to be the most important bacteria to control inorder to prevent acidosis and the use of a narrow-spectrum antibiotic a powerful tool.

Virginiamycin – FounderguardA large number of antibiotic feed additives wereexamined to determine in vitro inhibition of lacticacid production during incubation of equine caecaland colonic digesta. Virginiamycin was identifiedas the best. Compounds such as avoparcin andflavomycin, while reducing lactic acid productiondo not achieve the same level of control (see Table1; as seen below).

Efficacy of virginiamycin (asFounderguard) in acute carbohy drateoverloadAn early experiment with avoparcin highlighted theimportance of an appropriate formulation to ensurethat the active enters the caecum in sufficient con-centrations to be effective. When administered asthe premix there was good activity in the colon but

81


81

Figure 2. The changes with time in D-lac-tate and blood bicarbonate measured followingdosing with ground wheat. The horses in one groupwere treated with Founderguard and those in theother received no medication (Control).

little or no effect on lactic acid production in thecaecum. The Founderguard formulation ofvirginiamycin was developed to overcome thisproblem identified with a premix.Eight standardbred horses were used for this experiment (Roweet al. 1994). Four animals received Founderguardand 4 animals received the same treatment but with-out Founderguard. The animals, which receivedFounderguard, were pre-dosed for two days priorto administration of the wheat slurry based on themodel developed by Garner et al. (1975). Thedoses of wheat administered on the third day pro-vided 12 g ground wheat/kg liveweight. This wasgiven in two equal amounts with an interval be-tween doses. The animals were examined at 8 hourintervals over a period of 48 hours. Each exami-nation included temperature, heart rate and respi-ration in addition to assessment of lameness by anindependent operator and samples for analysis ofblood gases, D-lactate and faecal pH. After 48hours all animals were euthanased.

The results are summarised below in Figures 2.These show that treatment with Founderguard pre-vented accumulation of lactate in the gut (as shownin blood D-lactate levels) and this had an impor-tant effect on blood gases and pH. D-lactate is animportant indicator. It provides evidence of lacticacid accumulation within the gut, of microbial ori-gin, and also indicates a breakdown in the integrityof the gut wall (Krueger et al. 1986; Ding et al.1998)

Of the animals treated with Founderguard there noanimal showed any signs of lameness. In contrastthree out of the four control animals, which receivedno Founderguard, developed Obel grade 2 lame-ness (Obel 1948). There was a significant (p<0.05)reduction in lameness associated with the use ofFounderguard. The assessment of lameness byphysical examination was confirmed by histologi-cal examination of hoof sections. There was a closecorrelation (p<0.002, R2=0.94) between lamenessassessed according to the Obel grades and the in-

cidence and severity estimated by histological ex-amination (Pollitt 1996).

Based on the fact that it appears to take 18 to 24hours following administration of carbohydratebefore lactic acid levels rise an experiment wasdesigned to examine the possible therapeutic useof Founderguard for animals discovered during ac-cidental exposure to grain. Founderguard was ad-ministered 8 hours after first dose of grain and com-pared with no treatment or 3 days prior treatment

82


82

Table 2 Effect of virginiamycin applied as Founderguard on faecal pH, faecal lactate andlameness following administration of ground grain (Rowe, Pethick and Colbourn, Unpublished)

Control Therapeutic Prophylactic

Faecal lactic acid (mmol/L) 81 29 8Faecal pH 5.8 5.5 6.4Lameness (Obel scores) 1.38 0.80 0

Figure 3 Relationship between the sum of allincidents of adverse behaviour (wood chewing,eating bedding and grasping) per horse duringthe total 14 hours of observation during the week,and the average faecal pH during the correspond-ing week. (Johnson et al. 1998)

with Founderguard. The results are summarisedin Table 2 and show that therapeutic use ofFounderguard cannot be recommended.

Vaccine possibility?Research into vaccination against bacteria in fer-mentation compartments such as the rumen encour-aged research into vaccines against S. bovis and S.equinus. Vaccination has the potential to offer sig-nificant advantages over daily prophylactic admin-istration. Although preliminary results have beenencouraging in terms of antibody production, in vivoprotection against acidosis and laminitis has notbeen achieved.

Clays and buffersAlthough clays such as bentonite and zeolite canincrease faecal dry matter and reduce cowpat faecesthey do not reduce the risk of fermentative acido-sis. Buffers, such as sodium bicarbonate have aneffect on blood bicarbonate and systemic acid-basebalance but do not reduce the risk of fermentativeacidosis and do not appear to have a role in man-agement of founder.

Additional benefits of controlling fermentative acidosisBehavioural changes in horses fed grain are com-mon and include increased chewing of wood andbedding as well as being more difficult to handle.An experiment reported by Johnson et al (1998)examined the effect of Founderguard on behaviouralchanges in horses fed increasing amounts of grainrelative to hay. There were marked changes in thebehaviour of horses fed increasing levels of grainwithout Founderguard. During the same time the

behaviour of the horses maintained on hay only re-mained normal indicating that the development ofabnormal behaviour was a result of change in dietrather than boredom at being housed in a stable.The behaviour of horses fed grain withFounderguard was marginally, but not significantlydifferent from those fed hay. In animals fed grainwithout Founderguard there was a significant de-creased in faecal pH with increasing levels of grainin the diet. The faecal pH of horses fed grain withFounderguard was similar to those fed hay. The in-cidence of adverse behaviour was closely relatedto faecal pH (r2=0.96) (see Figure 3). These re-sults are consistent with those of Willard et al(1976) who reported that behaviour such as wood

83


83

chewing and eating bedding was closely related tothe concentration of lactic acid in caecal contentsand negatively related to caecal pH.

Summary of experience withFounderguard

Founderguard has now been used for nearly 10 yearsand after approximately 7.5 million doses it is clearthat Founderguard provides an effective and safeway of reducing the risk of laminitis. Although mostuse of Founderguard has been in Australia and NewZealand there has been significant use in the UKover the last three years. Founderguard has there-fore been extensively tested under a range of envi-ronmental and dietary conditions and in differentbreeds and ages of horses.

Side effects are rare but there are some thatveterinarians should be aware of.· First introduction of Founderguard at the full

dose can reduce feed intake and cause mild con-stipation. This potential problem is overcomeby gradually increasing the amount ofFounderguard over 3 to 4 days before giving thefull dose. If constipation dose occur it has beenfound to respond well to conventional treatment.

· Discoloration of urine to an orange/red colourcan occur when virginiamycin is first adminis-tered. This phenomenon has also been observedin dairy cattle and is thought to be associatedwith pasture pigments present in lush green feedparticularly when clover is present. There donot appear to be any adverse effects on the ani-mal and discoloration is transitory, returning tonormal after a few days.

· There have been anecdotal reports of horsesdeveloping some swelling of the lower hind legswhen first given Founderguard. This appears tobe very rare and it is not certain that it is actu-ally associated with the use of Founderguard.The few horses that developed swelling werewithdrawn from further treatment.

High-dose toxicity does not appear to pose a prob-lem. A study by SmithKline showed no adverseeffects associated with 8 times the recommendeddose. There have also been a number of instanceswhere, through accidental exposure, a horse haseaten a whole 1 kg container full without apparentadverse effect.

References1. Ding, Z., Rowe, J. B., Godwin, I. R., Xu, Y.,

Ball, F. M., and Atkinson, S. (1998). No lacticacid absorbed from the caecum and rumen ofsheep. Australian Journal of AgriculturalResearch 49: 293-301.

2. Garner, H. E., Coffman, J., Hahn, A. W.,Hutcheson, D. P., and Tumbelson, M. E. (1975).Equine laminitis of alimentary origin: Anexperimental model. American Journal ofVeterinary Research 36: 441 – 444.

3. Johnson, K.G., Tyrrell, J., Rowe, J.B. andPethick D.W. (1998). Behavioural changes instabled horses given non-therapeutic levels ofvirginiamycin. Equine Veterinary Journal 30:139-43.

4. Krueger, A. S., Kinden, D. A., Garner, H. E.,and Sprouse, R. F. (1986). Ultrastructural studyof the equine caecum during onset of laminitis.American Journal of Veterinary Research 47:1804 - 1812.

5. Pollitt, C. C. (1996). Basement membranepathology: a feature of acute equine laminitis.Equine Veterinary Journal 28: 38 - 46.

6. Rowe, J. B., Lees, M. J., and Pethick, D. W.(1994). Prevention of acidosis and laminitisassociated with grain feeding in horses. Journalof Nutrition 124: 2742S - 2744S.

7. Schwartz, H. M., and Gilchrist, F. M. C. (1974).Microbial interactions with the diet and the hostanimal. In “Digestive Metabolism in theRuminant.” (I. W. McDonald and A. C. I. Warner,eds.), pp. 165 - 179. University of New EnglandPublishing Unit., Armidale.

84


84

Perioperative equine mortalities

G.F. Stegmann Department of CompanionAnimal Clinical Studies, Faculty of Veterinary

Sciences, University of Pretoria.

IntroductionPerioperative mortality in equines higher (1:100,colics excluded) compared to small animals (1:700)and human patients (1:10 000). The mortality ratefor non-colic surgeries is 0.9 % and for all equinesurgeries 1.9%.

Perioperative mortalitiesThe highest number of deaths (colic surgery ex-cluded) is associated with horses anaesthetised forfracture repair and are not only from euthanasiaafter refracture. Prolonged anaesthetic time be-comes a significant risk factor.

Table 1. Incidence of perioperative equine mortalities* SURGERY ALIVE DEAD % Non-colic Orth (general) 14 120 0.7 Orth (fracture) 1087 4.7 Urogenital 8386 0.83 Miscellaneous 4675 0.70

Total non-colic 35 107 0.9

Colic Colic 3 487 10.8 Other abdom 431 7.1

Total colics 3 918 10.4 Total all cases 39 025 1.9

* Modified from Johnson et al. Vet Anaesth & Analg. 2002, 29, 159-170

Cardiac arrest or cardiovascular collapse, fractures,abdominal complications and myopathy are the mostcommon causes of death after anaesthesia.

Table 2. Causes of perioperative equine mortalities* Cause of death Percentage Cardiac arrest or CV collapse 33.2 Fracture 25.6 Myopathy 7 Abdominal 13.1 CNS 5.5 Respiratory 3.7 Post-op haemorrhage 1.2 Found dead 4.6 Other 9.5

* Modified from Johnson et al. Vet Anaesth & Analg. 2002, 29, 159-170

Table 3. Significant factors for altered perioperative mortalities*Age ++ < 1 month

+++ > 14 yearsType of surgery +++ FractureTime of surgery +++ 00:00 – 06:00Day of surgery +++ Saturday & SundaySurgery time +++….Premed ++ No premed

+ Romifidine ???- - - ACP

Anaesthesia +++ Total inhalation ???- - - Total intravenous

+ increased risk, - decreased risk*Modified from Johnson et al. Vet Anaesth & Analg. 2002, 29, 159-170

Other significant factors involved in anaestheticmortalities are anaesthetic time, type of surgery,time and day of surgery, age group, premedicationand anaesthetic drugs used. Not using any premedi-cation increased the risk and ACP decreased therisk. A high risk was associated with inhalationinduction and maintenance but probably related tothe use of this regime for emergency surgery in neo-nates. The low risk with intravenous induction andmaintenance is mostly associated with a short an-aesthetic time, uncomplicated surgery performedon young healthy animals. Choice of intravenousinduction technique did not influence anaestheticmortalities.

85


85

Causes of cardiac arrest:Hypoxia from hypoventilation, apnoea or pulmonary disease

Respiratory obstruction from nasal oedemaAtelectasis from lateral recumbencyResidual anaesthetic respiratory depression

Hypotension, toxaemia, shock and anaphylaxisInhalation anaesthetic drugsEndotoxaemia during colicHypocalcaemia

Overdose of anaestheticsRelative – CV compromisedAbsolute - ponies

Vasovagal reflex responses to surgeryCardiac disease, or trauma

Arrhythmias (AV-blocks) (African horse sickness ??)

Hypothermia

Comments on the “ideal” equinerecovery stable designü shape - round or octagonalü shape - rectangular 3X4 m: width allow

horse to lay in lateral recumbency, andlength a little longer to prevent the horsepicking up speed into the wall of death

ü size – as small as possible, when the horselies flat the ears should touch one side andfeet the opposite wall

ü floor - non-slip (Linatex rubber) withsoftish walls

ü ceiling should be high enough to hoist thehorse off the floor

ü door - half-high to see in and pull ropes forrecovery

ü door - opens at the top with platform laddersto man the head and tail rope (no peopledoors at floor level)

ü assistance - use head rope on everythingand have tail rope available

Current research in methods to minimize emergenceexcitement associated with inhalation anaesthesiais to administer IV anaesthetics consisting ofpropofol combinations during recovery.

Conclusion1. Prognosis plays an important role in mortality

rate e.g. abdominal surgery and fracture repair.

2. Prolonged surgical time a significant risk factorindependent from type of surgery.

3. Cardiac arrest, fractures during recovery, ab-dominal complications and myopathy are mostcommon factors in postoperative period.

4. Equine recovery stable design may have someinfluence on incidence of fractures during re-covery.

References1. Johnson G M, Eastment J K, Wood J L N, Tay-

lor P M 2002 The confidential enquiry intoperioperative equine fatalities: mortality resultsof Phases 1 and 2. Veterinary Anaesthesia andAnalgesia 29: 159-170

2. Grubb T L, Muir W W 1998 Anaesthetic emer-gencies and complications – Part 1 Equine Vet-erinary Education 10: 98-109

3. Hubbell J A E 1999 Recovery from anesthesiain horses. Equine Veterinary Education 11: 160-167

86


86

Equine DentalDiseaseG.B. Edwards

University of Liverpool

IntroductionThe equine species has evolved as a continuouslygrazing animal, developing its own dental form andfunction along the way. Every aspect of dental formis designed to provide the animal with an ability todetect, prehend, masticate and begin the digestionof forage. Horses are selective grazers and tend toavoid eating grass in areas polluted with faeces orhorse urine. Horses confirmed to stalls and al-lowed free access to hay exhibit the same feedingpatterns observed in free-ranging animals and usu-ally eat 10-12 hrs daily in sessions lasting 30-180minutes.

In contrast, confined horses eat concentrate orpelleted feed more rapidly and spend the remain-ing time in boredom.

The range of motion of the mandible during masti-cation is affected by the nature and size of the foodparticles being ingested. Horses on concentrateand pelleted diets have a limited range of jaw mo-tion when chewing compared with horses on grassor long-stemmed hay roughage. The jaw excursionpattern has an effect on molar tooth wear and couldexplain why confined horses seem to have moreproblems with upper buccal and lower lingualenamel points on their molar arcades

The dentition of the horse is classified in the het-erodont group of animals and is further divided intohypsodont and brachyodont types. The canine andfirst premolar teeth are brachyodont, having asimple root and a short crown to root ratio. Theseteeth are not in occlusal contact with the opposing

teeth, therefore the need for continual eruption toreplace crown wear is not necessary.

The incisors and molarised cheek teeth (premolar2, 3, 4 and molar 1, 2 3) are hypsodont, having thefollowing characteristics:

1. long anatomical crowns when the horse ismature and before it is mature and before it issubjected to occlusal attrition.

2. much of the crown is held in reservesubgingivally in the alveolar bone.

3. the root apices complete their developmentafter the tooth has erupted.

4. once fully formed, no further longitudinalgrowth takes place in the root apices.

5. teeth erupt throughout life at 2-3 mm per year asocclusal wear takes place, from grinding andcutting forage with a high concentration of bio-logic silica.

The eruption of teeth into persistent occlusion andfunction causes the reserve crown length to de-crease. The functional crown height and anatomi-cal root length remain relatively the same from thetime of tooth maturity, but the position of the rootapex migrates coronally as the height of the reservecrown decreases. By having reserve crown in thealveolar bone that erupts until the crown length isexhausted, horses are able to maintain a functionaldental apparatus well into old age.

Due to the dependence on accurate occlusal articu-lation of the teeth, which is responsible for evencrown wear, any disturbance in the integrity of thedental arcades as the result of jaw fractures, mal-occlusions or tooth loss can have serious dental re-percussions. Pathological over-eruption, toothdrifting, feed packing between the teeth and rootovercrowding lead to serious dental disease. Theapical foramen of hypsodont teeth become con-stricted once the tooth is fully mature. Therefore,they do not possess the extraordinary healing po-tential of the pulps of elodont teeth. The maturemouth of the horse will contain six incisors each in

87


87

both the upper and lower jaws and six upper andsix lower cheek teeth on each side of the mouth.Three cheek teeth are premolars and three are mo-lars. The molarised premolars have deciduous andpermanent sets. Molars come in at an older ageand only one set is present.

The first premolar or ‘wolf tooth’ is only presentin the upper jaw of some individuals. A furthervariation occurs between the sexes. The male nor-mally has all four canines while in the mare, al-though vestigial canines are not uncommon, theyusually fail to erupt.

It is customary to refer to cheek teeth 1 to 6 ratherthan premolars 2, 3 and 4 and molars 1,2 and 3.The modified Triadan system has been introducedto provide a more logical and easy to learn methodof identifying individual teeth.

The horse is anisonathic, which means that the bot-tom jaw is narrower than the upper, and the lateralexcursion of the jaw favours occlusal wear of thebuccal aspect of the lower and the palatal aspect ofthe upper molar arcades. The dental arches widenfrom rostral to caudal with more spaces betweenthe last molars than the first premolars. The oc-clusal surfaces of all six cheek teeth are compressedtightly together forming a single grinding unit, thuspreventing food from accumulating between theteeth.

The occlusal tables of the molarised cheek teethare sloped at an angle of 10-15° from dorsal lin-gual to buccal ventral. As the horse chews, the jawmoves in a rotating or circular motion from side-to-side with a limited rostral caudal excursion. Asthe jaw moves through a masticatory cycle, thesloped molar arcades on one side make contact.As the sloped arcades grind over one another, the10-15° pitch of the grinding surface drops the man-dible slightly, bringing the incisor arcades out ofcontact. In a well-balanced mouth, the jaws movefreely from side to side and the even grind of thecheek teeth can be heard.

The construction of the molars with interdigitationsof enamel, cementum and dentine allow for unevenwear with a sharp serrating surface when the horseis continually grazing as intended.

Malocclusion of the incisor arcades perpetuatesabnormal wear patterns that eventually lead to se-vere dental pathology.

The relationship of the upper cheek teeth to theparanasal sinuses has important clinical implica-tions. The bony sockets of the last four cheek teethproject into the maxillary sinus. (The root of the3rd cheek tooth may project fully or partially intothe sinus. As the horse gets older, the volume ofthe sinus increases as the teeth are extruded.

The teeth are composed of 3 calcified tissues:enamel produced by ameloblasts, dentine producedby odontoblasts and cement produced bycementoblasts. Pulp is the major soft tissue com-ponent of the teeth. Dentine is second in hardnessto enamel and forms the bulk of the tooth. The com-bination of the very hard but brittle enamel dentalskeleton, combined with a slightly softer but moremalleable dentine and cement, results in a structurewith high resistance to wear and shearing forces.The distribution of enamel cement and dentine en-sures a hard-wearing grinding surface on the tablewhich, although fairly flat overall, has various abra-sive ridges where the enamel wears down lessreadily than the softer cement and dentine. (Fig. 3).

Cement is the peripheral component in the toothinto which the periodontal ligament attaching thetooth to the alveolar bone inserts and which alsofills the infundibula. The infundibula of the cheekteeth frequently have development defects of thecement. The recently erupted cheek tooth has anenamel shell with a relatively low proportion ofprimary dentine and wide open pulp cavity at theapices. With age the deposition of secondary den-tine on the periphery of the pulp cavity as the tootherupts, results in an increase in the relative pro-

88


88

portion of dentine in the tooth. Consequently cheekteeth in young horses are brittle and should not becut with molar cutters, to avoid fracture with pulpexposure. Excessive overgrowths should be re-duced with manual mechanical rasps, whilst inolder horses molar cutters may be used with lessrisk of dental fracture. These more solid, older(7/8 year old) teeth require more effort to rasp com-pared to the softer teeth of young horses.

The mechanism of dental eruption is unclear butthe equine periodontal ligament appears to be adynamic structure as demonstrated by the occur-rence of temporary periodontal disease during erup-tion of the permanent cheek teeth in some horseswhich later resolves spontaneously.

The pulp is the gelatinous vascular tissue in thecentre of the tooth, the viability of which is neces-sary for production of secondary dentine through-out the life of the tooth.

Diagnosis of Dental Disease

Clinical Signs of Dental DiseaseThe clinical signs include the following either sin-gly or in combination with each other:-1. Difficulty in mastication2. Quidding (i.e. dropping pledgelets of partly

chewed food from the mouth)3 Loss of condition due to anorexia or improper

mastication4. Facial or mandibular swellings5. Maxillary infection and nasal discharge6. Discharging sinuses on maxilla or mandible7. Halitosis8. Adverse reaction to bit pressure

Examination of Equine TeethThe equine incisors and canine teeth are readilyexamined but satisfactory examination of the cheekteeth depends largely on the temperament of the

animal. Sedation and sometimes general anaesthe-sia may be necessary. Due to a combination of fac-tors, including the limited angle of opening of theequine mouth, the rostral positioning of the lipcommissives and the great length of the dental ar-cade, it is difficult to visually examine the cheekteeth, particularly the caudal cheek teeth.

Observation

1. Look for swelling of the maxillary region ormandible, purulent, often foetid, nasal discharge,or discharging sinuses. Observe the horse eat-ing and look for restricted mandibular movementswhich may be totally confined to one side of themouth. Listen to see whether there is a reduc-tion in the normal grinding sounds. The degreeof lateral mandibular movement and the animal’sresponse to manipulation can be manually as-sessed by fixing the maxilla with one hand withthe horse’s mouth closed, and sliding the man-dible transversely.

2. Palpate the cheek teeth through the cheeks. Feelfor evidence of food pocketing, or major irregu-larities such as a missing or deviated tooth.Check for evidence of pain when the cheek ispressed against the teeth which would suggestthe presence of sharp enamel points.

3. Examine the incisors for angle and abnormalwear (e.g. due to crib biting).

4. Check for the presence of wolf teeth.

5. Although a cursory examination of the more ros-tral cheek teeth can be carried out by withdraw-ing the tongue to each side in turn and illuminat-ing the buccal cavity with a torch, a detailedequine oral examination can only be performedusing a full mouth speculum (gag) such as aHausmann gag. Horses tolerate having this some-what cumbersome piece of equipment in their

89


89

mouth remarkable well. Care should be takento ensure that you or your assistant are not struckin the face should the horse throw its head about.Although some practitioners use a gag inunsedated horses, sedation facilitates the exami-nation and reduces the risk of injury. If it isdifficult to open the horse’s mouth using the gag,first check that the noseband is sufficiently loose.Pushing a thumb against the hard palate will usu-ally prompt the horse to open its mouth further.Food retained in the oral cavity should be re-moved by flushing the oral cavity with water.Manual removal of remaining food accumula-tions may be necessary after flushing. The useof a head light (a pen torch is much less satis-factory) and a long metal ‘toothpick’ greatly fa-cilitates the examination. Major problems, es-pecially of the caudal upper and lower cheekteeth and of the adjacent periodontal membranes,can be easily missed unless all the teeth. andadjacent soft tissues (gums) are carefully visu-ally examined and palpated.

1. Examine the upper and lower arcades for evi-dence of sharp edges, hooks, fractured or devi-ated teeth, food impacted in gaps between theteeth and evidence of separation at the gum mar-gin.

ii. Examine the cheeks and tongue for abrasion orulceration.

iii. Smell your fingers after completing the oralexamination. A foetid smell indicates anaero-bic infections most commonly of the periodon-tal tissues, but also of the teeth themselves.

iv. Check the occlusal surfaces for irregular con-tour associated with wave or step mouth. Manyequine cheek teeth disorders, especially in theyounger horse, are due to localised periapicalabscessation, but in most cases, little or nochange is usually visible at the occlusal surfaceof the crown, except in some maxillary teeth

apical infections where fractures and gross den-tal caries may be present.

Radiography of Equine Teeth

Dental radiography is especially valuable for evalu-ation of localised apical infections, traumatic andother types of dental fracture, supernumerary andmisaligned cheek teeth, and dental related tumours.Because of the excellent contrast between the air-filled nasal cavity and sinuses, and the teeth andsupporting bones, high powered x-ray machines arenot necessary to obtain diagnostic radiographs ofequine dental disease.

In most cases root and reserve crown detail ratherthan exposed crown detail is required. Therefore,oblique views are essential to project the roots un-der scrutiny, clear of the contra-lateral side. Theradiographic changes are often subtle and their dem-onstration requires high quality radiographs whichdepend on careful positioning, correct beam angleand absence of movement.

Although it is technically easier to obtain dentalradiographs with the horse under general anaesthe-sia, satisfactory radiographs can be safely taken inthe standing horse provided certain procedures andprecautions are taken.

· Heavy sedation is helpful in that it results in low-ering of the head and reduces the likelihoodof movement

· When taking lateral films, the cassette shouldbe placed in contact with the side of the headcorresponding with the affected dental arcade

· Grids are not required· Handlers should wear lead gowns, gloves and a

radiation exposure badge· A cassette holder should be used where pos-

sible· Handlers should stand clear of the main beam

which should be collimated· A fabric, webbed head-collar without metal

90


90

components should be used· Centre the beam on the suspect tooth at the middle

of the arcade. Always include cheek tooth 1 or6 to allow identification of individual teeth

· If an external sinus tract is present in the man-dible or the rostral maxillary region, a straightmalleable, metallic probe should be inserted intothe tract prior to taking the radiograph

Lateral radiographs

This view is obtained with the x-ray plate in a ver-tical position as close as possible to the affectedside of the head, with the x-ray beam centred onthe suspect tooth and perpendicular to the screen.The main disadvantage of this projection is thatboth teeth arcades are superimposed. However, itis valuable in demonstrating fluid lines in the max-illary sinuses which can be caused by periapicaldisease of cheek teeth 3 to 6. If the paranasal si-nuses are full of inspissated pus, this will have tobe removed by lavage via a trephine hole prior totaking projections to show the tooth roots.

To identify disorders of the erupted crown, an openmouth latero-oblique projection is useful. Themouth is held open with a piece of plastic pipingor wood and a latero-oblique projection of 15° istaken.

Lateral Oblique Radiographs of theMaxil lary Teeth

Latero-ventral radiographs taken at 30° to 35°angles (higher in smaller animals) are necessaryto outline the separate apices of the maxillary teeth.The x-ray plate is placed vertically close to theaffected side and the x-ray tube is placed at a higherlevel on the opposite side and is directed ventro-laterally at the appropriate angle. Care should betaken to avoid rostro-caudal angulation. Accuratepositioning is critical.

Latero-oblique Radiographs of Man

dibular Cheek Teeth

Similarly, latero-dorsal projections of 45° outlinethe apices of the mandibular cheek teeth.

Dorso ventral Radiographs

Dorso ventral radiographs must be taken with thebeam centred very accurately because the mandibu-lar cheek teeth rows are so close together. Conse-quently slightly oblique projections will not out-line the medial aspect of the cheek teeth.

The limited areas of the nasal cavity and sinusesthat are exposed medial to the mandible can exhibitdystrophic nasal calcification and sinus empyema.Lateral displacement of sagittal maxillary cheektooth fractures, and gross destructive dental changes,can also be detected as can mandibular and maxil-lary fractures.

Intra-oral Occlusa RadiographsEvaluation of incisor teeth is best done using intra-oral ventro-dorsal or dorso-ventral projections.

Radiographic Signs of Dental Disease

Experience of the normal is essential. The appear-ance of the normal permanent teeth varies with theage of the horse and the stage of development of theteeth. Eruption is brought about by an increase inpulp vascularity which is seen as a cystic disten-sion of the lamina dura (a radiographic white linewhich represents the interface of the periodontalligament and alveolar bone). These distensions canvary is size between individual horses and give riseto concern if they are large. However, they can bedistinguished from apical abscesses by their asso-ciation with an erupting tooth, their regular outlineand absence of sclerosis and periosteal reaction.

The radiographic appearance of apical infectionsvaries greatly. Change include loss of definition ofthe lamina dura, loss of normal outline of the tooth

91


91

apex, irregular bone lysis surrounded by irregularsclerosis, clubbing of the tooth root due to cementdeposition and occasionally discrete spherical ag-gregations of cement.

The apices of normal, recently erupted cheek teethwill have a radiolucent appearance when comparedwith more mature teeth but there is no surroundingsclerosis. For example, major radiographic dif-ferences are present between the apices of the 3rd

and 4th cheek teeth in a 4 year old horse becausethe 4th cheek tooth is 3 years older than the 3rd.Therefore, caution must be exercised when com-paring the radiographic appearance of adjacentcheek tooth apices in young horses.

A more marked sclerosis develops around the api-ces of all of the mandibular teeth and upper cheekteeth 1-3 which are positioned in denser bone thanthe thin alveolar bone covering the roots of cheekteeth 4-6 within the maxillary sinuses. In some earlycases of periapical infection in the maxillary si-nuses, a rounded, soft tissue granuloma or, later, anencapsulated abscess, may be apparent over theinfected apex.

Even experienced clinicians can differ greatly intheir radiographic interpretation of dental infectionsespecially in early cases. Because of the seriousconsequences of removing the wrong tooth or com-plications which could arise from removing a toothunnecessarily, it is better to have a very conserva-tive approach to these cases. If it is not clearwhether a tooth needs to be removed, it is better toerr on the side of caution and to re-evaluate radio-graphically 4-6 weeks later.

Additional Diagnostic Aids

ScintigraphyScintigraphy can be useful in identifying preciselywhich tooth has apical infection when conventionalradiography and clinical examination has failed to

provide unequivocal evidence of disease.

Gamma scintigraphic examination of the equinehead can be performed easily and relatively quicklyin the standing patient. Sedation, the use of blink-ers and plugging the ears with cotton wool help toreduce the frequency of movement in response toexternal stimuli. Providing a stable headrest alsohelped to reduce movement.

Ten MBq/kg cwt 99m technetium methylenediphosphonate is administered via an indwelling1/v vatheter and images are obtained 3-4 hours later.Right lateral, left lateral, dorsal and ventral viewsare obtained. The arcades of the maxillary andmandibular premolar and molar teeth are identi-fied as regions of high radioisotope uptake (RU) inall views. There is no RU in the teeth themselves.However, RU in the alveolar and periodontal boneresults in multiple arch-like intensities in the max-illary and less prominently in the mandilular ar-cades. There are striking differences between im-ages taken from horses of different age groups onthe lateral views of the dental arcades. In horses <6 years of age, the multiple arch-like intensitiesare clearly defined, particularly in the maxillarycheek teeth and it is easy to identify the site of eachcheek tooth. In contrast, in horses > 11 years ofage, the definition of these arches is reduced and itis increasingly difficult to define the outline of in-dividual teeth.

In horses with dental disease, scintigraphic exami-nation will show discrete areas of radionuclideuptake indicating increased bone metabolism as-sociated with periapical infection and periodontaldisease. The radionuclide uptake is seen in theinterproximal and periapical bone. The presenceof periapical infection leads to discrete focal ar-eas of increased RU in the periapical alveolar boneassociated with dental infection. The presence ofperiodontal disease causes an increase in RU inthe interproximal bone, sometimes of multiple teeth.

92


92

Scintigraphy therefore, can provide complemen-tary information to radiography, allowing for amore accurate diagnosis of periapical dental in-fection in horses. A study evaluating the use ofscintigraphy for detection of dental disease showedthat it had a high sensitivity (90%) but a moderatespecificity (75%) for the detection of periapicalinfection. In comparison, radiography had a mod-erate sensitivity (66.7%) but a high specificity(95.2%). When radiography and scintigraphy wereused together, there was a high sensitivity (93%)and a high specificity (95.2%).

Computed tomography and magnetic resonance im-aging provide a means of obtaining detailed im-ages of dental abnormalities but will not be widelyavailable for economic reasons for the foreseeablefuture.

DENTAL DISEASES

A. Developmental Diseases

Developmental dental anomalies that occur inhorses include supernumerary teeth, odontomas andtumours including teratomas, impactions, missingteeth, retention of primary teeth, maleruption, mal-occlusion and malposition of teeth and the devel-opmental absence of cementum.

PolydontiaThis term refers to any anomaly in which the num-ber of permanent teeth exceeds the normal dentalformula. The supernumerary teeth lie inside or out-side the dental arcade, but in the case of the molararcade are usually lingual.

Treatment is indicated when mastication is impairedby inflammation following mechanical injury toadjacent soft tissues.Supernumerary cheek teeth are not uncommon. Theteeth are usually abnormally large and irregularlyshaped as if formed from two or even threevestigeal cheek teeth. They most commonly occur

at the caudal aspect of the cheek teeth arcade. Foodpocketing occurs between them and the 6th cheektooth with resulting pain and possibly deeper in-fections. If unopposed, they will later form largeovergrowths. Either the tooth or the overgrowthmay require removal.

Retained Deciduous TeethThe term pseudopolydontia is sometimes appliedto persistence of the temporary teeth which resultsfrom the faulty positioning of the correspondingpermanent tooth and the absence of the mechanicalpressure necessary to result in root resorption ofthe milk tooth and its eventual expulsion. They arerelatively common in the incisor arcade. If the per-sistent tooth is pushed labially, it can cause ulcer-ation of the mucosa of the lip. Removal is simple.

Retention of remnants of the deciduous cheek teethcan occur in horses between 2-6 years of age. Whenvery loose, or just partially retained by gingivalattachments, they may cause oral irritation. Affectedhorses may quid, or suffer bitting problems and oc-casional loss of appetite for a day or two. Suchsigns in horses in this age group warrant a carefulexamination of the rostral 3 cheek teeth for evidenceof loose ‘caps’. If present, they should be removedusing a specialised ‘cap extractor’ or a long slimscrewdriver.

DiastemaThe occlusal surfaces of all 6 cheek teeth are nor-mally compressed tightly together and the cheekteeth function as a single grinding unit. Even withage (the cheek teeth taper in slightly from crown toapex) the progressively smaller reserve crownsusually remain tightly compressed at the occlusalsurface.However, if spaces (often 2-5 mm wide) which aretermed diastema to develop, clinical problems willoccur. In some cases, the diastemata will be due toinsufficient angulation of the cheek teeth to supplyenough compression. In other cases, diastemataoccur along with displacements and apparently nor-

93


93

mal angulation indicating that the dental buds de-veloped too far apart.

Food will become impacted into these abnormalinterdental spaces and will lead to progressivelydeeper secondary periodontal disease. Diagnosiscan be difficult without the use of an endoscope.

Treatment is problematical . Many horses mayshow severe clinical signs when fed hay but im-prove greatly when at grass. If marked diastemataare present between a small number of teeth, ex-traction of a tooth on one side of the diastema willoften result in a complete cessation of quidding.

Inferior Brachygnathia or ‘ParrotMouth’

This developmental abnormality in which the up-per incisors lie in front of the lower ones is com-mon in horses. It causes little or no difficulty inprehension but rostral positioning of the maxillaryarcades relative to their mandibular counterpartswill, in time, lead to the development of largeovergrowths (hooks) on the first upper and lastlower cheek teeth. Regular removal of the 1st up-per CT hook using a carbide rasp or power tool isrequired throughout the horse’s life.

The overgrowths on the caudal aspect of the 6th(caudal) lower cheek teeth frequently go undetec-ted and can lacerate the adjacent mucosa. There isvery little space between the occlusal surfaces ofthe caudal cheek teeth and even less if a large over-growth is present. There is also little space be-tween these teeth and the vertical ramus of the man-dible so it is easy to damage this bone when vigor-ously rasping the lower cheek teeth.

Molar cutters and percussion guillotines can beused to remove these overgrowths but fracture ofthe tooth with exposure of the pulp can occur, es-pecially in small breeds which have marked dor-sal curvature of the caudal surface of the cheek teeth.Such fractures and pulp exposure can lead to sep-

tic infection of the mandibular and pharyngeal ar-eas. Consequently, power tools are now commonlyused to safely and controllably remove theseovergrowths.

Displacement of Cheek TeethTwo causes of cheek teeth displacement arerecognised. In most cases, the medial or lateraldisplacements appear to be due to overcrowdingof the dental rows during eruption and this type ofdisplacement is usually bilateral. Rotation of thedisplaced tooth is also sometimes present. Grossovergrowths then develop on areas of the displacedtooth and their occlusal counterparts which are notin contact.

Acquired cheek teeth displacements (usually man-dibular) can develop in older horses and are asso-ciated with less displacement and limitedovergrowths. These acquired displacements arebelieved to be caused by abnormal angulation ofthe occlusal surfaces.

The protruding parts of the teeth and theovergrowths can lacerate the oral soft tissues andin some cases deep food pocketing can lead to pe-riodontal disease. In these cases, the displacedtooth has to be extracted. Less severe cases can bemanaged by regular removal of protrusions with amotorised tool.

Dental Tumours

1. OdontomaThis tumour can arise from any one of a combina-tion of various mesodermal elements making up thetooth. It may become cyst-like and is most com-monly sited in the mandible. Treatment comprisescurettage under general anaesthesia.

2. AdamantinomaThis tumour is epithelial in origin and arises fromthe ameoloblasts in the enamel organ. Occasion-ally it may undergo malignant changes and invadesurrounding tissues.

94


94

Temporal Teratomas (Dentigerous cysts)A dentigerous cyst is a special form of dental ter-atoma characterised by the presence of dental tis-sue at the base of a draining sinus tract. It appearsas a fluctuating swelling at the base of the ear in ayoung horse, often accompanied by a dischargingfistula which opens part of the way up the marginof the pinna. In some cases, the swelling com-prises a cyst without aberrant dental tissue.

Treatment comprises surgical excision. An obliqueradiograph will give some indication how closelythe tooth is related to the skull. Care must be takenwhen freeing the tooth not to fracture the temporalbone.

B. Acquired Disorders of theCheek Teeth

1, Disorders of WearDue to their prolonged eruption (circa 20-25 years),any areas of equine teeth that are not in full occlu-sion will continue to erupt and such areas will even-tually project beyond the normal occlusa surfaceas overgrowths.

The normal movement of the narrower mandibulardental arcade across the maxillary arcade resultsin the outer (buccal) edges of the maxillary teethand the inner (lingual) edges of the mandibularcheek teeth becoming sharp. During mastication,food lying between the maxillary and mandibularcheek teeth is initially crushed by closing the jaws. This is followed by a sideways medial move-ment of the mandible which involves the medial(lingual) edges of the mandibular teeth movingacross the lateral (buccal) surface of the maxillaryteeth in a shearing action that is referred to as the‘power stroke’. The buccal aspect of the maxil-lary cheek teeth and the lingual aspect of the man-dibular teeth are consistently the leading edges butundergo the least wear due to anisognathism.

The power stroke is exerted on either the right orleft side and food is frequently masticated on thesame side repeatedly before being moved to thecontra lateral side or swallowed. It appears thatthe amplitude of the lateral mandibular movementis greater when chewing forage compared to con-centrate feeds. While eating more particulate con-centrate feeds which may have a reduced tendencyto bind as a bolus compared to forage, a restrictedlateral mandibular movement maintains the food inclose proximity to the cheeks. This may result inreduced wear of the leading edges of the arcadesand subsequent development of enamel points.

Food stagnation will occur at the gum margin dueto lack of normal movement of food and salivaaround the oral cavity and this will lead to second-ary periodontal disease. As dental eruption is de-pendent upon the presence of a healthy periodontalmembrane, teeth that have marked periodontal dis-ease will erupt more slowly than the adjacent teethwith healthy periodontal membranes. This may leadto the occlusal surface of the cheek teeth develop-ing an uneven or undulating occlusal surface, termedwavemouth. Some cases of wavemouth, however,are unrelated to periodontal disease.

Step MouthThe height of adjacent teeth due to defective growth,or extraction of a tooth.

Sheer MouthThis is an extreme form of cheek tooth malocclu-sion with reduction of the lingual surfaces of themaxillary teeth and buccal surfaces of the mandibularteeth. There is complementary overgrowth of thebuccal surfaces of the maxillary teeth and lingualsurfaces of the mandibular teeth. The result is se-vere malalignment of the cheek teeth surfaces andextremely sharp ineffective edges.

In advanced cases of dental overgrowths, affectedanimals may not be able to fully clear their mouthof food. Semi-permanent hamster-like cheek swell-

95


95

ings may occur in badly affected horses, due to theaccumulation of fibrous food wedges between thelateral aspects of the cheek teeth and the cheeks. Inthe presence of oral pain, and later also due to me-chanical factors due to large overgrowths, somehorses chew very slowly and don’t make the nor-mal vigorous crunching sounds when eating for-age. Some horses may use just one side of theirmouth for chewing rather than using alternativesides, or they may hold their head in an abnormalposition during chewing.

Treatment of these abnormalities includes removalof major overgrowths using specialised dentalshears, chisels, guillotines, power tools or embryo-tomy wire followed by careful rasping. As unop-posed cheek teeth may erupt abnormally quickly,there is a danger that if a large cheek tooth over-growth (e.g. a 3cm long stepmouth) is cut to thelevel of the remaining cheek teeth, the pulp may beexposed. This is because sufficient secondary den-tine may not have developed at that level to oc-clude the pulp cavity. This prevent such end-stagedisorders as severe periodontal disease and looseteeth by regular (twice yearly) dental inspectionsand removal of any detected overgrowths therebyencouraging normal chewing action and allowingthe free movement of food and saliva around theoral cavity.Smooth mouth, i.e. absence of enamelon the occlusal surface of cheek teeth, is commonin old horses. Teeth without enamel are ineffec-tive at grinding food.

C. Dental Diseases

Periodontal disease

Inflammation of the periodontium is usually due toinfection of its fibrous layer from the oral cavity.

In older horses it starts following gingival retrac-tion, or loosening of some teeth due to senile atro-phy of the bony support apparatus, or altered pres-

sure during mastication brought about by irregularocclusal wear.

In young horses, the disease is due to congenitaldefects (polydontia, diastema) or disturbances ineruption of the cheek teeth. Only the cheek teethare usually affected.

Periodontal disease in the horse has been dividedinto four categories based on the evaluation of theseverity of the lesion.

1. Local gingivitis with hyperaemia andoedema.

2. Erosion of the gingival margin 5mm andperiodontal pocket.

3. Periodontitis with loss of gum.

4. Gross periodontal pocketing, lysis of alveolar bone, loosening of bone support.

Horses with grades 1 & 2 periodontal disease maynot show overt signs of oral discomfort. The care-ful owner may notice some excess salivation and asensitivity to cold water. Halitosis is the pathog-nomonic sign for severe periodontal disease in thehorse.

As soon as the tooth and mucoperiosteum separate,feed and debris accumulate and bacterial fermen-tation leads to progressive infection of the peri-odontal membrane and eventually the alveolar wall.The tooth loosens as the dental supporting struc-tures are gradually destroyed. In the upper cheekteeth, the infection may break through into the nasalcavity or into the maxillary sinus.

Treatment

Prevention is better than treatment. Once gum re-cession and loss has occurred, it is not possible toundertake a treatment regime which will result in

96


96

re-attachment of gum and a reduction of gingivalpocket size. In the horse, consequently, the equineclinician’s role is to eliminate irregularities of wear,oral ulcers and other conditions that may initiatethe progressive process of periodontal pathology.

In horses with major irregularities of wear and ad-vanced periodontal pocketing, treatment is aimedat restoring as closely as possible, normal or nearnormal occlusion. Loose teeth should be extractedand periodontal pockets enlarged and irrigated.

Dental Decay and Endodontic DiseaseIn many species, and particularly in man, dentalcaries is the most common cause of dental decay.Caries is a disease of the calcified tissues of theteeth characterised by demineralisation of the in-organic, and destruction of the organic, substanceof the tooth.

Dental caries does occur in the horse but the termhas been subjected to various interpretations basedon aetiopathogenesis. Horse caries occur under anumber of circumstances. Some foods that are car-ies forming may adhere to the tooth crowns (sweetfeeds, high molasses content).

It has frequently been misinterpreted that infundibu-lar cemental hypoplasia is in fact caries but histo-pathological examination reveals that this is notthe case.

Despite the confusion over the incidence and sig-nificance of maxillary teeth cemental hypoplasia,there is no doubt that the presence of food materialimpacted into areas of hypoplastic cement does cre-ate the potential for bacterial fermentation, acidproduction and caries of cement to be initiated.Dental caries is a progressive localised destruc-tion of dental tissue due to chemical and bacterialprocesses. It requires an initial mechanical injuryto the outer cement layer and the upper cheek teethare commonly involved due to the pattern of the

infundibulum. Extension of the necrosis eventuallyleads to involvement of the pulp cavity.

Pulpitisnflammation of the pulp cavity, which has both bloodand nerve supply, usually results from caries, hy-poplasia of the cement lakes or, occasionally, frac-tures of the teeth, although the last mentioned is of-ten secondary. The inflammation may be confinedinitially to one root. Pulpitis leads to periapicalabscess with swelling and fistula formation or in-fection of the maxillary sinus depending on the toothinvolved.

Dental Surgery

Cheek Tooth ExtractionCheek teeth may be removed via the mouth, by ret-ropulsion via trephine holes or, in the case of themore rostral teeth, by lateral buccotomy.

Oral extraction of cheek teeth in very old horseswhose teeth have very little reserve crown remain-ing, or grossly diseased or fractured teeth, is rela-tively straightforward. In recent years with theavailability of effective sedatives and improvedinstrumentation, there has been a move towards oralextraction of cheek teeth in much younger horses.

General anaesthesia, preferably with a cuffed en-dotracheal tube to prevent aspiration of blood clotor debris, is essential if a tooth is to be removed bytrephination or by lateral buccostomy.

Thorough radiological and clinical examinationshould be carried out to determine the tooth or teethinvolved and the nature of the condition. On thebasis of this examination the site for trephination ischosen, bearing in mind that variations occur in theposition of the dental root relative to the crowns asthe horse gets older.

The operator must be aware of the location of im-portant structures such as the infra-orbital and fa-

97


97

cial nerves, facial artery and vein and parotid ductwhich may encroach on the proposed site of trephi-nation or buccostomy.

Mandibular TeethThe trephine hole is made over the root of the af-fected tooth on the ventral border of the jaw. Oncethe tooth root is exposed, the tooth is repelled us-ing an 8mm x 25cm punch and a heavy steel ortho-paedic mallet. Care must be taken to ensure thatthe correct tooth is removed and that the punch doesnot slip off the root damaging the adjacent tooth orthe medial or lateral mandibular plates. In rela-tively young animals the tooth must be struck re-peatedly for several minutes before any progressis made. The sudden loosening and movement ofthe tooth is heralded by a distinct change in tone asthe punch is struck.

Maxillary Teeth (Fig. 5)The course of the nasolachrimal duct correspondsto a line drawn from the medial canthus of the eyeto the angle formed by the nasal and premaxillabones. Therefore, to avoid injury to it, the trephineholes must be placed below this line.

Cheek teeth 1 and 2 lie in front of the sinus; 3, 4and 5 are approached via the maxillary sinus and6, which is only rarely affected, via the frontal si-nus and the fronto-maxillary opening. Because ofthe curvature of the face, a suitably angled punch isnecessary in order to apply the necessary forcealong the long axis of the tooth.

Following retropulsion of a tooth, it is examined tocheck that it is complete. The alveolus is searchedwith a finger and any fragments of bone are re-moved by curetting the cavity. If possible, postop-erative radiographs are taken to ensure that all po-tential sequestra have been removed. Alternatively,insertion of a wide endoscope into the mouth en-ables fragments of tooth to be identified. In orderto prevent food entering the sinuses or alveolus,the oral entrance of the alveolus is plugged with

gutta-percha softened in warm water. The remain-der of the mandibular alveolus, or trephine hole inthe maxillary sinus is plugged with a roll of gauzewhich can be removed to allow daily irrigation untilhealing is well advanced.

Although the majority of cases heal satisfactorily,a significant proportion (50% or more) require fur-ther surgical intervention because of persistent al-veolar infection due to sequestra.

Extraction of Cheek Teeth by LateralBuccotomy (Fig. 6)This technique affords direct vision to remove thebuccal alveolar bone before sectioning the toothand delivery of the segments. The advantages ofthis approach are the safety of adjacent teeth andthe simplicity of aftercare.

Vital anatomical structures in the area must beavoided. (7th cranial nerve, and parotid duct es-pecially in the region of cheek teeth 2 to 4, the fa-cial branches of the external maxillary artery andvein, and the buccal venous plexus).

A horizontal skin incision is made at the level ofthe occlusal surface of the tooth in question.Branches of the facial nerve are identified and thebuccinator muscle incised without damage to thenerve. This exposes the tooth. A muco-periostealflap is created and the exposed buccal bone is re-moved with an osteotome or drill. The tooth isthen sectioned longitudinally and the two halveselevated and removed. Any fragments of root arecarefully removed.

The socket is packed with ribbon gauze soaked inmetronidazole exited through a stab incision in theface. The mucoperiosteal flap and the skin are su-tured.

The technique is most frequently employed in theremoval of upper and lower cheek teeth 1 and 2 butcan be employed to remove the 5th lower cheek

98


98

tooth which is sometimes displaced medially. Thisrequires an incision along the rostral margin of themasseter muscle, care being taken to avoid damageto the parotid duct and vessels. The masseter muscleis then separated from the underlying mandible, suf-ficiently far caudally to expose the alveolar bonecovering the reserve crown of the 5th tooth.

Extraction via the MouthMore recently there has been a move back to ex-tracting cheek teeth via the mouth.

Improved sedative techniques and instrumentationallow teeth to be removed in the standing horse.Proper extraction technique based on sound dentalsurgical principles minimises postoperative discom-fort and encourages rapid healing of associated softtissues.

Oral extraction can be performed on any tooth butspecial consideration should be given to teeth withgross caries as these crowns may disintegrate dur-ing extraction. Diseased caudal maxillary teeth areoften associated with secondary sinusitis and surgi-cal drainage of the sinuses is required. The morecaudally situated teeth are more difficult to accessthrough the mouth making instrument placement andmanoeuvring more challenging.

Careful preoperative examination of the patient isimportant and all aspects of the approach should beplanned before surgery is undertaken. Special con-sideration should be given to the age of the horse,type of dental pathology, position and number of rootapices and to the structural integrity of the toothcrown. Radiographic and endoscopic examinationsshould be carried out pre- and post-operatively tosupport the clinical findings.

Instruments required include:-

1. Molar spreader or separators2. A set (4) of molar extraction forceps

3. Dental fulcrum4. Molar cutter5. Set of dental elevators and curettes

Oral extraction cannot be performed without firstloosening the tooth (400-500 kg force is requiredto extract a cheek tooth from a fresh cadaver skull).

1. The molar spreaders are used to place pressureon the periodontal ligaments, stretching thembeyond the elastic limit over a 5-10 minute pe-riod.

2. The gingival mucosa is separated from the buc-cal and lingual edges of the tooth crown with asharp dental elevator to expose enough crownto allow forceps placement.

3. Proper sized extraction forceps are placed onthe tooth crown and the handles tied together.The forceps are rocked from side to side untilthe tooth is felt to loosen indicated by a suckingsound. Undue haste or too great a force must beavoided. It may take 1-2 hours in younger horsesbefore the tooth becomes loose.

4. Once the tooth is loose, the forceps should berepositioned to get a firmgrip of the crown andwith the aid of a fulcrum block placed near thehead of the forceps the tooth is removed usinggradual firm traction.

5. Check to make sure the tooth has been removedin its entirety.

Endodontic Therapy

Endodontics is the branch of dentistry that coversthe diagnosis, management and prophylaxis of dis-ease of the dental pulp and periapical tissues. Someof the principles of endodontic therapy used in mancan be applied to the horse. In horses in which adiagnosis of pulp infection is based on clinical andradiographic findings the selection of endodontic

99


99

therapy versus tooth extraction is based upon thesummation of the following observations:-

a. absence of other significant diseaseb. the localisation of the peri radicular disease pro-

cessc. the availability of equipment and operative dis-

eased. economic factors

In young horses (4-6 years old), there may not beadequate maturation of the tooth roots to enable feel-ing to be achieved.

1. In very simple terms the procedure involves ex-posure of the apex of the diseased tooth fol-lowed by transection.

2. Sterilisation of the diseased pulp chamber byphysical removal of all the non-vital necroticpulp tissue with a file followed by high volumeirrigation of the cavities with sterile saline and2.5% sodium hypochlorine solution. The com-plexity of the shape of the pulp chambers in thehorse means that complete cleansing is almostimpossible.

3. Complete filling of the exposed pulp chamber.The cavity must be dry. Best material is a com-bination of gutta percha and a mixture of zincoxide and eugenol. The zinc oxide and eugenolis mixed and injected via a syringe. The pulpchamber is then lined by this material and filledwith gutta percha.

4. Apical Seal: The apex is sealed with multiplemixes of standard amalgam.

Results

Best results reported in mandibular teeth. Eighty-four per cent absence of complications. If the tech-nique fails, tooth extraction is performed.

Equine Dental Equipment

Dental Rasps (floats)

In order to effectively rasp (float) a horse’s teeth, aset of dental rasps (floats) are required. A mini-mum of 4 different shaped or length handles arerequired.

1. A long straight handled rasp for the caudal 2 or3 (or even all) of the lower cheek teeth.

2. A short straight float for the rostral lower cheekteeth.

3. A short handled rasp with an angled or offsethead to rasp the first and second upper cheekteeth.

4. A long handled, obtuse angled rasp for the cau-dal upper cheek teeth.

Rasp bladesTwo main types of rasp blades are currentlyutilised:-

a Metal blades with particles of tungsten carbidechips attached which can vary from fine, me-dium to coarse. They are inexpensive and ro-bust, and are suitable for removing routineenamel point but are very ineffective at remov-ing major overgrowths which, if extensive, couldtake hours of manual rasping to reduce.

b Solid tungsten carbide blades which can be flator concave. They can havea variety of cuttingsurfaces varying from fine, medium, to coarsecutting edges; the latter is too aggressive for rou-tine dental rasping (floating). These blades areboth very expensive and brittle, and need to becarefully looked after. They can, however, beused to quickly remove all but the largest dentalovergrowths relatively quickly. In young horsescare should be taken not to excessively rasp theteeth with these blades. Due to the fact that theseblades cut in only one direction, the bladesshould be set in the handle to cut in a rostraldirection (‘on the pull’) for the caudal cheekteeth overgrowths, in order to prevent trauma to

100


100

the vertical ramus of the mandible. Likewise,shorter rasps with solid carbide blades fitted tocut in a caudal direction (‘on the push’) are usedfor removing rostral mandibular cheek teethovergrowths.

‘S’-FloatsThese floats usually come as short (30cm long) andlong (45cm) floats. The shorter S float is usuallygritted with tungsten carbide chips on both sides,often with fine gut on one side and coarse gut onthe other. Consequently, when using such a floatthe soft tissues of the mouth should be protectedfrom the back of the float by keeping the operatorsfingers on the back of the blade.

The longer S-float which is mainly used for thecaudal cheek teeth, is gritted on one side only. S-floats are very versatile and essential instruments,especially for awkward areas in the horse’s mouth.

A bucket with a brush attached to the inside is nec-essary to allow dental debris to be readily removedfrom the rasp blades during dental procedures. Itshould be filled with lukewarm water containing adilute disinfectant such as povidone iodine orchlorhexidine.

Motorised Equine Dental InstrumentsMotorised dental tools have the advantage of re-ducing operator fatigue and allowing even the largeovergrowths to be quickly, fully and controllablyremoved. A large variety of such instruments areavailable. Some with a wide diameter are not ef-fective at removing overgrowths at the caudal as-pect of the equine mouth. This is especially true ofovergrowths of the 6th lower cheek teeth.

One instrument (Eisenhuit) has a blade that is rela-tively atraumatic to soft tissue and which rotateshorizontal to the occlusal surface of the teeth. Op-erators should use face masks and safety goggleswhen using such instruments.

These power instruments are used mainly for re-moval of major dental overgrowths but are beingused increasingly for routine prophylactic dentaltreatment. Due to their great power, there is a riskof over-rasping the teeth and leaving the occlusalsurface smooth. This will prevent proper chewingof forage in the short term until differential wearbetween occlusal enamel, cement and dentine re-stores the grinding surface, and in the long term willreduce the longevity of the teeth.

Dental ShearsDental shears have been the instruments tradition-ally used to remove larger dental overgrowths.Molar cutters can have single or compound joints,and either A type jaws which have no space be-tween the blades or D type jaws where the bladesare over 2cm apart when closed.

They should not be used in younger horses (< 8 yrsof age) whose teeth are shell-like because of thehigh proportion of brittle enamel with minimalamounts of secondary dentine; these teeth are likelyto fracture if cut with shears. Motorised instru-ments are used in these cases.

Percussion InstrumentsPercussion instruments can also be used to removefocal overgrowths but again, due to the risk of frac-ture, they should be confined to tall narrowovergrowths of the caudal cheek teeth, particularlyin older horses.crotic pulp tissue with a file fol-lowed by high volume irrigation of the cavities withsterile saline and 2.5% sodium hypochlorine solu-tion. The complexity of the shape of the pulp cham-bers in the horse means that complete cleansing isalmost impossible.

3. Complete filling of the exposed pulp chamber.The cavity must be dry. Best material is a com-bination of gutta percha and a mixture of zincoxide and eugenol. The zinc oxide and eugenolis mixed and injected via a syringe. The pulpchamber is then lined by this material and filled

101


101

with gutta percha.

4. Apical Seal: The apex is sealed with multiplemixes of standard amalgam.

Results

Best results reported in mandibular teeth. Eighty-four per cent absence of complications. If the tech-nique fails, tooth extraction is performed.

Equine Dental Equipment

Dental Rasps (floats)In order to effectively rasp (float) a horse’s teeth, aset of dental rasps (floats) are required. A mini-mum of 4 different shaped or length handles arerequired.

1. A long straight handled rasp for the caudal 2 or3 (or even all) of the lower cheek teeth.

2. A short straight float for the rostral lower cheekteeth.

3. A short handled rasp with an angled or off sethead to rasp the first and second upper cheekteeth.

4. A long handled, obtuse angled rasp for the cau-dal upper cheek teeth.

Rasp bladesTwo main types of rasp blades are currentlyutilised:-

a Metal blades with particles of tungsten carbidechips attached which can vary from fine, mediumto coarse. They are inexpensive and robust, andare suitable for removing routine enamel point butare very ineffective at removing major overgrowthswhich, if extensive, could take hours of manual rasp-ing to reduce.

b Solid tungsten carbide blades which can be flator concave. They can havea variety of cuttingsurfaces varying from fine, medium, to coarsecutting edges; the latter is too aggressive for rou-tine dental rasping (floating). These blades areboth very expensive and brittle, and need to becarefully looked after. They can, however, beused to quickly remove all but the largest dentalovergrowths relatively quickly. In young horsescare should be taken not to excessively rasp theteeth with these blades. Due to the fact that theseblades cut in only one direction, the blades shouldbe set in the handle to cut in a rostral direction(‘on the pull’) for the caudal cheek teethovergrowths, in order to prevent trauma to thevertical ramus of the mandible. Likewise,shorter rasps with solid carbide blades fitted tocut in a caudal direction (‘on the push’) are usedfor removing rostral mandibular cheek teethovergrowths.

‘S’-FloatsThese floats usually come as short (30cm long) andlong (45cm) floats. The shorter S float is usuallygritted with tungsten carbide chips on both sides,often with fine gut on one side and coarse gut onthe other. Consequently, when using such a floatthe soft tissues of the mouth should be protectedfrom the back of the float by keeping the operatorsfingers on the back of the blade.

The longer S-float which is mainly used for thecaudal cheek teeth, is gritted on one side only. S-floats are very versatile and essential instruments,especially for awkward areas in the horse’s mouth.

A bucket with a brush attached to the inside is nec-essary to allow dental debris to be readily removedfrom the rasp blades during dental procedures. Itshould be filled with lukewarm water containing adilute disinfectant such as povidone iodine orchlorhexidine.

102


102

Motorised Equine Dental InstrumentsMotorised dental tools have the advantage of re-ducing operator fatigue and allowing even the largeovergrowths to be quickly, fully and controllablyremoved. A large variety of such instruments areavailable. Some with a wide diameter are not ef-fective at removing overgrowths at the caudal as-pect of the equine mouth. This is especially true ofovergrowths of the 6th lower cheek teeth.

One instrument (Eisenhuit) has a blade that is rela-tively atraumatic to soft tissue and which rotateshorizontal to the occlusal surface of the teeth. Op-erators should use face masks and safety goggleswhen using such instruments.

These power instruments are used mainly for re-moval of major dental overgrowths but are beingused increasingly for routine prophylactic dentaltreatment. Due to their great power, there is a riskof over-rasping the teeth and leaving the occlusalsurface smooth. This will prevent proper chewingof forage in the short term until differential wearbetween occlusal enamel, cement and dentine re-stores the grinding surface, and in the long termwill reduce the longevity of the teeth.

Dental ShearsDental shears have been the instruments tradition-ally used to remove larger dental overgrowths.Molar cutters can have single or compound joints,and either A type jaws which have no space be-tween the blades or D type jaws where the bladesare over 2cm apart when closed.

They should not be used in younger horses (< 8 yrsof age) whose teeth are shell-like because of thehigh proportion of brittle enamel with minimalamounts of secondary dentine; these teeth are likelyto fracture if cut with shears. Motorised instru-ments are used in these cases.

Percussion InstrumentsPercussion instruments can also be used to remove

focal overgrowths but again, due to the risk of frac-ture, they should be confined to tall narrowovergrowths of the caudal cheek teeth, particularlyin older horses.

Further Reading

Equine DentistryEdited by J. Baker & J. Easley.W.B. Saunders.

Dixon, P.M. et al. (1999).Equine Dental Disease Pt. I. A long term studyof 400 cases: Disorders of incisor canine and1st premolar teeth.Eq. Vet. J. 31, 369-377.

Dixon, P.M. et al. (1999)Equine Dental Disease Pt. II. A long term study of400 case: Disorders of development, eruption andvariations in position of the cheek teeth.Eq. Vet. J. 31, 519-528.

Dixon, P.M. et al. (2000).Equine Dental Disease Pt. III. A long term study of400 cases: Disorders of wear, traumatic damageand idiopathic fractures, tumours and miscellaneousdisorders of the cheek teeth.Eq. Vet. J. 32(1), 9-18.

Dixon et al. (2000).Equine Dental Disease Pt. IV. A long term study of400 cases: Apical infections of cheek teeth.Eq. Vet. J. 32, in press.

Lane, J.G. (1994).A review of dental disorders of the horse, their treat-ment and possible fresh approaches to management.Eq. Vet. Educ. 6, 13-21.

Wyn Jones, G. (185).Interpreting radiographs of the head.Eq. Vet. J. 17, 274-275 and 417-425.·

103


103

104


104

Endoscopy ofthe upper

Respiratory tractof young horses:

What does it mean in thecontext of Pre-purchase

Examinations?

J. Geoffrey Lane BVetMed DESTSFRCVS

University of Bristol, Department ofClinical Veterinary Science, Langford

House, Langford, BRISTOL BS 405DU, United Kingdom

IntroductionGrading of recurrent laryngeal neuropathy(RLN)Clinicians are generally obsessed with scoring orgrading the disorders with which they come intocontact whether it be the severity of feather peck-ing in chickens, hip dysplasia in dogs or the func-tion of the equine larynx. The purpose is invariablyto provide an objective and repeatable method todocument observations so that the clinician will beable to know with confidence the state of a condi-tion on a given day or, should the proverbial buscome around the corner at an inopportune moment,others will be able to use the clinical data to goodeffect.

The five point scheme shown here to grade the en-doscopic perception of equine laryngeal motilityat rest in the stable, including on return from exer-

cise – quiet breathing - has been used at Bristolsince the early 1980s and in Australasia since1993(Lane, 1993, Kannegeiter and Dore, 1995). It isnot very different from the 4-point scale used inNorth America (Rakestraw et al,,1991) and hasbeen continued simply because it has been found tobe workable in everyday equine laryngologicalpractice.

Grade 1.All movements, both adductory and abductory aresynchronised and symmetrical regardless of whethersedated or examined before or after exercise. A‘mirror’ effect is achieved through a perspectiveartifact whereby the right arytenoid appears lessabducted when the endoscopy is performed throughthe right nostril and the left is similarly less ab-ducted when the larynx is viewed via the left nasalchamber

Grade 2.All major movements are symmetrical and a fullrange is achieved. Transient asynchrony, flutter ordelayed opening may be seen (Baker, 1983)

Grade 3.There is asymmetry of the rima glottidis at rest dueto reduced motility by the left arytenoid cartilageand vocal fold, but there are occasions, typicallyafter swallowing or during the nostril closure ma-noeuvre, when full symmetrical abduction isachieved

Grade 4.There is consistent asymmetry of the rima glottidisbut with some residual active motility by the leftarytenoid cartilage and vocal fold. Full abductionis not achieved at any stage

Grade 5.True hemiplegia. There is obvious and consistentasymmetry of the rima glottidis with no residualactive motility by the left arytenoid cartilage andvocal fold. No responses to the ‘slap’ test are pro-voked

105


105

Total: 3497

RLN Grading

1 2 3 4 5 Not Graded

784 2008 618 69 9 12

22.4% 57.4% 17.6% 2.0% 0.26% 0.34%

Authors Group Size Population RLN Incidence(sic. Grades 4 and 5)

Pascoe et al (1981) 235 Horses in training 2.6%

Raphael (1982) 479 “ 3.3%

Baker (1983) 537 “ 4.7%

Lane et al (1987) 6860 Yearlings at sale 0.96%

Sweeney et al (1991) 678 Horses in training 1.8%

Survey of 3500 yearlingsAt the request of a major owner/breeder video-endoscopic recordings were made of the upper res-piratory tracts of 3500 yearlings during a 15 yearstudy and the findings have been reviewed. Thestudy has provided a unique opportunity to esti-mate the prevalence of laryngeal disorders as wellas to assess the distribution of functional anoma-lies in the Thoroughbred.

Although the subjects represent an elite group ofhorses on the basis of genetic selection, unlike pre-vious investigations (Pascoe, et al, 1981; Raphael,1982; Baker, 1983; Lane et al, 1987; Sweeney, etal, 1991), these were unbroken and therefore un-tried animals. Initially approximately half of theyearlings had been purchased, some privately andsome at auction, and half were homebred. In recentyears the majority of the yearlings examined havebeen homebred and yet the distribution of the find-ings has remained constant. The findings in regardto the distribution of gradings was as follows:The twelve yearlings for which no grade was as-signed included seven animals afflicted with thefourth branchial arch defect syndrome and an addi-

tional five where there was mal-function on the rightside and where no physical explanation was dis-covered

The value, or otherwise, of using any system ofgrading equine laryngeal function during quietbreathing, will be discussed later in this workshop.It is sufficient to say here that all horses showingGrade 5 were later confirmed to show severe ob-structive dyspnoea and that most of the Grade 4horses were also clinically diseased.

This is in line with previous findings (Morris andSeeherman, 1991) which showed that dynamic col-lapse of the left arytenoid cartilage (ACC) and vo-cal fold (VCC) developed in the overwhelmingmajority – 20 out of 27 horses with Grade 4 (sic)motility at rest. The prevalence of clinically sig-nificant RLN, i.e. Grades 4 and 5, was found to be2.26% and this can be regarded as a base level foran unselected population of Thoroughbred horses.It compares with previous reports of selectedgroups (see below):

The greatest diversity of opinion hinges on the sig-nificance of Grade 3 motility and whether this rep-resents a performance-limiting malfunction, orwhether it should be viewed as a variant of nor-mality. This grading does not discriminate betweenthe abilities to achieve and to maintain full abduc-tion as these are subjective judgements. A largenumber of group, listed and stakes race winners

106


106

have come from the horses with this grading. Thenumbers of Grade 3 horses which required or weresubjected to corrective surgery later in life is notknown but from studies of animals examined byhighspeed treadmill endoscopy (see later) it is safeto conclude that the majority are ‘normal’ showingsustained symmetrical abduction of the arytenoidcartilages and vocal folds throughout exercise.However, horses with Grade 3 RLN are at a sig-nificantly greater risk of sustaining ACC and orVCC at exercise than horses with Grades 1 and 2RLN.

Although the designation of a Grade 1 or 2 scoreduring quiet breathing does not convey absoluteprotection against ACC or VCC during exercise,susceptible horses invariably show other featuressuch as palpable atrophy of the crico-arytenoideusdorsalis muscle and a progressive inspiratory noiseat exercise.

In conclusion, the 5-point grading scheme for RLNhas proved to be a practicable means to assess la-ryngeal function in Thoroughbred horses which hasa useful predictive value in regard to the likeli-hood of clinical disease provided that it is used inconjunction with other techniques such as palpa-tion and an exercise test. Assessments of upper res-piratory tract function which rely on endoscopyduring quiet breathing alone should be regarded asinadequate.

Long-term longitudinal study of laryngealfunction in 187 foalsThe sale of foals to be retained to go into trainingor to be resold as yearlings - “pin-hooking” formsa major component in the marketplace for Thor-oughbred horses. Prospective purchasers seek totake precautions to ensure that the animals con-cerned will be suitable for resale, or can be trainedeffectively for racing. It has become fashionablefor foals to be subjected to endoscopic examina-tions on behalf of prospective purchasers prior to

sale. Some breeders also seek endoscopic exami-nations of foals ahead of sales if only for peace ofmind. However, is endoscopy of foals a worthwhileprocedure and are the results dependable?

A number of congenital structural abnormalities ofthe URT can be diagnosed accurately by a combi-nation of palpation and endoscopy (Embertson,1997). These conditions include midline clefts andother defects of the palate, pharyngeal and sub-epi-glottal cysts and fourth branchial arch defects. Theseabnormalities are collectively relatively unusualand arise in no more than 0.5% of Thoroughbredsborn (see later). A major interest for foal purchas-ers often centres on laryngeal function and the iden-tification of RLN.

In order to assess the reliability of the interpreta-tion of laryngeal function a group of 197 foals wereexamined by endoscopy and 187 were availablefor re-examination one year later. The video-endo-scopic records were reviewed “blindly” - the find-ings are shown in the table below and the obviousconclusion to be drawn is that there are inconsis-tencies in the two series of results.

The laryngeal function of some foals appeared tobe within normal limits, but then to have ‘deterio-rated’ over the following 12 months, while otherswhich would have been damned had they been ex-amined prior to sale as foals turned out to be totallynormal. Chance would have it that there was nofoal or yearling in the group studied which was af-flicted with any of the congenital abnormalitiesmentioned above. In summary, endoscopy of foalsis not an absolutely dependable technique and de-cisions on whether to buy or to reject should not bebased upon this technique.

A review of subsequent racing performances at 2,3 and 4 years of age showed that the median stakeswinnings of the yearlings in this study were great-est in the Grade 3 group.

107


107

Laryngeal 1 2 3 4 5Grade (32) (112) (37) (6) (0)

MedianWinnings 1933 5358 5367 724 0(£)

Thus, the median stakes winnings of the yearlingsin this study were greatest in the Grade 3 group.

Conditions of sale at public auctionsrelating to respiratory impediments

The implementation of Conditions of Sale relatingto respiratory impediments at public auctions iscontroversial. The justification for such proceduresis obvious when obstructions of the URT are knownto be performance-limiting and purchasers shouldhave the confidence that the animals which they arebuying have a chance equal with others to be trainedand race effectively if not successfully. ‘Wind’ test-ing at sales also has a deterrent effect against theunscrupulous vendor who may wish to pass off ahorse knowing it to be defective. In order to giveconfidence ‘wind’ testing must be practicable, safeand provide consistent results. Suffice it to say herethat there is not, and cannot ever be, a system whichtales account of every rare situation and deliversthe correct decision in all cases.

At North American sales yearlings and horses intraining are deemed returnable to vendor if theyare found to be afflicted with one or more of a speci-fied list of disorders: “laryngeal hemiplegia (com-plete immobility or inability to fully abduct (!) thearytenoid cartilage); rostral displacement of thepalato-pharyngeal arch; clefts of the palate; epig-lottal entrapment; permanent dorsal displacementof the soft palate; severe arytenoid chondritis orchondroma; and sub-epiglottal cyst or cysts. TheseConditions of Sale are implemented solely on thebasis of endoscopic examinations of the standinghorse.

In the UK ‘wind’ Conditions of Sale are limited toRLN so that other, albeit rarer, disorders are notproscribed. This was the case at Goffs until thisyear when a list of specified diseases similar tothose itemised in the USA has been included. Themajor difference between the UK/Ireland and theUSA is that in order to be returnable the lot mustalso produce a characteristic inspiratory noise whenactively exercised as well as showing endoscopicevidence of disease. Horses are usually lunged soonafter sale by a veterinary surgeon engaged by thepurchaser and, provided that he/she is satisfied thatthe lot is unsatisfactory on both counts, the horse isreferred for adjudication by a veterinary panel ap-

Yearling Grades (187)

1 (32) 2 (112) 3 (37) 4 (6) 5 (0) NR

Foal Grades (197)

1 (36) 12 14 4 0 0 6

2 (123) 17 86 16 1 0 3

3 (29) 3 11 12 2 0 1

4 (9) 0 1 5 3 0 0

5 (0) 0 0 0 0 0 0

108


108

pointed by the auctioneers. The role of the panel isto assist the auctioneers in the interpretation of theirConditions of Sale, not to represent the interests ofbreeders, purchasers or insurance underwriters,and nor are they engaged to forecast changes whichmay take place at a later date. Their role is simplyto determine on the day whether or not the featuresshown by the horse fulfill the criteria for it to bereturned to the vendor.

Between 1987 – 1995 the total number of year-lings sold at Tattersalls Houghton and October saleswas 9524 of which 78.8% were examined by pur-chasers’ veterinary surgeons. 149 (1.56%) werereferred for a panel assessment and 59 (0.65%)were found to be returnable to vendor. Such a levelof ‘failure’ confirms that a selection process hasalready taken place when yearlings are presentedfor sale – the 0.65% failure rate should be com-pared with the 2.26% with Grades 4 and 5 RLN inthe unselected population – and/or that ‘wind’ Con-ditions of Sale do indeed have a deterrent effect.The fate of all horses presented to the panel hasbeen reviewed in order to check on the validity of‘wind’ procedures. A cohort of control horses wascreated by reference to the sales’ catalogues andtaking the two horses sold on either side of eachhorse referred to the panel.

Between 1984 and 2002 no yearling has sustaineda significant injury during the ‘wind’ testing pro-cess and, thus, the procedures can be regarded assafe. The overwhelming majority of panel deci-sions were made unanimously and in the rare caseswhere there was dissent this was generally on thebasis of whether the noises heard were ‘character-istic’. A review of the racing records of the horsesat 2, 3 and 4 years of age together with their life-time performance data has shown that the ‘failed’group were less successful at all levels.

They were twice as likely to be unraced (34% vs17% of the control group), had fewer race startsand were less likely to win or be placed. No infor-

mation is available regarding which of the returnedhorses, if any, was subjected to corrective surgery.In regard to the 90 horses which were ‘passed’ bythe panel after referral there was no statisticallysignificant disparity between them and the controlcohort using any of the parameters above. The re-sults of this review support the view that in a fieldwhich will inevitably produce instances of injus-tice the panel scheme is successful in safely iden-tifying a group of horses which will perform belowexpectation.

ReferencesBaker, G.J. (1983) Laryngeal asynchrony in thehorse: definition and significance. In: Equine Exer-cise Physiology, Eds. D.H.Snow, S.G.B.Persson andR.J.Rose. Granta Editions, Cambridge, 46 – 50

Embertson, R.M. (1997) Weanling and yearling up-per airway evaluation. In: Current techniques inEquine Surgery and Lameness, eds White, N.A andMoore, J.N. Philadelphia: W.B.Saunders Co. 122-127

Kannegeiter, N.J. and Dore, M.L. (1995) Endos-copy of the upper respiratory tract during treadmillexercise: a clinical study of 100 horses. Aus. vet.J.72, 101 – 107

Lane, J.G., Ellis, D.E. and Greet, T.R.C. (1987)Observations on the examination of Thoroughbredyearlings for idiopathic laryngeal hemiplegia.Equine vet. J. 19, 531 – 536

Lane, J.G. (1993) Equine recurrent laryngeal neur-opathy (RLN): current attitudes to aetiology, diag-nosis and treatment. Proceedings of the 15th Bain-Fallon Memorial Lectures, Australian Equine Vet-erinary Association, 173 - 192

Morris, E.A. and Seeherman, H.J. (1991) Clinicalevaluation of poor performance in the racehorse:the results of 275 evaluations. Equine vet. J. 23,169 - 174

109


109

Pascoe, J.R., Ferraro, G.L., Cannon, J.H., Arthur,R.M. and Wheat, J.D. (1981) Exercise-inducedpulmonary haemorrhage in racing Thoroughbreds:a preliminary survey. Am. J. vet Res. 42, 703 –707

Rakestraw, P.C., Hackett, R.P., Ducharme, N.G.,Nielen, G.J. and Erb, H.N. (1991) Arytenoid carti-lage movement in resting and exercising horses. Vet.Surgery 20, 122 – 127

Raphael, C.F. (1982) Endoscopic findings in theupper respiratory tract of 479 horses. J.Am. vet.med. Assoc. 181, 470 – 473

Sweeney, C.R., Maxson, A.D. and Soma, L.R.(1991) Endoscopic findings in the upper respira-tory tract of 678 Thoroughbred racehorses. J. Am.vet med. Assoc. 198, 1037 - 1038

110


110

External Herniasin Horses

Barry EdwardsUniversity of Liverpool

Definition of an External Hernia: -The protrusion of a viscus, or part of a viscus,through a naturally occurring opening in the abdomi-nal wall to produce a swelling covered by skin.They include umbilical and scrotal/inguinal her-nia. The term rupture is often used loosely insteadof hernia, but strictly speaking applies to an abnor-mal opening in the abdominal wall.

A hernia may be reducible or irreducible. Mosthernias are reducible and the contents of the her-nial sac can be returned to the abdomen by gentlepressure, allowing the defect to be readily palpated.Hernias become irreducible when the contents be-come incarcerated within the hernial sac or arefixed by adhesions.

The contents of the hernial sac may comprise smallintestine, caecum, or omentum.

An incarcerated hernia is one where distension ofthe herniated viscus increases its diameter to thepoint where it is tightly held at the hernial ring. Atthis early stage, there is no vascular impairment ofthe bowel and the bolus of gas or ingesta may moveon spontaneously or respond to gentle pressure. If

the intestine remains trapped, the constricting pres-sure obstructs the venous and lymphatic drainage,causing an increase in mural thickness and quicklyleads to arterial occlusion (strangulated hernia).This complication frequently develops in animalswhich have had a reducible hernia for severalweeks or months. Intermediate sized hernial ringsare potentially the most serious because they arebig enough to allow intestine through, but not largeenough to accommodate any sudden increase in di-ameter due to distension.

Strangulated hernias require immediate surgicalcorrection. Animals with incarcerated herniaswhich reduce spontaneously, or in response to ma-nipulation, should undergo surgery to close the ab-dominal defect without too much delay to avoid thesame complication recurring. A Richter type her-nia involves protrusion of only part of the total di-ameter of intestine causing only partial occlusionof its lumen. If corrected promptly, the degree ofischaemic damage is such that it will often resolvewithout resection. However, if not surgically cor-rect, such hernias which most commonly involveileum or caecum in the horse and abomasum incattle, result in necrosis of the viscus and anenterocutaneous fistula.

The term ventral hernia is applied to hernias (?rup-tures) involving any part of the ventral abdominalwall excluding the umbilicus and inguinal canals.They include traumatic ruptures which commonlyoccur at a particular site associated with inherentweakness of the abdominal wall, and incisionalhernias.

Types of hernia rupture and species in which they are seen most commonly

Horses Cattle Sheep Goat PigsUmbilical + + +Congenial Scrotal + +Acquired Inguinal / Scrotal + + +Ventral ruptures + + + +Incisional + +

111


111

Umbilical hernias

HorsesRelatively common. Present at birth or soon after-wards. More common in filly than in colt foals.Possibly a hereditary factor. An American studysuggested that they are less common when the cordis allowed to break naturally. The defect variesfrom 1 finger to 4-5 finger diameter, but most aresmall. Those of 1-2 finger diameter may resolvespontaneously as the foal grows. For this reasonsurgery is often delayed until after weaning.

However, it is routine on the Newmarket studs toapply rubber elastrator rings across the base of thehernial sac in young foals after careful manipula-tion of its contents back into the abdomen. Thisprocedure may be performed with the foal standingor alternatively under sedation with the foal re-strained on its back. The umbilical sac sloughs 3-4 weeks after application of the ring. Surprisinglymaybe, foals with defects up to 3-4 fingers in di-ameters, healing takes place without apparent prob-lems. Personally I prefer to close the ring withsutures where the defect is 3 fingers or greater inwidth.

Diagnosis

In uncomplicated cases palpation of the swellingat the umbilicus allows the contents to be easilyreduced allowing the defect in the abdominal wallto be identified and a hernia confirmed. The size,shape and rigidity of the margin of the defect shouldbe assessed as this may influence choice of treat-ment method. Infections of the umbilical remnantsin foals are much less common than in calves andare rarely a complicating factor in diagnosis.

When incarceration of a viscus occurs the foalshows sudden onset colicky pain and the previouslyrelatively flaccid hernial sac is now tense and pal-pation is resented. Ultrasonographic evaluationwill demonstrate an entrapped viscus and allow

any thickening of its wall to be identified.

Surgical Repair

The surgery is performed under general anaesthe-sia with the foal in dorsal recumbency. After rou-tine preparation, the skin is incised in the mid lineextending from just caudal to the ring to a similardistance cranial to it. Encircling the umbilical scarleaving it attached to the peritoneal sac provides auseful point for application of fixation forceps dur-ing dissection of the sac. In most small herniasremoval of excess skin is unnecessary, but if re-quired, it is useful to mark the location of the ellip-tical incision at this stage in the surgery by makinga very superficial incision of the skin.

The dissection is now continued through the nu-merous layers of connective tissue which can beseen to separate as the knife is drawn across untilthe peritoneal sac, which is usually relatively thick,is reached. Once this is identified, the remainingdissection can proceed quite quickly to the samelevel allowing the peritoneal sac to be isolateddown to the abdominal wall.

I prefer to leave the peritoneal sac intact and insertit into the abdomen. In the majority of cases, thedefect in the abdominal wall can be closed usinginterrupted, modified mayo sutures which overlapthe margins for a few mm. In some cases, the sizeand/or rigidity of the defect makes it necessary touse a piece of mesh to fill the defect rather thanattempting closure with suture which could be dis-rupted be excessive tension. Applying fixation for-ceps to either side of the ring and attempting tooverlap the edges will give an indication of thedegree of traction necessary. If considered to bequite difficult to overlap the edges, it is preferableto use mesh bearing in mind the tension on the ab-dominal wall will be significantly greater when theanimal is standing.

Closure with suture

112


112

Non-absorbable suture material such as prolene isused. I prefer to use a multifilament sheathed ny-lon suture (supramid) because of greater ease ofhandling. Using a round bodied needle 3-5 modi-fied mayo sutures are laid, but not tied off. Byintroducing a finger below the margin of the de-fect, thereby pushing the peritoneal lining againstthe underneath surface of the abdominal wall, anyrisk of damage to intestine can be eliminated. Whenall the sutures are in place, traction is applied toall at the same time allowing the edges to be over-lapped. This traction is maintained until all thesesutures have been tied. If excess skin needs to beremoved, it is excised at this stage. The amplesubcutaneous connective tissue which was previ-ously dissected from the peritoneal sac is closedwith a continuous suture of 0 vicryl followed bythe skin with interrupted non-absorbable suturesor staples. Any potential dead space can be oblit-erated using a stent, or if necessary, a belly bandwhich can be removed 72 hours later.

Mesh ClosureThe surgical procedure up to the stage of returningthe peritoneal sac to the abdominal cavity is iden-tical to that described. A piece of woven polypro-pylene mesh (Marlex mesh ) is cut to shape, sothat it overlaps the margin of the defect by 2cm.Sutures of 1 prolene are placed in the mesh N, S,E, & W and points in between and held in arteryforceps. The suture at one pole of the mesh is thentaken through the margin of the defect from insideto out taking the same precaution to avoid damageto the intestine as previously described. This istied securely. The procedure is repeated with theremaining sutures, alternating between the twosides. By ensuring that the sutures are placed thesame distance apart as in the mesh, the mesh willbe placed under even tension giving the appear-ance of the top of a trampoline. Closure of subcu-taneous connective tissue and removal of excessskin is as previously described.

Ventral HerniasFlank ruptures

Although these can involve any part of the abdomi-nal wall, they most commonly occur at a specificsite which is the same in all the species. This sitelocated just in front of the stifle joint correspondswith the weakest part of the abdominal wall justlateral to the border of the rectus muscle. Here thetwo oblique muscles and the transversalis muscleare aponeurotic. Most of these ruptures result froma sudden increase in intra-abdominal pressure due,in the horse, to collisions with vehicles or, morecommonly, becoming straddled over a gate.

The animal presents with a swelling which may besmall and well defined if the peritoneum remainsintact, or large and diffuse if it too has ruptures. Inthe latter case, there is nothing to prevent intestinewhich has left the abdominal cavity from trackingalong the plane of least resistance, which is deep tothe cutaneous muscle. The breach in the abdominalwall takes the form of splits along the direction ofthe fibres of the aponeuroses creating in effect agrid iron incision. Surprisingly, despite this andthe long length of gut which herniates, intestinal ob-struction and resultant colic signs are unusual.

The diagnosis of these flank ruptures is less simplethan for umbilical hernias, because the nature of thedefect prevents the contents being returned to theabdominal cavity by manipulation. In some cases afew cm of the margins of the tears in the variousaponeuroses may be palpable but this is far lessconvincing that being able to palpate the whole cir-cumference of an umbilical ring. The differentialdiagnoses are abscess and haematoma. Both resultin swellings of a similar size and location becauseblood and purulent material like intestine track alonglines of least resistance. Both conditions are fre-quently the result of trauma and in all cases oedemamay further complicate diagnosis.

It is unwise to tap the swelling at this early stage ifthe possibility of a haematoma or hernia exists. In-troduction of a needle into a haematoma may resultin the bleeding recommencing due to release of pres-

113


113

sure and lead to abscess formation despite everyattempt to sterilise the skin. Our main aim at thisstage is to eliminate or confirm the presence of her-niated bowel.

Rectal examination is not helpful because thebreach in the abdominal wall is out of reach. Aus-cultation over the swelling will often give the im-pression that borborygmi are close to the surfacewhen a hernia is present. However, the availabil-ity of ultrasonography has greatly simplified thediagnosis. In the case of a hernia, loops of smallintestine, or occasionally large intestine, can bedemonstrated located deep to the cutaneous muscleand surrounded by fluid. Ultrasonography is alsohelpful in identifying abscess and haematoma.

In cases in which herniation has led to intestinalobstruction and colic, immediate surgery is neces-sary to expose an evaluate the viability of smallintestine which, if healthy is returned to the abdo-men prior to an attempt at closing the defect. Anydevitalised intestine must be resected. Returningthe intestine to the abdomen is often difficult be-cause it has to be eased back through each apo-neuroses tear in turn. When large lengths of smallintestine are involved, it is often necessary to makea short midline abdominal incision to allow trac-tion to be applied to the herniated bowel.

Closure of the defect is attempted using interruptedsutures of 2 vicryl in each of the layers in turn.However, in these fresh cases, because the fibreseither side of the splits have frequently separated,when the sutures are tied, further defects are cre-ated. Even if this is not apparent at the time ofsurgery, the repair may dehisce during attempts tostand on recovery from anaesthesia. The recur-rence of an identical swelling as before, an hour orso later will confirm that this has happened. Forthat reason, surgery is delayed 7-10 days or some-times longer in those horses which do not have in-testinal obstruction. By this time, deposition ofcollagen at the site of trauma will have significantly

increased the tensile strength of the tissues whichare to be repaired. In these cases, I prefer to closethe transverses and peritoneum and internal obliqueaponeuroses with 1 vicryl and to place a piece ofpolypropylene mesh between the oblique aponeuro-ses sutured to the external oblique. The subcutane-ous tissues and skin are closed in the usual manner.A Penrose or continuous suction drain may be re-quired to prevent accumulation of inflammatoryexudate in the dead space.

The same procedures are applicable in cattle andsmall ruminants with the same problem. Herniaswhich are located immediately caudal to the bor-der of the rib cage present problems because thereis no muscle along the cranial border to suture orattach mesh to. If the defect is relatively small andthere has been no suggestion that incarceration islikely, they are probably best left untouched. Al-ternatively, mesh may be anchored to the rib.

Incisional Hernias

With the increasing number of midline laparoto-mies performed in horses, particularly for colicsurgery, more cases of incisional hernia are encoun-tered. The incidence is reported to vary from 1-16%. A number of risk factors have been reported(Table 1, see next page).

Infection plays a significant part in the develop-ment of incisional hernias. Reports on postopera-tive complications after colic surgery have indi-cated that between 10 and 25% of cases developsubcutaneous midline infection.

Of 40 horses with incisional hernias referred to theLiverpool University Equine Hospital, 37 had un-dergone ventral midline laparotomy for colic; ofwhich 7 had had a relaparotomy through the sameincision. The hernia had first been noticed 3-24weeks after surgery. The majority were seen whenthe horses were first turned out or resumed lightwork. Most of the horses were large with a mean

114


114

Wilson et al 1995

White 1996

Kobluk et al 1989Trostle et al 1984

Gibson et al 1989Kobluk et al 1989

Kawak and Stashak 1995

Intestinal surgery Large horses

Wound Infection Postoperative leucocytosis Relaparotomy at the same site Chronic catgut closure

Geldings Excessive incisional oedema Excessive exercise at termination of box rest

Nutritional deficiencies Prolonged Shock Excessive recumbency

Strenuous recovery Abdominal distension Near-far-far-Near suture Polypropylene/polyester suture

Wilson et al 1995

weight of 510kg. Eleven horses had developedmild incisional infection postoperatively. Of these,70% had had an enteratomy or enterectomy per-formed. The size of the defect varied consider-ably between individual cases depending on thelength of the original incision and the proportionwhich had broken down. The largest deficit mea-sured 35cm x 20cm. 36 horses had a single defectwhile the remaining 4 had 2 or 3 defects separatedby a ‘bridge’ of intact abdominal wall. Most de-fects involved the cranial end of the incision wherethe thinner abdominal wall and greater weight bear-ing were likely to be significant factors.

Surgery was delayed until 16 weeks after the origi-nal colic surgery by which time all infection hadresolved, the margin of the defect was firm andwell-defined and the skin had healed. Horses inthe latter half of the series underwentultrasonographic scanning of the swelling to checkfor evidence of adhesions, but none were found.However, one horse was found at surgery to havea focal adhesion between the caecum and the her-nial sac. Although there are several reports of re-pair of incisional hernias using a variety of suturematerials and patterns to close the abdominal walldefects, I much prefer to use a mesh prosthesis.

The horses are starved for 24 hours prior to sur-gery to reduce the bulk of the intestinal contents.The defect was repaired in all 40 cases using asingle piece of woven polypropylene mesh placedbetween the peritoneum and the inner sheath of therectus muscle without encroaching on the perito-neal cavity. The midline skin incision extends from3cms cranial to 3cms caudal to the palpable defect.Dissection is continued through the remaining ab-dominal tunic to the peritoneal sac. Once the sac isidentified, the dissection is continued in this planeto a distance of 3cms beyond the defect. The peri-toneum is carefully dissected free from the marginof the defect and a shelf created along the plane ofthe retroperitoneal fat for whatever distance neces-sary to provide adequate support for the prosthe-sis. The mesh is then cut to size so that it overlapsthe margin of the defect by 3cms and is then suturedin place using 4 metric monofilament polypropy-lene. The sutures are placed in the mesh and ab-dominal wall in such a way that the mesh is undereven tension and a degree of traction is applied tothe margin of the defect. In those cases with morethan one defect, the bridge of intact abdominal wallis left to provide additional support for the singlepiece of mesh. The subcutaneous tissues are thenclosed with a continuous suture of 0 polyglactin.

115


115

The decision as to how much, if any, excess skinneeds to be removed to minimise dead space istaken at this point. The horses with the largest de-fects are fitted with an elasticated belly band for 2-5 days postoperatively. Postoperative ultrasoundwas used to check the position of the mesh prior todischarge from the hospital 7-10 days after sur-gery. Healing is usually uneventful; any localisedswelling quickly resolves. One horse in this serieshad slight incisional drainage, while a second de-veloped an abscess, which was surgically drained.Both healed uneventfully. These results show thata single piece of polypropylene mesh is sufficienteven for very large hernias thus simplifying the sur-gery and reducing cost. Infection is very uncom-mon and if it does occur, quickly responds to drain-age.

Inguinal/Scrotal Hernias

Inguinal/scrotal hernias can be classed as congeni-tal or acquired.

Congenital Scrotal Hernias occur principally infoals and pigs and are present at birth or soon af-terwards. Considerable lengths of small intestinepass through the deep inguinal ring to come to liewithin the vaginal sac in contact with the testis andcord. This is designated an indirect hernia. Thecondition is usually unilateral and results in grossenlargement of the hemiscrotum. The intestine iseasily reducible and there is no tendency for ob-struction to occur.

However, in the foal, rupture of the vaginal sac canoccur just distal to the deep inguinal ring after theintestine leaves the abdominal cavity allowing it topass through into the subcutaneous region. Thesmall size of the hole quickly leads to strangulationof the bowel. The foal, which is usually 1-2 daysold, presents with severe colic and extensiveoedematous swelling extending forwards from thescrotum along the abdominal wall. This is the re-sult of peritoneal fluid escaping through the defect

in the vaginal sac. These foals require immediatesurgery to free and resect the affected bowel. Cas-tration allows recurrence of hernia to be avoidedby twisting the vaginal sac into a pedical prior toligating it.

Management of scrotal hernias in foals may be con-servative or surgical. In many cases, repeated ma-nipulation of the intestine back into the abdomenduring the first few weeks of life results in sponta-neous resolution of the problem. It is probable how-ever, that these cases have a greater risk of hernia-tion at castration if an open technique is used.

In those foals where the hernia persists, surgicalrepair is performed at a few months of age. Undergeneral anaesthesia, an oblique incision is madefrom the scrotum in the direction of the externalinguinal ring. The vaginal tunic is carefully dis-sected free from the overlying skin and connectivetissue down to the level of the ring. In the process,most of the herniated intestine will fall back in tothe abdominal cavity under gravity. Usually thesmall testis can be held fixed in the vaginal sac, butif it too has fallen back into the abdomen may re-quire the sac to be opened in order to locate it.The sac is progressively twisted into a pedicle,thereby gently returning any remaining intestine tothe abdomen. One or two transfixing ligatures areplaced as high up the pedical as possible, one ofwhich is anchored to the external inguinal ring be-fore the testis and excess sac are removed withscissors or emasculator. Further sutures may beused to close the ring if necessary. The procedureis repeated on the other side even though there maybe no overt evidence of hernia.

Acquired Inguinal Hernia

HorseAlthough it can occur in almost any breed, inguinalhernia is most common in standardbreds,warmbloods and, to a lesser extent, shires. In mostcases, the onset of the problem is sudden and acute,

116


116

but occasionally the horse may have had short boutsof discomfort which have resolved spontaneously.It is not uncommon for the stallion to have justserved a mare or have been exercised prior to theonset of colic. It is important that any stallionshowing colic should undergo examination of itsscrotum to identify, or eliminate , an inguinal her-nia. The hernia is unilateral and most frequentlyoccurs to the left side. Only a short length of smallintestine, most commonly ileum, passes through thedeep inguinal ring to lie high up in the inguinalcanal. No intestine can be palpated within the scro-tal sac. However, there is marked enlargement ofthe scrotum on the affected side because obstruc-tion to its lymphatic and venous drainage due tocompression of the cord by the herniated loop ofintestine rapidly leads to severe engorgement ofthe testis. The testis is large, firm and cool to thetouch. The major differential condition is 360° orgreater torsion of the testis which leads to similarsevere colic and unilateral scrotal enlargement. Incases of inguinal hernia, distended small intestinemay be felt per rectum at the deep inguinal ring.Ultrasonography of the scrotum in both conditionsmerely shows dilation of vessels. It is usually im-possible to scan high enough up the inguinal canalin the standing horse to demonstrate herniated in-testine. It is possible, however, with the horse indorsal recumbency under general anaesthesia.

Except in cases referred very soon after herniationof gut has occurred, irreversible ischaemic changeswill have occurred in the testis necessitating itsremoval. This also applied to a testis which hasundergone torsion. This simplifies surgery to oblit-erate the inguinal ring in horses with hernia. Boththe midline and the scrotal areas are prepared forsurgery. With the horse in dorsal recumbency, anoblique incision is made in the skin extending fromthe scrotum towards the external inguinal ring. Thescrotal sac is dissected free from the surroundingtissues down to the external inguinal ring. Thescrotal sac is incised to reveal the darkly congestedtestis and, deep in the inguinal canal, the short loop

of intestine which will show varying degrees of dis-tension, mural oedema and serosal petechiation orcyanosis depending on the length of time the herniahas been in existence. The testis can be removed atthis stage following ligation of the cord. Only verylimited decompression can be achieved by needlesuction. In most cases a short ventral midline ab-dominal incision is necessary to allow traction tobe applied to the small intestine at the deep inguinalring. Even then it can be difficult because the in-testine is gripped by a constricting band of tissuecomprising the vaginal sac 1-2cm distal to the deepinguinal ring where the short funnel-shaped first partof the vaginal process ends. Carefully making asmall cut in this band using the tip of a pair of bluntended scissors will relieve the pressure and allowthe intestine to be drawn back into the abdomen.The herniated segment is withdrawn from the ab-domen and evaluated objectively as to its viability.If any doubt exists it is replaced in the abdominalcavity and re-evaluated after the scrotal sac hasbeen obliterated by twisting into a pedicle and twotransfixing ligatures of 1 vicryl applied which areanchored to the external ring.

Experience has shown that short lengths of strangu-lated small intestine < 30cm remain viable evenwhen they have been trapped for several hours. Itis unusual for resection and anastomosis to be nec-essary. Because of the possibility that the condi-tion is hereditary, it is debatable whether or not theother testis should also be removed. The mattershould be discussed with the owner prior to sur-gery. Stallions can function perfectly well with onetestis, should be decision be made to carry outhemicastration.

With the development of laparoscopes andlaparoscopic instruments, techniques have been re-ported allowing early cases of incarceration to becorrected by gently withdrawing the herniated in-testine from the deep inguinal ring followed by par-tial obliteration of the ring using polypropylenemesh.

117


117

Miscellaneous Topics:Fourth branchial

Arch defects,Epiglottal

Entrapment,Sub-epiglottal Cysts

and ArytenoidChondropathy

J. Geoffrey LaneBVetMed DESTS FRCVS


House, Langford, BRISTOL BS 405DU, U K

Fourth branchial arch defects (4-BAD)

AetiopathogenesisHast (1972) has described the development of thelarynx in the early human embryo and showed thatthe extrinsic structures are derived from the fourthbranchial arch and the intrinsic structures from thesixth arch. 4-BAD is a syndrome of irreparablecongenital defects resulting from a failure of de-velopment of some or all of the derivatives of thefourth branchial arch. The structures which may bedefective are the wings of the thyroid cartilage, thecrico-thyroid articulation, the crico-thyroideusmuscles and the crico-pharyngeal sphincter muscles.Any permutation of aplasia or hypoplasia of thesestructures may arise uni- or bilaterally. The absenceof a firm bond between the wing of the thyroid andthe cricoid cartilages deprives the larynx of a stableskeleton to facilitate the function of its intrinsic

musculature. For example, in the face of such de-fects, the action of the crico-arytenoideus dorsalismuscle will be ineffective and the extent of arytenoidabduction is reduced. Clearly, this may convey afalse impression of RLN on the affected side orsides. The absence of the crico-pharyngeus muscleshas two obvious effects, firstly the inability to closethe upper oesophageal sphincter which results ininvoluntary aerophagia. Secondly, there is nomeans to anchor the palatal pillars into a positioncaudal to the apices of the corniculate cartilagesresulting in rostral displacement of the palatal arch(RDPA).

PrevalenceSurveys of structural and functional abnormalitiesof the upper respiratory tract of the horse have pre-viously been based upon selected populations forexample those submitted to public sales (Lane etal, 1987) or in training (Pascoe, et al, 1981;Raphael, 1982; Baker, 1983; Sweeney, et. al,1991), where unsaleable or untrainable individu-als will have been excluded earlier. In addition, nosurvey of dynamic dysfunctional conditions, occur-ring only under exercise conditions, has been at-tempted to date. Thus, it is generally held that dor-sal displacement of the soft palate (DDSP) and re-current laryngeal neuropathy (RLN) are the two mostfrequently encountered disorders of the region. Theprevalence of non-RLN URT disorders found dur-ing the video-endoscopic study of 3500 yearlingswas as follows:

Fourth branchial arch defects (4-BAD) 7 cases 0.20%

Sub-epiglottal cyst (SEC) 5 cases 0.14%

Epiglottal entrapment (EE) 2 cases 0.06%

Right laryngeal malfunction

5 cases 0.14%

118


118

The condition has been identified in other breedssuch as the Hanovarian, warmbloods, Welsh Sec-tion A ponies and the Haflinger (Cook, 1974;Goulden et al 1976; Wilson et al, 1986; Deegan etal 1987; Klein et al 1989; Dixon et al) As often asnot it has been reported under titles such as rostraldisplacement of the palato-pharyngeal arch (RDPA)or cricopharyngeal-laryngeal dysplasia.

Clinical findingsThe author has reviewed the findings in 60 4-BAD-afflicted Thoroughbred horses and the results aresummarised here. The presenting signs of horseswith 4-BAD are variable and reflect the severityof the absence of the structures involved. However,in order of frequency, the signs are abnormal res-piratory sounds at exercise (50 out of the 60 horses),belching (13), nasal discharge (10), coughing (10)and recurrent colic (5). The involuntary aeroph-agia and eructation sometimes may be confusedwith the noises produced by ‘wind-suckers’.

There is no current evidence that the syndrome isgenetically transmitted.

A complete evaluation of the extent of 4-BAD canonly be made at exploratory surgery or autopsy butthe combined findings of palpation, endoscopyand radiography are generally sufficient to justifya diagnosis. When the cartilage components aredefective, an unusually wide gap can be palpatedbetween the caudal margin of the thyroid and therostral edge of the cricoid whereas in the normallarynx the two structures overlap. The two endo-scopic features to alert the clinician to the possi-bility of 4-BAD are RDPA (33 cases) where thecaudal pillars of the soft palate form a cowl whichpartly obscures the corniculate processes dorsallyand defective arytenoid motility (45 cases). 4-BADis the commonest explanation for apparent right-sided RLN and there is be a marked over-repre-sentation of right-sided cases. In the 60 cases 15were bilateral, 39 were right unilateral and in 6 thedefects were confined to the left side. In one in-

stance 4-BAD was only detected as dynamic RDPAduring treadmill exercise. RDPA itself is simply anendoscopic symptom of a major underlying laryn-geal disorder and should not be regarded as a dis-ease in its own right. It arises when the upper oe-sophageal sphincter muscles are not present to pro-vide an anchor for the palatal arch caudal to theapices of the corniculate processes of the arytenoidcartilages. When the crico- and thyro-pharyngeusmuscles are absent there is a failure to close theupper oesophagus so that lateral radiographs willreveal a continuous column of air extending fromthe pharynx into the oesophagus. The RDPA is seenas a ‘dew drop’ intruding into this air column fromthe dorsal wall. Repeated aerophagia leaves thoseanimals without an upper oesophageal sphinctersusceptible to episodes of colic which may be lifethreatening. Three horses have died or been de-stroyed through tympanitic and one other has re-quired surgical decompression.

The performance records of 51 of the horses havebeen traced: 22 were un-named; 29 were namedbut unraced; 11 raced but were unplaced; 4 wereplaced and 7 won albeit all in minor competitions.Thus, horses afflicted with 4-BAD are generallyineffective athletes.

Prevalence of other laryngeal disordersin young horsesFive cases of right laryngeal malfunction, other thanthe 7 cases of 4-BAD, were identified in the studsurvey of yearlings. Three of these were later sub-jected to surgery with a view to prosthetic laryn-goplasty but were found to be inoperable by virtueof hypoplasia of the muscular process of the rightarytenoid cartilage. Given that the arytenoidcartilages develop from the sixth branchial arch darewe contemplate adding a 6-BAD syndrome to theclinical vocabulary!?

It is generally believed that sub-epiglottal cysts arecongenital and if this is so the incidence of 0.14%demonstrates that the disorder is indeed rare. In

119


119

contrast the aetiopathogenesis of epiglottalentrapment is not known and the results of repeatedendoscopic examinations confirm that at least somecases are acquired. Thus, the identification of only2 cases in 3497 yearlings does not reflect the overallincidence. Similarly arytenoid chondropathy isknown to be an acquired disorder and a failure torecord a single case even in quite a large populationof young horses is not significant.

Epiglottal entrapment (EE)

AetiopathogenesisIn this condition the cartilage of the epiglottis be-comes enveloped by a fold of glosso-epiglotticmucosa which arises between the epiglottis itselfand the base of the tongue and extends laterally asthe aryepiglottic folds. The aetiology of EE is usu-ally not known as the condition can be reproducedon most equine laryngeal post-mortem specimensand it is not clear why some horses develop theclinical condition and others do not. The aetiol-ogy of EE is more straightforward when the epig-lottis is congenitally hypoplastic or where it is as-sociated with a sub-epiglottic cyst. These possi-bilities should be checked by endoscopy and/orradiography before surgical correction is attempted.

Clinical signsThe signs associated with EE are highly variableand include exercise intolerance with inspiratoryand/or expiratory noises at exercise, intermittentgurgling from secondary DDSP and coughing aftereating. The noises which are associated with EEare usually vibrant and are more readily provokedthan those of dynamic DDSP. In addition, it shouldbe noted that EE may be a chance endoscopic find-ing in horses which are asymptomatic.

Reports of the prevalence of EE in endoscopic sur-veys of athletic horses at rest suggest an incidencein the range of 0.75% to 3.3%. However in theauthor’s video-endoscopic survey of an unselectedpopulation of 2522 yearlings only 2 cases were

identified - in the same survey there were 3 sub-epiglottal cysts and 6 yearlings afflicted with fourthbranchial arch defects. The implication is that EEis an acquired disorder rather than a congenitaldefect

The relationship between EE and dynamic DDSPis confusing. Treadmill studies have confirmedwhat has been suspected for some time inasmuchas EE is likely to provoke secondary DDSP duringexercise. However this does not explain the clini-cal observation that horses which have been af-flicted with EE and have been subjected to surgi-cal correction may become susceptible to DDSPlater, and vice versa.

Diagnosis of epiglottal entrapmentDefinitive diagnosis of EE is achieved by endos-copy: the normal epiglottis has a sharply definedwrinkled cartilage outline and the superficial bloodvessels on the dorsal surface are clearly visible.In EE the epiglottis loses its wrinkled cartilageborder and the superficial blood vessels are ob-scured by the entrapping mucosa. However, a struc-ture with the overall shape of the epiglottis remainspresent. In a proportion of cases the mucosa over-lying the epiglottis is ulcerated.

EE may be intermittent and it is important, as aroutine part of endoscopic procedure, to stimulatea series of deglutition sequences in an attempt toidentify the condition.

Occasionally the free border of the soft palate isfound to be dorsally displaced throughout the en-doscopic examination of a horse showing abnor-mal respiratory sounds at exercise. Epiglottal en-trapment and sub-epiglottic cyst are the two mostcommon explanations for persistent DDSP in thehorse at rest. Attempts should be made to stimulateswallowing while the endoscope is in place in thehope that the epiglottis can be brought into viewbecause, in the face of persistent DDSP, it shouldbe obvious that the epiglottis cannot be seen at all.

120


120

Should this manoeuvre prove to be ineffective alateral radiograph of the pharynx is indicated todetermine whether or not entrapment is present. Onthis projection the epiglottis should measure at least7.0 cm from tip to hyoid articulation; an epiglottiswith a length less than 5.5 cm is indicative of hy-poplasia and surgery is contra-indicated.

In rare cases EE may be present only during vigor-ous exercise so that high speed treadmill endos-copy provides the best opportunity to establish adiagnosis of this form of intermittent entrapment.

Treatment of epiglottal entrapment

The treatment options for epiglottal entrapment are:

a. resection of the entrapping mucous membranevia ventral laryngofissure

b. axial division of the entrapping mucosa per osc. axial division of the entrapping mucosa per

nasumd. transendoscopic Nd: YAG laser resection per

nasum

Methods (a) and (b) require general anaesthesiabut both (c) and (d) can be performed on the stand-ing horse with the obvious advantage of minimaldisruption of training and racing schedules.

Methods (b) and (c) utilise a hooked bistoury tomake a longitudinal cut in the loose mucous mem-brane overlying the epiglottal cartilage. The mostimportant practical limitation of these methods isthe stability of the entrapment. Whenever the en-trapment is insecure or intermittent it may not bepossible to make a satisfactory section of the re-dundant mucosa because the forward pull of thebistoury may displace the entrapment from the apexof the epiglottis. An inadequate incision is likelyto be followed by recurrence within a short time.

However, if the entrapment is secure the hookedbistoury techniques are applicable. Obviously asharp instrument introduced into the pharynx of a

fractious horse in method (c) has the potential forcausing serious injury. Thus, it is essential that thepatient is thoroughly sedated and the pharynx isdesensitised by the infusion of local anaestheticsolution. The procedure of axial section of the EEis performed under endoscopic surveillance - theendoscope is passed through one nostril while thebistoury is introduced through the other. The aryepi-glottic mucosa is quite tough and care is requiredto prevent a disastrous palatal injury when the hooksuddenly cuts free from the entrapment. Method(b) is safer, albeit with the risk of anaesthesia, andrepresents the technique of choice in those clinicswhich do not possess a laser facility .

Surgical relief via laryngotomy uses a conventionalapproach through the crico-thyroid membrane. Forthe resection itself the endotracheal tube must bewithdrawn so that the entrapped epiglottis can bereverted towards the incision. It is sensible to placea stay suture through the tissue to be excised at anearly point in the procedure. An elongated ovalsection of mucosa 6 cm x 1 cm is removed and it ispreferable to commence with incisions from lat-eral to medial through the doubled layer of mucosa.

Care is taken not to traumatise or cut into the carti-lage of the epiglottis. Haemorrhage is usually mini-mal and surgical closure of the defect in the sub-epiglottic mucosa is unnecessary.

Regardless of the technique used, endoscopy per-formed in the days after surgery should confirm thatthe entrapment has been successfully relieved al-though the epiglottis itself may appear swollen andflaccid. Hence anti-inflammatory medication shouldbe provided routinely after treatment of EE.

Prognosis

All of the methods of treatment mentioned aboveyield a high rate of uncomplicated resolution of EE.The possibility of recurrence of entrapment is great-est with the axial section techniques but even this is

121


121

uncommon. Iatrogenic trauma to the epiglottal car-tilage can provoke granulomas and other distor-tions which may compromise the relationship be-tween the epiglottis and the soft palate. Chroniccoughing associated with low grade dysphagia is arare but recognised complication of resection ofthe glosso-epiglottal mucosa.

Sub-epiglottal Cysts

AetiopathogenesisDevelopmental cysts are occasionally recognisedin the pharynx of horses and represent causes ofdyspnoea and/or dysphagia. The most frequentlyencountered of these lesions is the sub-epiglotticcyst which is thought to be derived from the em-bryological remnants of the thyroglossal duct, astructure which runs from the level of the epiglottisto the anterior mediastinum. However, it is strangethat comparable cysts do not arise elsewhere in thecourse of this duct. It is believed that sub-epiglot-tic cysts are present from birth although they maynot be discovered until the horse is mature and com-mences training. An overall incidence of 1 per 1000Thoroughbreds born was indicated in the surveyoutlined above. The cysts themselves consist ofsmooth-walled, sometimes multilobular, structuresfilled with straw-coloured slightly tenacious fluid.They arise from within the loose glosso-epiglotticmucosa lying between the base of the tongue andthe epiglottis. It is uncommon for a sub-epiglotticcyst to be found which is not located within an epi-glottal entrapment.

Clinical signsThe age and manner by which the cysts cause clini-cal signs is dependant on their size. Large cystscan be a cause of dysphagia and respiratory ob-struction in foals. Such foals may present within afew days of birth with reflux of milk from the naresand will require an endoscopic examination for dif-ferentiation from foals with palatal clefts. Oftenaspiration of fluids into the trachea will lead on toinhalation pneumonia and in addition to surgical

relief, vigorous antibiotic medication will be re-quired.

Older animals with cysts may present with a vari-ety of respiratory signs including nasal discharge from dysphagia and abnormal respiratory sounds atexercise. Horses with small sub-epiglottic cystsmay present with a history of choking up under ex-ertion and will require differentiation from DDSP.

DiagnosisThe diagnosis is easily established by endoscopyprovided that the cystic lesions are available to beseen. In some horses with this condition persistentDDSP is present, in which case it will be neces-sary to resort to other diagnostic procedures suchas plain and contrast radiography.

The cysts may be intermittently obscured by thepalatal arch when the cartilage of the epiglottis liesabove the palate and the cyst is trapped below. Pa-tient inspection with repeated stimulation of de-glutition should always be part of the endoscopicroutine for horses with suspected pharyngeal le-sions such as entrapment or cysts. Endoscopy peros with the patient anaesthetised is a justifiable tech-nique if endoscopy per nasum and radiography havefailed to provide a definitive explanation for per-sistent DDSP, .

TreatmentThe objective of treatment is to ablate the cyst bysharp excision which can be achieved per os usingan ecraseur provided that the mouth of the horse islarge, and the hand of the surgeon is small, for ac-curate placement of the ecraseur loop around thecyst without risk of injury to adjacent structures,most notably the epiglottis itself. Resection by con-ventional ventral laryngofissure is generally sim-pler and safer.

The technique is similar to that used for the treat-ment of epiglottal entrapment and, again, once thetip of the epiglottis has been retroverted towards

122


122

the laryngotomy incision, stay sutures to stabilisethe tissues before resection are a useful practicalprecaution. Haemorrhage is usually slight and thereis no need for closure of the mucosal defect fol-lowing excision.

Nd : YAG laser destruction of the cysts can also beused when the facility is available.

PrognosisThe cystic lesions can often be excised intact andeven if they should be ruptured during removal afavourable prognosis can be given. Unlike thyro-glossal cysts in man, recurrence is most unlikely tooccur after excision in the horse.

Arytenoid chondritis

AetiopathogenesisArytenoid chondritis (chondropathy) consists of thedevelopment of suppuration within the matrix ofone or both arytenoid cartilages. The mechanismof development of micro-abscessation with dis-charging tracts to the luminal surfaces is not clearbut young male Thoroughbreds are usually in-volved. The condition appears to be more preva-lent in the USA than Europe. The condition canarise in horses of any breed and at any age andpresumably pyogenic organisms become inoculatedthrough the muco-perichondrium into the cartilagefrom the luminal surface.

Clinical findingsThe signs associated with arytenoid chondritis arisethrough a combination of airway obstruction andcompromised glottic protection. Thus, stridorousnoises are heard when the horse is exerted and ifthere is bilateral involvement there may be airwayobstruction at rest. Coughing may be evident at anystage.

The diagnosis of arytenoid chondritis is primarilymade by endoscopy showing distortion of the af-fected cartilage. As the micro-abscesses develop

the cartilage thickens and shows axial displacementtowards the midline and reduced motility. In theearly stages, particularly when the left side is in-volved, casual endoscopy may suggest a diagnosisof RLN. As the condition advances, so the distor-tion of the cartilage becomes more obvious andgranulomatous eruptions appear on the medial faceof the corniculate process. Contact lesions may de-velop on the contralateral arytenoid cartilage.

Lateral radiographs of the larynx usually show fo-cal mineralisation even in early cases.

Progress and managementThe progress of arytenoid chondritis may be ar-rested in the early stages by the prolonged (i.e. sixweeks) use of potentiated sulphonamide medica-tion per os but once the chronic stage has beenreached, the only treatment option is arytenoidec-tomy.

Total arytenoidectomy implies that the entirearytenoid cartilage together with the corniculateprocess is removed. In partial arytenoidectomythe muscular process and articular facet are left insitu and in sub-total arytenoidectomy part or allof the corniculate process is also left in place. Thegreater the extent of cartilage resection the greateris the possibility that the ability of the larynx toprotect the lower airways during deglutition willbe compromised and that marked dysphagia withaspiration pneumonia will ensue. Partialarytenoidectomy offers the best compromise to sal-vage a horse afflicted with laryngeal chondritis forbreeding or for quiet exercise but full athletic ca-pacity cannot be restored by any surgery.

123


123

HOW TODIAGNOSE

HIGH SUSPENSORY

DISEASEIngrid Cilliers

Companion Animal Clinical Studies,Faculty of Veterinary Science, Univer-

sity of Pretoria, Onderstepoort.

Acute cases of high suspensory disease may presentwith slight, palmar (plantar), oedematous swell-ing, heat distension of the medial palmar (plantar)vein and/or pain. Chronic cases or those restedimmediately after onset of lameness usually haveno detectable clinical signs suggestive of the sourceof pain. In these cases local analgesia is requiredto identify pain in the proximal metacarpal (meta-tarsal region). Diagnosis often requires a combi-nation of diagnostic local analgesic techniques anddiagnostic imaging techniques, including ultrasonog-raphy, radiography and nuclear scintigraphy.

AnatomyIn the forelimb the third interosseous muscle(TIOM) / suspensory ligament (SL) arises proxi-mally from the distal row of carpal bones and fromthe adjacent parts of the palmar aspect of the proxi-mal extremity of the metacarpal bones, principallythe third metacarpal bone. The proximal part ofthe TIOM is incompletely separated into two maindivisions originating from the second and third car-pal bones. The distopalmar outpouchings of thecarpometacarpal joint, located between the axialsurfaces of the second and fourth metacarpal bonesand the abaxial surface of the suspensory ligament,

extend distally a mean distance of 2,5 cm 3. Theseoutpouchings lie in close proximity to the palmarmetacarpal nerves in the proximal metacarpal re-gion. In the hindlimb, the main area of attachmentis at the proximal and plantaromedial aspect of thethird metatarsal bone: there is less attachment tothe plantar tubercle of the first, third and fourth tar-sal bones. A distal recess of the tarsometatarsaljoint is in contact with the lateral aspect of the proxi-mal TIOM in some horses 1.

The body of the TIOM descends between the sec-ond and fourth metacarpal (metatarsal) bones, andgradually is separated from the palmar aspect ofthe third metacarpal bone. The level at which itdivides into two branches is approximately betweenmid-metacarpus and the distal fourth of this area.These branches insert on the abaxial surface of thecorresponding proximal sesamoid bone.

In the forelimb, the TIOM is rectangular, strong,and about 20 to 25 cm long. In the hindlimb, it isthinner, round and 25 to 30 cm long. It is mainlycollagenous and contains variable amounts of stri-ated muscular fibres, especially in the proximal anddeep part.

The interosseous muscle is innervated by the deepbranch of the lateral palmar nerve which emergesat the level of the midcarpal region and containsfibres from both the ulnar and the median nerves.The level at which the deep branch detaches fromthe lateral palmar nerve is not clear. It has beendescribed by some authors to arise proximal to themetacarpus and others describe it as distal to thecommunication between the ulnar and the mediannerves 2.

It is therefore not clear whether a high palmarmetacarpal nerve block would include the stem ofthe deep branch of the lateral palmar nerve andthus desensitise the insertion of the TIOM. Proxi-mal diffusion of local anaesthetic solution may re-sult in effective desensitisation. However, a pal-mar metacarpal nerve block, 4.5 cm or less distal

124


124

to the carpometacarpal joint, carries the risk of anintra-articular anaesthesia 3.

Diagnostic analgesic techniques for theforelimb:Infiltration at the origin of the suspensoryligament.The carpus is held in slight flexion with the fetlockextended. A 3,8 cm, 18G needle is inserted at thepalpable junction of the head and shaft of MCIVon the axial surface. The needle is directed be-tween the suspensory ligament and the distal ac-cessory ligament of the deep digital flexor tendon.

Subcarpal lateral palmar and medial andlateral palmar metacarpal nerve blocks performed at the proximal end of the metacarpususing 6 to 8ml of mepivicaine (1 %)4. To avoidpenetration of the distopalmar outpouchings theneedle must be inserted perpendicular to the skinsurface, more than 4.5cm from the carpometacar-pal joint 3. At this level, however, these nerveblocks may not desensitize proximal metacarpallesions and are not effective in desensitizing theorigin of the suspensory ligament.

Palmar and palmar metacarpal nerve blocksat the level of the accessory carpal bone.The carpus is held in slight flexion and the fetlockextended, a 1.5 cm, 25G needle is inserted to thehub in a palmarolateral to dorsomedial directionat the distal aspect of the accessory carpal bone.With this technique perineural infiltration of thelateral palmar nerve is obtained. At this level, thelateral palmar nerve is a continuation of the pal-mar branch of the ulanar nerve and a portion of themedian nerve, and located just proximal to the deepbranch of the lateral palmar nerve, which dividesinto the medial and lateral palmar metacarpalnerves.

The medial palmar nerve can not be infiltrated atthe level of the accesory carpal bone because it

lies within the carpal synovial sheath 3. This methodis advantageous because the lateral palmar nerveis desensitized before the deep branch of the lat-eral palmar nerve is given off. With this tech-nique, it is not necessary to use a large volume offluid to infiltrate the origin of the suspensory liga-ment and risk injection into the distal carpal joints.

Diagnostic analgesic techniques for thehindlimbSubtarsal nerve block.Dyson performs this block with the limb bearingweight. A small volume (1ml) of local anaestheticis deposited subcutaneously plantar to the base(head) of MTIV approximately1.5 cm distal to TMTusing a 0.9 x 40mm needle. The needle is insertedmore deeply, directed medial to the fourth metatar-sal bone and dorsally until resistance is encoun-tered. After aspiration to ensure that synovial fluidis not withdrawn, 3ml of local anesthetic is injected;if resistance is met the needle is withdrawn slightlywhile injection proceeded.

The needle is withdrawn partially, directed furtherdorsomedially and an additional 3ml of local anes-thetic is deposited. If there is excessive resistanceto the injection, the needle is withdrawn slightlyprior to injection. The lameness is re-evaluatedafter standing for 15 mins and if no improvement,again after a total of 30 mins.

Inadvertent local anaesthetic injected into the tar-sometatarsal joint may alleviate pain from the tar-sometatarsal and centrodistal joint, from the inser-tions of the tibialis cranialis and / or fibularis ter-tius, and in some cases from the tarsal sheath andDDFT. False negative results for subtarsal analge-sia may be achieved by inadvertent injection intothe tarsal sheath or into a blood or lymphatic ves-sel5 .

Dyson and Romero’s (1993) results indicate thatextension of local anesthetic solution into the TMTjoint probably occurs infrequently, in contrast to the

125


125

relatively high risk of infiltration of the combinedmiddle carpal and carpometacarpal joint capsuleafter some techniques of proximal metacarpal an-algesia (Ford et al. 1989).

Tibial nerve block.This block alleviates pain associated with PSDwithout significantly influencing tarsal pain. Twentyminutes may be required before analgesia is effec-tively achieved due to the large diameter of thisnerve.

UltrasonographyHigh quality ultrasonographic images are essentialfor accurate diagnosis. Abnormalities associatedwith PSD include the following:4,6,7,8

• Enlargement of the cross-sectional area. Thismay result in reduction of space between theSL and the palmar cortex of MCIII, or reducedspace between the SL and the accesssoryligamnet of the deep digital flexor tendon.

• Poor demarcation of the margins of the SL,especially the dorsal margin.

• Focal or diffuse areas of reduced echogenicity.These may extend less than 1 cmproximodistally and occupy less than 10% toup to the entire cross-sectional area of theligament.

• Focal anechoic core lesions.• Reduced strength of fiber pattern.• Focal mineralization

Central, circular hypoechoic lesions were mostcommon in the forelimb, whereas in the hindlimb adiffuse decrease in echogenicity of two-thirds ormore of the cross-sectional area of the ligamentwas the most frequent lesion in studies done byDyson 4.

RadiographyThere are usually no detectable radiographicabnormalities of MCIII (MTIII) in acute cases ofPSD. In chronic cases the followingabnormalities may be seen:4,7

• Increased opacity of the proximal aspect ofMCIII (MTIII) seen in dorsopalmar views.

This may represent sclerosis of the trabeculaeand / or entheseophyte formation on the palmar(plantar) aspect of the bone. It should bedifferentiated from sclerosis associated with apalmar cortical fatigue fracture.

• If entheseophyte formation is extensive, it mayalso be seen in a lateromedial view as anopacity on the palmar (plantar) aspect of thebone superimposed on the second and/or fourthmetacarpal (metatarsal) bones.

• The trabeculae in the subchondral bone on thepalmar (plantar) aspect of MCIII (MTIII) maybe more obliquely orientated and coarser, withor without sclerosis.

Secondary bony changes in a forelimb areassociated with a more guarded prognosis6.

Nuclear scintigraphyNuclear scintigraphy is generally unnecessary fordiagnosing PSD, provided that good qualityultrasonographic images are obtained, but may giveadditional information about associated bone turn-over at the insertion of the SL. Not all horses withPSD have detectable abnormalities if examinedusing nuclear scintigraphy. In bone phase imagesthere may be an increased radiopharmoceutical(RPU) uptake in the proximoplantar (palmar) as-pect of MTIII (MCIII) in some, but not all cases ofPSD. Abnormal RPU in the bone phase, seen inabsence of ultrasonographic and radiographic ab-normalities, is more likely to reflect a primarypathological condition of the bone 6 .

References

1. Denoix JM. Functional anatomy of tendons andligaments in the distal limbs

(manus and pes). Veterinary Clinics of NorthAmerica: Equine Practice 10: 2: 273- 321, 1994

126


126

2. Muylle S, Desmet P, Simoens P, Lauwers H,Vlaminck L. Histological study of theinnervation of the suspensory ligament of theforelimb of the horse. The Veterinary Record142:606, 1998

3. Ford TS, Michael WR, Orsini PG. Acomparison of methods for proximal palmarmetacarpal analgesia in horses. VeterinarySurgery 18: 2: 146-150, 1989.

4. Dyson S. Proximal suspensory desmitis:clinical, ultrasonographic and radiographicfeatures. Equine Veterinary journal 23:1: 25-31, 1991

5. Dyson S, Romero SJ. An investigation ofinjection techniques for local analgesia of theequine distal tarsus and proximal metatarsus.Equine Veterinary Journal 25: 1: 30-35,1993

6. Dyson SJ, Genovese RL. The suspensoryapparatus. Diagnosis and management oflameness in the horse. 654-662, 2003.

7. Dyson S. Proximal suspensory desmitis in theforelimb and the hindlimb. AAEP ProceedingsVol 46: 137-142, 2000

8. Dyson S. Proximal suspensory desmitis in thehindlimb: 42 cases. British Veterinary Journal150:279-291, 1994

127


127

How to Investigate and treat cardiac Dysrhythmias in the horse

David Sutton, BVSc, MRCVS, PhDCompanion Animal Clinical Studies,

Faculty of Veterinary science, Univer-sity of Pretoria, Onderstepoort

P Q S T

P-R interval

QRS complex

Q-T interval

R

The detection of dysrhythmias on auscultation ofthe equine heart, with or without associated pulsedeficit, is not uncommon and frequently does nothave clinical significance. Atrioventricular conduc-tion delays are reported to be the most commonequine conduction disorders and first and seconddegree atrioventricular blocks (AVB) may be nor-mal variations in this species, closely related tovagal tone. Such physiologic dysrhythmias arelikely to disappear after moderate exercise, andinclusion of an exercise test is therefore a valuableaddition to the initial investigation of these cases.Pathologic equine dysrhythmias often occur sec-ondary to underlying cardiac or gastrointestinal dis-ease, metabolic disorders or endotoxaemia, and a

thorough clinical examination is required in eachcase plus assessment of peripheral biochemicalparameters and electrolytes. However, significantdysrhythmias such as atrial fibrillation may alsooccur in the absence of detectable clinicopatho-logical abnormalities due to the large size of theequine heart. In order to accurately diagnose andtreat rhythm disturbances it is essential to obtain anappropriate electrocardiogram (ECG).

COLLECTION OF AN ECGIn many cases, collection of a resting ECG using abase-apex system with a paper trace machine issufficient: place right arm (red/negative) electrodeover the right jugular groove, and attach the leftarm (yellow/positive) electrode over the left heartbase, with the final earth electrode distant from theheart. Readings should then be collected from ‘LeadI’ to record electrical flow from base to apex. Toimprove the quality of the trace the horse must bekept as still as possible; contact between the skinand electrodes is improved by application of spirit,or adhesive electrode pads may be used on areasof shaved skin; background noise can be reducedusing the filter setting on most ECG machines. Apaper speed of 25 mm/s and deflection setting of10 mm/mV is usually adequate unless QRS com-plexes are extremely rapid or bizarre. However,certain dysrhythmias may occur infrequently or bepresent only at exercise such that further technol-ogy is required to collect a diagnostic ECG. Appli-cation of these further techniques will be discussedin detail in this talk:

128


128

Continuous Holter Monitoring:These continuous ambulatory monitors require just2 electrodes, generally positioned under a surcingle,and can record and store ECG data for at least a 24h period. The ECG is analysed retrospectively andthis may be performed automatically by softwaresuch as the Medilog Excel Ambulatory ECG sys-tem. At rest, holter monitoring is particular usefulfor detection of periodic (ventricular) dysrhythmiasthat may be involved in episodic collapse cases.Recordings taken during exercise facilitate the di-agnosis of dysrhythmias such as paroxysmal atrialfibrillation that may resolve spontaneously at rest.

·Radiotelemetric recording:As a radiosignal transmits the ECG trace to a dis-tant monitor, this technique offers the advantage ofproviding a real-time display of the ECG at exer-cise, and is useful for interventional therapy if re-quired. Due to the signal strength, exercise mustusually be restricted to a treadmill rather than aracetrack.

Digital recording:Palmtop computers and small digital holter record-ers now offer an innovative, cheaper alternative totraditional equine holter monitoring. The light 2-lead monitor is set to record by a Psion Palmtopcomputer, which is subsequently used to downloadand display the ECG trace. This light system is re-sistant to movement artifact and has been used toproduce excellent traces from racehorses at fullgallop (e.g. Oxford Cardiology Products).

INTERPRETATION OF THE ECGHeart rate should be calculated from the R-R inter-vals, and an assessment made of the overall rhythm:is it regular or (regularly/irregularly) irregular?Each QRS complex should be similar (narrow andnegative in lead I), and preceded by a P wave. Insupraventricular complexes the P waves are ab-sent, but the QRS complex is of normal form. Thisis different to ventricular complexes in which boththe QRS complex and T wave will be wide and

different to usual. When ventricular depolarisationarises from the junctional tissue, the QRS complexeswill be of supraventricular form but frequently besuperimposed by the P wave. Fluctuation of the P-R interval and of P wave morphology may be seenwith supraventricular ectopic beats, whilst replace-ment of the P waves with a fluctuating baseline ofF waves is seen in atrial fibrillation. Examples ofECG traces will be presented from horses with bothphysiologic and pathologic dysrhythmias – differ-entiation between these is essential before progress-ing further with the case. Having identified a patho-logical dysrhythmia, all attempts should be madeto identify the underlying cause so that a more ra-tional approach can be used to design the treatmentplan. Correction of electrolyte or acid-base de-rangements may resolve the dysrhythmia withoutfurther treatment, whilst failure to address suchproblems may cause specific pharmacological in-tervention to fail. Assay of serum cardiac troponinI concentration may be useful to confirm a diagno-sis of myocarditis. This myocardial polypeptide isa highly sensitive and specific biomarker of myo-cardial injury in people and dogs, and a serum ref-erence range has been established recently for thor-oughbreds. Echocardiographic evaluation (B-mode,M-mode and Colour flow Doppler) should also beperformed in each case to identify significant val-vular regurgitation, chamber enlargement or myo-cardial disease. Drugs and dosages used for thetreatment of pathologic equine dysrhythmias areshown in Table 1.

PATHALOGICBRADYDYSRHYTHMIAS:DIAGNOSIS AND THERAPYSinus node failure in older horses or in neoplasticconditions may occasionally lead to a pathologicalsinus bradycardia, resulting in episodic collapse.The ECG is characterised by normal complexes,but shows profound resting bradycardia (< 20 beats/min) and variable R-R interval. Compensatorychamber enlargement is likely to occur as the con-dition is progressive; treatment by pacing is pos-

129


129

sible but unlikely to be economic.

Atrioventricular Block:Pathological second degree AVB is not common,but is generally characterized by an irregularly ir-regular bradycardia. The resting ECG shows mul-tiple successive P waves that are not followed by aQRS complex, and the periods of AVB do not dis-appear at exercise. In third degree AVB, the ven-tricular rate is also slow but the condition is markedby complete dissociation of atrial and ventricularelectrical activity. The ECG trace shows variableQRS complexes with unrelated regular P waves.The morphology of the QRS complexes is depen-

Table 1 Doses of drugs commonly used to treat cardiac dysrhythmias in the horse

Drug Indication DoseAtropine Severe vagal bradycardia 0.01-0.1 mg/kg IVBretylium tosylate Life-threatening ventricular tachycardia (VF) 3-5 mg/kg IV, repeated

up to 10 mg/kg totalDexamethasone VPCs; atrial arrhythmias and VT 0.05-0.22 mg/kg IVDigoxin Congestive heart failure 2.2 mcg/kg IV q12 h or

11 mcg/kg PO q12 hRapid atrial dysrhythmias (AF) 11 mcg/kg PO q12 h

Enalapril Vasodilatation in congestive heart failure 0.5 mg/kg PO q24 hGlycopyrrolate Severe vagal bradycardia 0.005 mg/kg IVLignocaine Ventricular tachycardia 20-50 mcg/kg/min IV or

0.5 mg/kg very slowly IVto effect; repeat in 5-10min

Magnesium sulphate Ventricular tachycardia 1-2.5g/450 kg/min IV not to exceed 50 mg/kg total

Phenytoin Digoxin-induced ventricular tachycardia 7.5 mg/kg IV or10 mg/kg PO q24 h

Procainamide Ventricular tachycardia, atrial fibrillation 1 mg/kg/min IV, not toexceed 20 mg/kg total or25-35 mg/kg q8 h PO

Propanolol Refractory VT and SVT (quinidine toxicity) 0.03-0.16 mg/kg q12 h IV 0.38-0.78 mg/kg PO q8 h

Quinidine gluconate Acute onset atrial fibrillation 1.1-2.2 mg/kg IV q10 minVentricular tachycardia not to exceed 12 mg/kg total

Quinidine sulphate Atrial fibrillation 22 mg/kg PO q2 h untilconverted, toxic or plasma[quinidine] = 3-4 mcg/ml

Verapamil Supraventricular tachycardia 0.025-0.05 mg/kg IV q30min up to 0.2 mg/kg total

dent on their origin, and will be normal if from asupraventricular idionodal pacemaker, but wide andbizarre if from a ventricular pacemaker. The ven-tricular rate is markedly slower than the atrial ratein third degree AVB.

Both of these conditions may be caused byhyperkalaemia (e.g. in foals with a ruptured blad-der) or myocarditis. Hyperkalaemia must be cor-rected by diuresis or infusions of dextrose and in-sulin to lower circulating levels if the condition iscritical. If myocarditis is present, dexamethasonetherapy is recommended. Transvenous pacing is theonly further treatment option for third degree AVB.

130


130

Atrial fibrillationThis is the commonest pathologic dysrhythmia inhorses, and of the greatest economic importance asit may occur in fit racehorses. On auscultation thepulse is irregularly irregular with a low, normal orraised heart rate and a fluctuating systolic murmurmay be present. The diagnosis must be confirmedby ECG, which demonstrates normal narrow QRScomplexes with an irregularly irregular R-R inter-val and no preceding P waves. The baseline ismarked by characteristic fibrillation (‘F’) waves.The diagnosis of paroxysmal AF (which resolvesonce exercise has stopped) requires telemetric orholter electrocardiography at exercise.

A normal horse is capable of sustaining reentrantpathways within the atrial myocardium due to thelarge atrial size and predominant vagal tone. Thepresence of this dysrhythmia does not indicate car-diac pathology, but concurrent echocardiographicexamination should always be performed beforeconsidering treatment.

Both mitral valve incompetence and severe tricus-pid regurgitation may cause sufficient right atrialenlargement and stretching to cause AF. This dys-rhythmia is therefore common in horses with con-gestive heart failure. The major clinical importancein the different aetiologies of AF is that medicalantidysrhythmic therapy is likely to be less suc-cessful in conversion to sinus rhythm in horses withconcurrent pathological heart enlargement. Thereis likely to be a higher incidence of side effects inthe latter group also due to the higher dose of qui-nidine sulphate required, and a greater rate of re-currence.

The most common treatment for AF remains oraldosing with incremental quantities of quinidine sul-phate (see Table 1) at 22 mg/kg until conversion ifachieved; 5 doses have been given, or toxic sideeffects have appeared. The administration of thistreatment is simple, but the management of poten-tial complications such as life-threatening supraven-

tricular or ventricular tachycardia is more difficultand advance preparation for dealing with such prob-lems is essential. Much research has been per-formed on the indications for treatment, differenttherapeutic strategies and management of the po-tentially life threatening complications that mayarise from attempted atrial conversion in the horseand the reader is directed to the reference list. Con-version to sinus rhythm is most successful whenthe duration of AF is less than 4 months, auscul-tated murmurs of less than grade 3/6 and the restingheart rate is below 60 beats per minute. With care-ful case selection, a successful outcome can beachieved in approximately 85% cases of uncom-plicated AF.

TACHYDYSRHYTHMIAS ANDECTOPIC BEATSSupraventricular ectopic beats:Atrial premature depolarizations (APDs) may oc-cur in normal horses, but frequent APDs may pre-dispose to AF. The APDs have different P waveform to the preceding complex and occur prema-turely within the cardiac cycle but are often fol-lowed by a normal QRS complex if the ventriclesare repolarised. Frequent APDs may resolve withrest at pasture but treatment options should includecorrection of electrolyte abnormalities and use ofcorticosteroids where myocarditis is suspected.

Supraventricular tachydysrhythmias:Supraventricular tachycardia (SVT) is defined asa run of APDs with a sustained rapid ventricularresponse. If the heart rate exceeds 100 bpm in theabsence of underlying cardiac disease, quinidinesulphate can be used successfully. In the presenceof AF and congestive heart failure, then digoxintherapy is most useful as it decreases ventricularresponse by delaying conduction through the AVnode and is a positive inotrope. When used for over3 days, therapeutic drug monitoring is recommendedto ensure that plasma digoxin concentrations remainwithin the therapeutic range (0.5 – 2 ng/ml).

131


131

Ventricular ectopic beats:Ventricular premature contractions (VPCs) are seenas wide QRS complexes, followed by abnormal Twaves and are not preceded by a P wave. Up to 5isolated VPCs occurring over a 24 h monitoringperiod has been reported as a normal finding inhealthy horses. However, runs of greater than 4VPCs (paroxysmal ventricular tachycardia) mayrequire prophylactic treatment, particularly if heartrate is greater than 80 bpm. Such dysrhythmias fre-quently occur secondary to colitis, endotoxaemiaor myocarditis and may resolve spontaneously.Monitoring is required to ensure that ventriculartachycardia, with a sustained rate of over 100 bpmdoes not occur. Good success has been reportedwith phenytoin (20-22 mg/kg PO q12 h) for the treat-ment of persistent ventricular ectopy: after 4 doses,ectopy was resolved in 9/9 horses. Oral dosingshould be adjusted to maintain a plasma concentra-tion of approximately 9 mg/ml as sedation and ex-citement can occur at higher concentrations.

Ventricular tachydysrhythmias: Uniform VT occurs when the ectopic focus origi-nates from one place in the ventricle, creating onlyone abnormal QRS and T wave complex. This car-ries a better prognosis than multiform VT in whichmultiple different forms of QRS and T complex maybe present. The latter is indicative of increased elec-trical heterogeneity and instability and has an in-creased risk of progression to terminal ventricularfibrillation. Close examination for the ‘R on T’ phe-nomenon, when a QRS complex occurs within thepreceding T wave should also be performed, asthis indicates urgent requirement forantidysrhythmic therapy. Specific treatment of thiscondition is recommended if heart rate exceeds 100bpm or if there is evidence of cardiac output re-duction or ‘danger’ complexes in the ECG.Procainamide infusion (1 mg/kg/min) may be theoptimum treatment for VT in the conscious horseas this Class 1A antidysrhythmic does not not havevagolytic effects, such that it is unlikely to producevagotension. However, it is very expensive and an

infusion of quinidine gluconate (0.64% solution at1l per h per 500 kg) is a reasonable, cheaper alter-native. But, quinidine gluconate should not be givenwhen there is concurrent hypotensive cardiac out-put failure as it promotes peripheral vasodilata-tion. Lignocaine infusion is a cheaper alternativeto both of the agents above, and is also effective atterminating VT. This class 1B antidysrhythmic isrecommended to be infused slowly at a rate of 20-50 mcg/kg/min. If side effects of exciteability dooccur (although this is rare in the author’s experi-ence), then these may be controlled with diazepam(0.05 mg/kg IV). If VT remains refractory to thistreatment, then further agents may be added to theregimen, such as bretylium tosylate or an infusionof magnesium sulphate (See Table 1). When VT isnot life-threatening, therapy should be approachedcarefully (and calmly!) using the minimum numberof different agents so as to minimize the likely sideeffects of treatments. It should be remembered thatall antidysrhythmic agents have potential undesir-able cardiac effects.

REFERENCESBowen, I.M. (2003) cardiac Dysrhythmias. In:Current Therapy in Equine Medicine V, Ed. N.E.Robinson, W.B. Saunders, pp 602-613.

Reef, V.B. (1999) Arrhythmias. In: Cardiology ofthe horse, Ed. C.M. Marr, W.B. Saunders, pp 179-209.

Reef, V.B., Levitan, C.W. and Spencer, P.A. (1988)Factors affecting prognosis and conversion inequine atrial fibrillation. J. Vet. Int. Med. 2, 1-6.

132


132

A logicalapproach to the

evaluation ofdysphagia



House, Langford, BRISTOL BS 405DU, UK

Deglutition is divided into three stages.1. The oral phase which includes the gathering of

food, movements within the oral cavity, masti-cation and the formation of boluses of ingesta atthe base of the tongue is under voluntary con-trol.

2. The presence of a bolus gathered at the tonguebase triggers the split-second sequence of re-flexes, collectively known as swallowing, whichpropel the ingesta from the pharynx - the pha-ryngeal phase – into the oesophagus. The glosso-pharyngeal nerve(IX) and the pharyngealbranches of the vagus (X) innervate the pharynxand larynx and their afferent and efferent path-ways are co-ordinated in the swallowing centrein the brainstem.

3. waves of peristalsis convey the ingesta alongthe oesophagus to the stomach – the oesophagealphase of deglutition.

Oral phase of deglutitionPrehension in the horse relies on the incisor teethto grasp and section herbage, on the lips up pick up

smaller pieces of ingesta as well as to contain itwithin the mouth and to manipulate food towardsthe cheek teeth. Prehension necessitates normalopening and closure of the incisor teeth and normalmotility of the lips.

The molar and premolar teeth are responsible forthe mechanical crushing of the fibrous diet prepa-ratory to the chemical breakdown of the cellulose-based ingesta in the lower alimentary tract. Thetongue and buccal musculature assist to manipulatethe ingesta between the maxillary and mandibulardental arcades. Mastication requires free openingand closure of the temporo-mandibular joints(TMJs) through the action of the masticatory muscles– the masseter, pterygoid and temporal musclesclose the jaws and gravity assisted by the digastricmuscles open them. The masticatory muscles re-ceive their innervation through the mandibularbranch of trigeminal (V). The shape of the articularsurfaces of the TMJs together with the presence ofmenisci permit lateral movements by the mandibu-lar teeth across the wearing surfaces of the uppercheek teeth.

The tip of the tongue assists in prehension andmoves the ingesta between the cheek teeth. Con-traction of the tongue base helps in the formation ofboluses and once collected each bolus is drivencaudally by the piston action of the tongue and it isthis which triggers the involuntary phases of de-glutition by driving food and fluid caudally fromthe oro-pharynx. The tongue is attached to the hy-oid apparatus and free movement at the tympano-hyoid articulation is required for the antero-poste-rior tongue motion which facilitates bolus forma-tion in the oro-pharynx. The glossal musculaturereceives its motor supply via the hypoglossal nerve(XII).

The action of the levator palatini muscles drawsthe soft palate dorsally to close off the naso-phar-ynx and prevents the nasal reflux of ingesta; thismarks the onset of the involuntary stages of degluti-

133


133

tion. The horse has an intra-narial larynx, i.e. thelarynx is locked into the caudal wall of the pharynxby the free border of the palatal arch – the arcuspalato-pharyngeus – at all times other than duringthe momentary disengagement for deglutition. Thelevator palatini muscles lie parallel with the drain-age ostia of the auditory tube diverticula (ATDs)so that when they contract the ostia shorten and opento allow exchanges of air for pressure equilibra-tion across the ear drum, between the middle earand the external ear canal.

Pharyngeal phase of deglutitionThe constrictor action of the circular muscles ofthe pharyngeal walls embraces both oro-pharynxand naso-pharynx – the latter can be appreciatedduring endoscopic examinations of the naso-phar-ynx. A wave of constriction follows the contrac-tion of the tongue base and passes from rostral tocaudal efficiently to empty the oro-pharynx – thepharyngeal “stripping wave” – leaving minimalquantities of ingesta at the base of the tongue.

Aspiration of food and fluid through the rimaglottidis is prevented primarily by the tight adduc-tion of the vocal folds and arytenoid cartilages andto a lesser extent by the retroversion of the apex ofthe epiglottis. Laryngeal adduction is achieved bythe action of the crico-arytenoideus lateralismuscles which, like the dorsal muscle, is inner-vated by the recurrent laryngeal branch of the va-gus (X). However, dysphagia is not a recognisedfeature of recurrent laryngeal neuropathy. Fluidboluses tend to pass the larynx in the lateral foodchannels and solids take the midline route over theretroverted epiglottis. Following deglutition thelarynx is restored into its intra-narial position, i.e.it is held in position within the caudal wall of thenasopharynx by the arcus palato-pharyngeus beforerespiration is resumed.

The upper oesophageal sphincter is formed by thethyro- and crico-pharyngeus muscles and these aremaintained in a state of contraction to prevent in-

voluntary aerophagia, especially during forced ex-ercise. Relaxation of the crico-pharynx simulta-neous with the pharyngeal stripping wave permitsthe food and fluid boluses to pass caudally into theproximal oesophagus.

Oesophageal phase of deglutitionIt is arbitrary whether the oesophageal phase be-gins with the relaxation of the crico-pharyngeusmuscle or with its subsequent closure. However,after each bolus has passed through into the proxi-mal oesophagus, primary peristaltic waves are ini-tiated by the active closure of the cricopharynx.Waves of reduced intra-luminal pressure precedethe bolus in the form of muscular relaxation whilewaves of increased pressure by muscular contrac-tion follow to propel food and fluid caudally. Pri-mary oesophageal peristalsis carries individualboluses to the cardia, but the process is not com-pletely efficient and small quantities of ingesta areleft at variable levels in both the cervical and tho-racic oesophagus even in normal horses. This in-gesta is either picked up in the bolus of a subse-quent primary wave or by locally generated sec-ondary peristalsis which is triggered by segmentalstretching responses.

Diagnostic approach to cases of dysph-agiaHistory – signs of dysphagiaThe signs of dysphagia include an unwillingness toeat; slow, messy feeding; halitosis; rejection ofsemi-masticated food onto the ground (“quidding”);productive coughing; and the nasal reflux of saliva,ingesta and fluids. Horses which are unable to mas-ticate ingesta efficiently may be prone to impactivecolic and will show abnormal quantities of undi-gested fibre in their faeces. Obviously, horses whichare unable to eat and swallow food are likely tolose weight rapidly but this process is acceleratedif the horse develops secondary inhalation pneu-monia, which is a common sequel of dysphagia. Amoist cough is typical of animals aspirating foodor saliva into the rima glottidis.

134


134

In addition to a clear case history recording thecircumstances and rate of onset of the dysphagia,careful observation of the patient’s attempts to eatand drink can be invaluable to deduce which phaseof deglutition is awry. Whenever a horse showsreturn of ingesta from the mouth, the site of the dys-function must lie in the oral cavity or the orophar-ynx, certainly no further caudal than the epiglottis.Nasal reflux of ingesta points to an abnormality ofthe pharyngeal or oesophageal phase of degluti-tion.

Physical examination, external and oral inspectionDuring the external assessment of the patient, evi-dence of systemic and/or toxic disease, includingStrep. equi infection, botulism, grass sickness, ra-bies, upper motor neurone disease, lead poisoningand tick paralysis should be sought. The inspec-tion should check for evidence of concurrent neu-ropathies such as facial palsy, Horner’s syndromeor head tilt. The mouth should be opened to checkjaw tone, painful responses on opening the mouthand tongue mobility. Thoracic auscultation shouldcheck for signs of inhalation pneumonia. Local lym-phadenopathies and firm distension of the oesopha-gus to the left side of the trachea are changes whichmight be found during palpation of the throat area.Useful information can be obtained by attemptingto pass a stomach tube.

This should determine whether pharyngeal swal-lowing reflexes are still present or whether the up-per alimentary tract is physically obstructed. Un-der sedation and, with a full mouth (Hausmann)gag in place, a detailed inspection of the oral cav-ity should look for evidence of dental malalignment,enamel pointing of the cheek teeth, fractures of thedental crowns, periodontitis, soft tissue lesions ofthe buccal cleft and palate, oral foreign bodies andlesions of the tongue. While an effective light isinvaluable the structures involved often requirehands-on manipulation to complete the examina-tion and a tell-tale foul smell points to the pres-

ence of stale entrapped ingesta. The faeces shouldbe inspected for abnormal quantities of undigestedfibre.

Defects of the palate cannot be appreciated from aconscious examination of the mouth because theyare generally restricted to the soft palate and therestricted opening of the equine jaws prevents directinspection of the more caudal oral cavity other thanwith a rigid endoscope passed into a securelygagged mouth.

Endoscopy per nasumConchal necrosis may accompany prolonged dentalsuppuration and may be seen on endoscopy of thenasal chambers.

Provided that an endoscope with an external diam-eter of 8.0 mm or less is available, the diagnosis ofcongenital palatal defects in foals should presentno difficulties. This requires an inspection of thefloor of the naso-pharynx per nasum. Some defectsoccur at the midline with no absolute absence oftissue, simply a failure of fusion of the secondarypalate while others represent a unilateral hypopla-sia of the soft palate.

Endoscopy per nasum is necessary to confirmwhether pharyngeal paralysis is present. The usualfindings consist of a mixture of saliva and ingestaon the walls of the nasopharynx, persistent dorsaldisplacement of the palatal arch, poor constrictoractivity during deglutition and failure of dilation ofone or both ATD ostia after swallowing which isstimulated by contact with a biopsy wire or by wa-ter passed through the endoscope. Many cases wherefunctional pharyngeal paralysis is diagnosed are,in fact, afflicted with pharyngeal hemiplegia, i.e.the glosso-pharyngeal neuropathy is unilateral, forexample in cases of guttural pouch mycosis. How-ever, true pharyngeal paralysis may be seen in casesof botulism or heavy metal poisoning. Whenever aneurological cause of dysphagia is suspected, it isalways correct to inspect the ATDs for evidence ofmycosis or diverticulitis.

135


135

Other abnormalities which may cause dysphagiaand which can be confirmed by endoscopy of thepharynx or larynx include:- iatrogenic palatal defects after “over-enthusias-

tic” palatal resection (staphylectomy)- intra-palatal, pharyngeal and sub-epiglottic cyst

formation- epiglottal entrapment, with or without a sub epi-

glottal cyst- evidence of a sub-epiglottal foreign body seen

as unilateral oedema in the region of the ary-epiglottal folds with partial unilateral entrap-ment

- fourth branchial arch defects (4-BAD syndrome)- nasopharyngeal cicatrix- pharyngeal neoplasia- pharyngeal compression by external compres

sive lesions such as abscesses- arytenoid chondropathy- evidence of previous laryngeal surgery

Clearly it is helpful to obtain an impression of theextent of the tracheal aspiration of ingesta whichaccompanies the dysphagia and tracheoscopy ishelpful in this context.

Oesophagoscopy is often a less rewarding tech-nique than might be imagined in the investigationof dysphagia simply because physical or functionalobstructions invariably lead to a build-up of in-gesta and saliva in the lumen which, in turn, inhib-its a satisfactory field of view of the segment undersuspicion. However, when the patient has beenstarved before endoscopy evidence of conditionssuch as oesophagitis, megoesophagus, stricture, rup-ture, tracheo-bronchial fistulation, diverticulum,intra-mural cyst and neoplasia may be found. Amajor caveat for those intending to performoesophagoscopy is the very real hazard of expen-sive if not irreparable damage to a flexible endo-scope should it retrovert against an obstruction andpass craniad towards the teeth!

Radiography and fluoroscopyPlain lateral radiographs of the pharynx, larynx and

cervical oesophagus are used to investigate therelationships between normal anatomical structuresand to identify intra-luminal, mural and extra-mu-ral soft tissue swellings. Contrast media can behelpful to outline these structures. Fluoroscopicstudies, again using contrast media, are requiredfor a dynamic investigation of deglutition. Clearlyit is preferable for the patient to take up the con-trast medium voluntarily and, in the author’s clinic,bran mash impregnated with barium sulphate is of-fered to the horses, although a variety of flavouringssuch as molasses are included to make the mealmore palatable.

The shortcomings of the technique are that it is de-pendent on the enthusiasm of the patient to eat, andalso it takes no account of those dysphagias whichvary in severity between foods of differing consis-tencies. The forced introduction of liquid bariumsulphate into the mouth (oro-pharygography)through a syringe is far from ideal but it can beuseful to outline intra-oral, pharyngeal and oesoph-ageal lesions. Although it has been found that seda-tion does not significantly distort the process ofdeglutition, most horses will take part in the inves-tigation without resentment once they have becomefamiliarised with the ambient noises of the radio-graphic equipment. The sequence of events whichmake up deglutition is very rapid and facilities forvideo-recording of the fluoroscopic images for sub-sequent analysis including slow-motion replay areinvaluable. Lateral radiographs of the chest are auseful aid to monitor the progress of aspirationpneumonia which shows a characteristic pattern ofconsolidation in the dependant lung lobes.

Oral examination under general anaesthesiaGeneral anaesthesia is necessary to complete theinspection of the oral cavity and the tendency of thesoft tissues to obscure the view particularly towardsthe base of the tongue can be overcome by the useof an endoscope passed through a polypropylenemare gynaecological speculum. Again, general ana-esthesia is required for a more detailed manual ex-amination of the caudal oral cavity, especially in

136


136

the region of the epiglottis and ary-epiglottic folds.

Aetiology of dysphagia: oral phaseabnormalities

Facial palsy and lip lesionsFacial paralysis inhibits the ability of a horse toprehend and retain ingesta in the oral cavity. Thelocation of the facial nerve injury can often belocalised by assessment of other structures inner-vated by the facial nerve. Flaccidity of the upperlip and nostril margins indicates injury to the dor-sal buccal branch of the nerve which separates fromthe ventral buccal branch as it crosses the lateralaspect of the masseter muscle. Dysfunction of theventral buccal nerve produces drooping of thelower lip with resultant messy feeding through aninability to retain food and saliva within the mouth.

Laceration wounds at the commissures of the lipscan arise when a horse becomes hooked at the cor-ner of the mouth and a major avulsion injury fol-lows. Careful anatomical reconstruction of the lipmargins is required to ensure normal function aswell as acceptance of a bit after the wound hashealed. Sarcoids may develop at the lip marginsespecially the commissures and the method oftherapy, be it excision, cryosurgery or chemical cau-tery, which is used to ablate the lesions must alsotake regard of the acceptance of a bit after healing.Temporomandibular joint and hyoiddisordersTMJ disorders are rare in the horse but when theydo occur they cause marked pain and a rapid lossof bodily condition. Disuse leads to obvious atro-phy of the masticatory muscles, most obviously themasseters. The superficial position of the TMJ ren-ders it vulnerable to trauma most common disor-der afflicting this joint is the penetrating woundwith septic arthritis. The joint is located at the cau-dal extremity of the zygomatic arch and it lendsitself to direct palpation. Clinical examination alsoshows resentment of attempts to open the mouth

and even under general anaesthesia the range ofopening may be severely reduced. Radiography ofthe TMJs is difficult and the best imaging modali-ties are ultrasonography and scintigraphy.

Hyoid apparatus involvement usually accompaniesotitis media in the horse and ankylosis of thetemporo-hyoid articulation is a likely result. Patho-logical fracture of the stylo-hyoid bone follows andone of the effects of this is to limit the horse’s abil-ity to move the tongue. Radiography of the area andendoscopy of the ATDs contributes to the diagno-sis. The dysphagia can be relieved by pre-emptingthe pathological fracture by osteotomy of the stylo-hyoid, or more accessible is the kerato-hyoid, andtreating the underlying otitis media with broad spec-trum antibiotics.

Lingual abnormalitiesHypoglossal nerve injuries with lingual paralysisare rare in the horse and trauma, either in the formof lacerated wounds or tongue-strap strictures, ac-counts for the majority of tongue lesions in this spe-cies. A horse with a severely injured tongue may beunable to manoeuvre ingesta around the mouth andis inclined to drop food or to collect it in the buccalcleft. Similarly horses which loose the rostral por-tion of the tongue through incisive wounds can main-tain normal bodily condition albeit showing messyfeeding patterns. Foreign bodies may become bur-ied in the lingual tissues and the painful suppura-tive response can reduce a horse’s inclination toeat.

Dental disordersDental disorders are discussed at length later inthese proceedings but the reason why dental dis-eases cause dysphagia is through oral pain. Thereis little evidence that horses are afflicted with“tooth-ache” per se, but soft tissue pain through lac-erations of the oral mucosa by sharp dental projec-tions and at the gingival margins in the form of pe-riodontitis is a major contributor to the inability tomasticate food adequately. The dental projections

137


137

may take the forms of enamel pointing from ne-glected abrasive wear, maleruptions and displaceddental fragments usually the result of pathologicalfracture of teeth.

Congenital and acquired palatal defectsThe presence of a defect in the soft palate preventsan effective seal between the oral cavity and thenaso-pharynx during the lingual propulsion of in-gesta towards the tongue base and during pharyn-geal contraction. The result is that food and fluidsare directed dorsally and are refluxed via the nasalchambers to the nares.

Not all palatal clefts occur as simple midline lin-ear defects although these provide the most com-mon explanation when younger patients are pre-sented with nasal reflux of milk. The various per-mutations of unilateral hypoplasia of the soft pal-ate and pseudo-uvula formation can escape confir-mation until the patient is considerably older. Theyoften occur in association with epiglottal entrap-ment. Although there have been descriptions in theveterinary literature of palatal reconstructive sur-gery using mandibular symphysectomy to gain ac-cess to the area the results are invariably disap-pointing if success is measured as rendering thehorse suitable for athletic endeavour. It may be pos-sible to control the dysphagia by this very radicalsurgery, but such is the subtle function of the pala-tal arch as an organ of respiration that it has neverbeen possible to create a stable relationship withthe larynx. Excessive palatal resection (staphyl-ectomy) in the treatment of DDSP is an ominouscomplication because it is irreparable for the rea-sons given above. Iatrogenic defects can usuallybe differentiated from congenital palatal deformi-ties at endoscopy because the end-points of the re-section are visible and the margin of the free bor-der has a more rounded appearance. Inadvertentsplits in the palate have been reported after the re-lief of epiglottal entrapment by section with ahooked bistoury passed per nasum in the standinghorse. This complication can be avoided by per-

forming a similar technique through the mouth withthe patient anaesthetised.

Other oral conditions: foreign bodies, neoplasiaThe most common foreign bodies in the oro-phar-ynx are brambles which become lodged in the sub-epiglottal area or in the lateral food channels caus-ing acute-onset dysphagia. Endoscopy per nasumwill show oedema in the ary-epiglottic folds evenif the foreign body itself cannot be seen. Such anendoscopic finding is an indication for an oral ex-amination, either by palpation or with a guardedendoscope, under general anaesthesia. Other for-eign bodies such as wire fragments may becomewedged between teeth.

Squamous cell carcinomas, lymphosarcoma andconnective tissue tumours arise sporadically inhorses and they tend to cause dysphagia simply byvirtue of space occupation. Although each must beconfirmed by biopsy and treated on its merits de-pending on location, size etc. they generally carrya poor prospect of successful treatment by the timethey are presented for investigation.

Aetiology of dysphagia:pharyngeal phase abnormalities

Pharyngeal paralysisParalysis or paresis of the pharyngeal constrictormuscles arises when the function of the glosso-pha-ryngeal nerve (IX) is compromised. When food andfluids are not propelled into the upper oesophagusthey may be returned via the nostrils, be aspiratedinto the laryngeal airway or are spilled out of themouth. The most common causes of pharyngeal pa-ralysis are guttural pouch mycosis, ATD diverticu-litis, botulism and heavy metal poisoning. It is al-ways correct to investigate the possibility of ATDdisease in cases of pharyngeal dysfunction. Whenthere is marked inhalation of ingesta leading tobroncho-pneumonia or evidence of dehydration,the condition of the patient demands euthanasia on

138


138

humane grounds. However, some horses with par-tial pharyngeal dysfunction may survive withoutdistress and simply show an occasional cough andnasal discharge without progress to aspirationpneumonia. Such horses should be given the ben-efit of the opportunity for the natural restoration ofpharyngeal function even if this takes many monthsto return.

Pharyngeal compression:strangles abscessationThe presence of extra-mural soft tissue swellingsadjacent to the pharynx may cause dysphagia be-cause of external compression of the pharynx andalso, in the case of abscessation, because of thepain associated with the movement of food bolusespast the lesions.

Pharyngeal cysts, palatal cystsThe origin of pharyngeal cysts is not known butintra-palatal cysts may well develop from salivarytissue which is normally distributed widely in thepalatal mucosa. Diagnosis of both conditions isby a combination of endoscopy and radiographyand again these lesions cause dysphagia by virtueof space-occupation. While cysts on the pharyn-geal walls or at the free border of the palate can beexcised, the lesions within the substance of the softpalate are not easily treated because fistulation ofthe palate is a likely sequel to surgery. Epiglottal lesions, including sub-epiglottic cystsBoth peracute and sub-acute inflammation of theepiglottis are described in horses. The per-acuteform of epiglottitis, with oedema and cellulitis, isprobably a complication of upper respiratory tractviral infections and can be so severe that a poten-tially fatal airway obstruction occurs. A less se-vere form of epiglottitis with swelling and distor-tion of the epiglottis may have a similar aetiologyand causes dysphagia and coughing presumablythrough discomfort during deglutition combinedwith reduced flexibility. Afflicted horses also pro-duce untoward respiratory sounds at exercise. The

diagnosis is established by endoscopy but it can bedifficult to differentiate this form of epiglottitis,which is likely to be responsive to vigorous antibi-otic therapy, from a para-epiglottic foreign body.

The increased mass of the epiglottis arising in en-trapment by the glosso-epiglottal mucosa but moreusually with sub-epiglottic cysts, causes dysphagiabecause of space-occupation and a restriction ofthe freedom for epiglottal retroversion. Secondarypersistent dorsal displacement of the palatal archis not uncommon and this will frustrate diagnosisby endoscopy because the displaced palate obscuresthe view of the epiglottis. Persistent DDSP is anindication for lateral radiography or oro-pharyngography using contrast medium. Both con-ditions are amenable to successful excisional sur-gery.

Laryngeal abnormalitiesCompromised glottic protection leading to the as-piration of ingesta into the lower airways may arisespontaneously in cases of arytenoid chondropathy,or through iatrogenic causes such as complicationsof prosthetic laryngoplasty or partial arytenoidec-tomy. The precise cause of post-laryngoplasty dys-phagia is not known but over-abduction of thearytenoid cartilage, cicatrisation associated withreactive implants and nerve injuries are amongstthe suggestions which have been proposed. Thepresence of ingesta in the trachea can be establishedby endoscopy as the cause of coughing and refluxof ingesta to the nostrils may provided outward evi-dence of this complication. Removal of the pros-thesis is often, but not always, effective in controlof the dysphagia, but, of course, the respiratory ob-struction for which the surgery was originally per-formed can be expected to return as the arytenoidcartilage reverts to its collapsed state.

Fourth branchial arch defects (4-BAD)When the 4-BAD syndrome includes aplasia or hy-poplasia of the crico- and thyro-pharyngeal musclesthe proximal oesophageal sphincter remains per-

139


139

manently open. Although horses with 4-BAD aremore likely to present with abnormal respiratorynoises at exercise, some may cough when eatingand drinking and show a nasal discharge. They alsoshow bizarre eructation-like noises at rest and maybe confused with wind-suckers. The failure to beable to generate primary peristaltic waves com-bined with an oesophagus which is dilated by aircould lead to confusion with megoesophagus. Inaddition, the involuntary aerophagia which accom-panies this condition predisposes afflicted horsesto colic.

Aetiology of dysphagia: oesophagealphase abnormalities

MegoesophagusMegoesophagus has been reported sporadically inthe horse, sometimes as a primary congenital dis-order and sometimes secondary to other conditionscausing obstruction of oesophageal function suchas vascular ring strictures. Coughing, nasal refluxof ingesta and distension of the cervical oesopha-gus may all be features. Confirmation of the diag-nosis is easily achieved by contrast radiography.

Oesophageal obstruction (“choke”)Obstruction of the oesophagus results from the im-paction of dry fibrous material occluding the lu-men of the oesophagus, typically in the cervicalsegment, and is the commonest cause of acute dys-phagia in the horse. Older horses seem to be moresusceptible but this may relate to the diets offeredto animals which are not being fed for competitiveexercise. However, at the opposite extreme, foalswhich are beginning to take herbage occasionallyplug the oesophagus with a bolus of dry grass.

Acute obstruction of the oesophagus by impacted,dry ingesta is typically associated with access toinadequately soaked sugar beet pulp in the UK andno doubt each geographical region will have itsindividual prevalent causal agent. The dry fibrousmaterial swells with the absorption of saliva and

an expanding bolus occludes the oesophageal lu-men. Subsequent boluses compound the obstruc-tion.

Horses with “choke” present in an acutely distressedstate with copious reflux particularly saliva to thenostrils. Cross-examination of the person respon-sible for feeding the horse does not always lead toa confession of guilt in regard to failure adequatelyto soak the sugar beet pulp or even to an admissionof access to this material at all.

The initial diagnostic challenge in cases of oesoph-ageal obstruction is to differentiate this conditionfrom other causes of acute dysphagia most notablypharyngeal paralysis. The cervical oesophagus maybe palpably distended with firm ingesta and thepassage of a stomach tube beyond the pharynx isgenerally not possible . Inhalation tracheitis is in-variably present and pneumonia is likely to followif treatment is not promptly instituted. Endoscopyof the pharynx and ATDs may be helpful when thecase history convincingly rules out access to thecommon causes of obstruction.

Although most “chokes” are relieved by heavy se-dation and the repeated administration ofspasmolytics, and it is correct to attempt this for afew hours, the distressed state of the patient andthe likelihood of serious respiratory complications,demand that conservative management should notbe prolonged. The author’s preferred approach inreferred cases, which have invariably receivedconservative therapy for at least 24 hours, ispromptly under general anaesthesia, to institute vig-orous lavage by stirrup pump through a stomachtube. Obviously the patient’s trachea should be in-tubated and the head is positioned over a support-ing bag with the nose inclined downwards. In thisway the impacted ingesta is progressively washedback out at the nostrils. Other clinicians prefer toattempt relief using a similar lavage technique withthe patient standing but sedated. The prognosis fora complete recovery after the relief of an oesoph-

140


140

ageal obstruction is good. The possibility of re-currence of the “choke” or of long-term stricturedevelopment can be reduced by withholding dryfibrous foods for at least 72 hours followed by thegradual re-introduction of a soft diet. Oesophagealmotility is likely to remain weak for several days.The inhalational tracheitis or bronchitis is usuallyself-limiting but broad spectrum antibiotic covershould be maintained for 7 – 10 days.

Oesophageal strictures/stenosisOesophageal strictures are thought to be the sequelof episodes of acute obstruction and horses withthis condition are presented with recurring “choke”.Confirmation of the diagnosis is best achieved bycontrast radiography. The most common site forstricture development is at the thoracic inlet. Re-section of the stenosed segment of oesophagus maybe attempted but a guarded prognosis is indicatedbecause recurrence of the stricture at the site ofanastomosis is a frequent complication.

Intra-mural oesophageal cystsCongenital intra-mural cysts may be encounteredin young horses and cause dysphagia through re-stricting peristalsis and the passage of oesophagealboluses. The lesions may be seen as swellings inthe oesophageal wall at endoscopy or be demon-strated by ultrasonography or contrast radiography.

Oesophageal ruptureRuptures of the oesophagus may arise throughtrauma or by rough misuse of a stomach tube. Re-gardless of the cause, the condition carries a poorprognosis unless cases are presented for treatmentsoon after the injury has occurred because of therapid advance of contamination and cellulitis intothe surrounding tissues. Most cases arise throughobvious external trauma by kicks or stake woundsbut a number of horses have been referred to theauthor’s clinic where rupture of the pharyngeal oroesophageal wall has occurred through excessivelyforceful attempts to pass a stomach tube or, in onecase, an endotracheal tube.

NeoplasiaTumours of the oesophagus are very rare in the horsebut squamous cell carcinoma at this site has beenreported.

“Wind-sucking”Recent research using simultaneous video-endos-copy and video-fluoroscopy has elucidated theevents which occur in the pharynx and upper oe-sophagus during wind-sucking behaviour. Contraryto popular belief, horses performing this stereotypydo not swallow air and deglutition is not part of thesequence of events. The muscles of the upper neckcontract to create a pressure gradient across the softtissues of the throat so that the walls of the pharynxand upper oesophagus are pulled apart. The suddenin-rush of air through the open crico-pharynx coin-cides with the gulping sound which is typically heardduring attacks of wind-sucking, but the majority ofthe air is returned from the oesophagus to the phar-ynx immediately.

Grass sickness“Grass sickness” is a dysautonomia which producesdysphagia in its acute form but colic in the sub-acute and chronic forms. The condition is seen inhorses of all ages throughout the United Kingdomand northern Europe. Afflicted horses are gener-ally severely depressed with patchy sweating, el-evated pulse and ileus. The dysphagia arises as apart of total gastro-intestinal stasis and nasal refluxof ingesta adds to the pitiful appearance of the pa-tients. There is currently no reliable in vitro diag-nostic test, apart from gut wall biopsy during ex-ploratory laparotomy, but the radiographic demon-stration of oesophageal stasis and the endoscopicidentification of ulceration of the oesophageal mu-cosa are helpful pointers to the likely diagnosis.

141


141

Introduction

Dorsal displacement of the soft palate (DDSP) isthe most frequent form of dynamic upper respira-tory tract obstruction to afflict the athletic horseand is primarily a disorder of the racehorse. In asurvey of UK trainers 4% of horses in training perannum were afflicted with this malfunction(Franklin, 2002) which compares with approxi-mately 2.5% per lifetime afflicted with recurrentlaryngeal neuropathy (RLN).

Functional concepts of the equineconducting airways

The horse is designed to be an obligatory nose-breathing animal and never to breathe through its

mouth. It is equipped with an intra-narial larynxwhereby the cartilages of the larynx are locked intothe caudal wall of the nasopharynx by the palato-pharyngeal arch which acts to provide an air-tightseal. In this context the anatomical and functionalintegrity of the palatal arch is essential to maintainthe stability of the conducting airways.

An oro-pharyngeal seal also exists through contactbetween the dorsal surface of the tongue and theventral surface of the soft palate. The palatal archmust be able to disengage momentarily for degluti-tion, but at all other times while the larynx remainsin its intra-narial position, the oro-pharynx is nomore than a potential space as the palate and tongueare in contact with one another. The nasopharynx isa musculo-membranous tube where the ventral as-pect is formed by the soft palate. Active effort bythe muscles of the palate - the tensor veli palatinus,the levator palatinus, the pharyngo-palatinus andthe palatinus - is required to maintain the anatomi-cal relationships during exertion, and particularlyto prevent the separation of the palate from the baseof the tongue.

Aetiopathogenesis of DDSP

DDSP arises as an acute respiratory obstructionwhich occurs while a horse is at fast exercise andwhen the free border of the palatal arch becomesdislodged from its normal sub-epiglottic positionso that the unsupported soft tissues occlude the rimaglottidis. Ventilation studies of DDSP-afflictedhorses confirm that the greater obstructive effectoccurs during expiration (Franklin et al. 2002, a).

Recent research has attempted to explain how DDSPoccurs with studies ranging from the slow-motionanalysis of the events leading up to displacementof the free border above the epiglottis, to selectivedenervation of the pharyngeal muscles. Treadmillendoscopy, performed in step-wise tests to the pointof fatigue in clinical cases of DDSP, has revealeda consistent sequence of events which leads to dy-

How cantreatments

currently used fordorsal

displacement ofthe soft palate be

rationalised?


University of Bristol, Department ofClinical Veterinary Science,

Langford House, Langford, BRISTOLBS 40 5DU, United Kingdom

142


142

namic DDSP. This commences with palatal insta-bility (PI) which may reflect progressive weaken-ing of the palatal musculature. PI is first seen aswave movements by the soft palate from its junc-tion with the hard palate backwards.

These billowing movements can only occur oncethe soft palate has become separated from the baseof the tongue. The observation that the billowingmovements are generated at the junction of the hardand soft palates suggests that the primary dysfunc-tion has little to do with the free border of the pal-ate, and yet this is the site at which much correc-tive surgery is directed! When the palate and tongueseparate, the oropharynx is no longer a potentialspace but becomes occupied by air. Once the softpalate is free, it rises against the ventral surface ofthe epiglottis so that the shape of the cartilagechanges as it becomes contoured to the palate. Inthe early stages of exercise the epiglottis has anindependent rigidity and little of its ventral surfaceis in contact with the soft palate.

In ‘normal’ horses this remains the situation untilthe exertion is completed. However, in those horseswhich are afflicted with palatal dysfunction, theepiglottis appears to become progressively moreflaccid as the soft palate rises against it, but this issimply a reflection of the unstable relationship be-tween the tongue base and the ventral surface of thepalate rather than an indication of some form ofepiglottal hypoplasia. Contraction by the hyo-epiglotticus muscle adds to the impression of flat-tening of the epiglottis against the soft palate.

Finally, but not in every horse, the palatal arch spon-taneously slips from beneath the epiglottis to ob-struct the rima glottidis. It is as if once air entersthe oro-pharynx, the palate behaves like a wet sailand flaps until it is finally freed from beneath theepiglottis. Deglutition rarely, if ever, triggers DDSP.

While an anatomical account of DDSP is relativelystraightforward, the underlying causes which have

been proposed are more complex. A series of stud-ies by Holcombe et. al. at Michigan State Univer-sity have provided food for thought:

1. Experimental section of the tendinous portion ofthe tensor palatini muscles at the level of thehamulus of the pterygoid leads to billowing move-ments by the rostral portion of the soft palate, butnot to full DDSP

2. Temporary denervation of the palatal musclesby the application of local anaestheticsolution tothe pharyngeal branch of the Vagus nerve as itcrosses the medial wall of the ATD causes charac-teristic DDSP

3. Denervation of the hyo-epiglotticus muscle,which serves to maintain the epiglottis in a de-pressed position, can be achieved by blocking thehypoglossal nerve. Such a technique leads to epig-lottal retroversion and does not provoke DDSP

The conclusions to be drawn from these studiesare multiple, but they are not in conflict with thetreadmill endoscopic observations outlined above.DDSP appears to represent the end-point of weak-ening of the palatal musculature as a whole ratherthan of any individual muscle leading to instability.The role of epiglottal anomalies has probably beenoverstated as a cause of DDSP and the observationthat PI and DDSP do not occur in the face of epig-lottal retroversion in naturally occurring cases sup-ports the view that the epiglottis is innocent.What remains to be clarified are the factors whichcompromise the function of the palatal musculatureso that it can no longer maintain stable contact withthe base of the tongue. From the survey of trainersin the UK (Franklin, 2002) it was concluded thatDDSP is often preceded by exposure to upper res-piratory tract viral infection.

Management of DDSP

Conservative measures

143


143

Every attempt should be made to eliminate the pre-disposing factors, including unfitness, oral discom-fort through dental disease and concurrent smallairway inflammation. Aids such as a dropped orcrossed noseband or a change of bit to a simplerubber snaffle, or even the use of a bitless bridle,all aim to prevent air gaining access to the orophar-ynx. Tongue straps or tongue-ties are used to dis-courage caudal retraction of the tongue and can berationalised on the basis that they help to maintainthe tongue/palate contact. Experemental studies withhorses exercised on a highspeed treadmill with andwithout the application of a tongue-tie producedinconclusive results (Franklin et al, 2002, b). Inthe author’s clinic, horses for which a face mask isused to record physiological data are much lesslikely to show DDSP than when the mask has beenremoved. One of the effects of the mask is to closethe mouth. Thus, the crossed noseband is theauthor’s preferred riding aid to inhibit DDSP.

Surgical TreatmentsWhenever a wide range of surgical remedies isavailable for a clinical disorder and none hasproved to be significantly superior to the others,there must be grounds to suspect that all are em-pirical and that the underlying causes are not un-derstood or cannot be reversed. The various op-erations proposed to inhibit DDSP fall into fivebroad groups where the perceived objectives arequite different, (1) interferences to the free borderof the palate, (2) resections of part of the strapmuscles, or their tendons, attaching to the larynxand/or hyoid apparatus, (3) techniques to renderthe epiglottis longer and more rigid (4) attempts toincrease tension in the rostral soft palate from itsoral surface, and (5) replacing a weakened thyro-hyoid muscle and thereby altering the shape of thenasopharynx. It is ironic that very similar ap-proaches have been employed as remedies for hu-man snoring which can also be attributed to weak-ness of the pharyngeal musculature in overweight,unfit people and that similarly unpredictable re-sults are achieved. In both species is it accepted

that there is no surgical method which makes themuscles of the palate stronger but whatever tech-nique is used it should avoid damage to these struc-tures. The palatal musculature lies immediatelybeneath the nasopharyngeal mucosa and dorsal tothe aponeurosis of the palate and thus, the recentvogue to apply trans-endoscopic laser cautery pernasum appears to be contra-indicated.

1. Staphylectomy comprises the resection of astrip of tissue from the anterior margin of the palato-pharyngeal arch. This technique appears to be quiteillogical inasmuch as the source of palatal dysfunc-tion does not lie at the free border of the palate.Also an effect of the surgery is to increase the sizeof the intra-pharyngeal ostium so that the intra-narialconfiguration of the larynx would be expected tobe less stable. Some advocates of the techniqueargue that the effect is more one of scarifying theborder of the arch. However, a proportion of horsesappear improved by staphylectomy - 59% in onesurvey - and it has been suggested that the improve-ment arises through a reduction in the mass of thetissues available to obstruct the rima glottidis. Themajor detractions of staphylectomy are the need forgeneral anaesthesia and the possibility that exces-sive removal of palatal tissue, or damage to thepharyngeal wall, will precipitate chronic palatalinstability with or without a permanent dysphagia.

2. Myectomy includes resection of a segment fromthe sterno-thyroideus and sterno-hyoideus muscles,and may be extended to include part of the omo-hyoideus muscle, or be limited to cutting the ten-don of insertion of the sterno-thyroid on each side.Protagonists of the technique claim that it inhibitsthe laryngeal retraction which they say precedesDDSP. The procedure can be performed on thestanding horse under local analgesia, or more safelyunder general anaesthesia. The overall ‘success’rate of 60% which has been recorded after myec-tomy is not significantly different from that achievedby staphylectomy. However, there is absolutely noendoscopic evidence or airflow data to support the

144


144

concept of laryngeal retraction as a trigger of DDSP,in fact studies in normal horses has shown that im-pedance in the URT is increased by this surgery(Holcombe et al, 1994).

Composite surgery - on the basis that myectomyand staphylectomy performed independently pro-duce approximately 60% success, some surgeonshold that the two techniques performed together in-crease the possibility of inhibiting DDSP. The“Llewellyn” procedure consists of a combinationof staphylectomy and sterno-thyroid tenotomy. Inpractice, the results of the composite operation arenot one iota superior to the component techniquesperformed independently.

3. Epiglottal augmentation has the objective toincrease the size and rigidity of the epiglottis in thebelief that hypoplasia of the cartilage is a signifi-cant factor in the aetiopathogenesis of DDSP. Epi-glottal hypoplasia may be defined as an epiglottalcartilage which is abnormally small or which lacksrigidity. It is a common observation that the epig-lottis of young horses appears flaccid but the natu-ral ageing process from foal to yearling to juvenilebrings increased rigidity. Thus, it is both unneces-sary and unjust to condemn yearlings at the time ofsale on account of their epiglottal conformation.Epiglottal hypoplasia based on the length of thecartilage is said to occur occasionally in Standard-breds but it is very rare indeed in Thoroughbreds.Treadmill endoscopic observations and the hypo-glossal nerve resection studies have cast consider-able doubt on the role of the epiglottis in the main-tenance of the intra-narial larynx - the epiglottis isnot necessary to “hold down the soft palate.”

In spite of the lack of reasoning behind the augmen-tation technique, a comparable level of success toother methods is reported. However, the potentialfor major complication cannot be overstated. Theepiglottis may not be as important in respiratoryfunction as previously thought but it is vital in theprotection of the lower airways during deglutition

and misplacement of the surgical Teflon may pre-cipitate irreversible dysphagia.

4. Tension palatoplasty techniques aim to stabilisethe contact between the palate and the base of thetongue by reducing flaccidity in the palatal tissuesin the area between the hard/soft palate junctionand the level of the fauces. Protagonists suggestthat such procedures prevent disruption of the oro-pharyngeal seal and thereby arrest DDSP at itssource. The palate is approached through the mouthbut only the structures ventral to the aponeurosis ofthe palate are tensioned. Thus, the palatal muscleswhich lie dorsal to the aponeurosis remain un-touched, and yet weakness of these muscles appearsto be a primary factor in the aetiology of DDSP.The methods used to increase tension in the softpalate include partial thickness resection of the pala-tal tissue (“Ahern” procedure), the injection of scle-rosing solutions and the physical cautery of the su-perficial palatal tissues per os. There are as yet nopublished results from any tension palatoplasty tech-nique.

5. Thyro-hyoid replacement – “tie-forward”.Recently Ducharme has proposed the use of bilat-eral prosthetic implants to replace the thyro-hyoidmuscle. These are placed ventrally between thebasi-hyoid bone and the thyroid cartilage. The rea-soning behind this proposal is that dynamic imag-ing of the region has suggested that the position ofthe hyoid apparatus in relation to the larynx is notnormal in DDSP-afflicted horses. Although his earlyresults are encouraging giving a superior level ofsuccess to all other reported techniques the posi-tion of the larynx as it is engaged through the arcuspalato-pharyngeus is altered but the dynamics ofdeglutition must also be compromised.

Prognosis and future developments

It is remarkable how consistently a “success” levelof 60% is achieved in the surgical management ofDDSP regardless of the method used. The obvious

145


145

unanswered question is what proportion of casesof DDSP would resolve spontaneously withouttreatment. Perhaps it is not surprising that manyveterinary reputations in this field have been es-tablished from surgery on 2 year old horses whichare improved in time for their 3 year old season.The role of upper respiratory tract infections in theonset of DDSP has not been explored and yet someform of subtle inflammatory change in the pharyn-geal musculature or its innervation could explainwhy DDSP can occur in “clusters” in the aftermathof URT infections.

146


146

The Hock accounts for most hind limb lameness inperformance horses. A large number of conditionsinvolving the tarsocrural joint, arthrodial joints,tendon sheaths, bursae, tendons or ligaments con-tribute to this high incidence.

Distal tarsal synovitis andosteoarthritis (Bone Spavin)

Bone spavin is an osteoarthritis and periostitis thatinvolves the distal intertarsal and tarsometatarsaland occasionally proximal intertarsal joints. It isconsidered to be the most common cause of tarsallameness. The vast majority of horses affected haveradiographic indicators of osteoarthritis but a smallpercentage lack physical or radiographic evidenceand are said to have occult or blind spavin. Theseanimals however may have scintigraphic evidenceof distal tarsal inflammation. Occult and distal tarsalosteoarthritis should be considered different stagesof the same process in which synovitis results fromradiographically inapparent cartilage lesions whichcan be found at autopsy. In addition, desmitis ofthe intertarsal ligaments can produce lameness.

Treatment of Distal TarsalOsteoarthritis

In most cases, determining how to treat horses withdistal tarsal osteoarthritis is more difficult thanmaking the diagnosis. There are a variety of treat-ment options available that can be tailored to theneeds of each affected horse. The success of thetreatment usually depends on the use of a combina-tion of specific treatments

Medical or non-surgical treatments

Most horses with D.T.O. respond favourably tovarious forms of medical management, includingintra-articular medication, combined with short-term rest, oral phenylbutazone and corrective shoe-ing. In general, medical management is attemptedinitially and if it is not satisfactory in restoring thehorse to its intended use, surgical options are thenconsidered. Medical management is consideredunsatisfactory when lameness does not improve orif repeat intra-articular medication is required inless than 8-10 weeks.

Reduced ExerciseIf the degree of disability is minimal and the per-formance demands of the owner are flexible, somehorses benefit from decreasing their workload andaltering their intended use.

Corrective ShoeingThe goal of corrective shoeing in healing DTOA isto reduce stress on the distal tarsus by encouragingbreakover of the hind foot and restoring hoof bal-ance. Breakover can be improved by squaring orrolling the toe and setting the shoe back on the hoof.

NSAIDSNSAIDS are often used as an adjunctive treatment.Phenylbutazone is used most often. Low doses ofphenylbutazone are often effective in managing painassociated with DTOA and may extend the perfor-mance longevity of the horse. Occasionally phe-nylbutazone may permit sufficient activity to achievefunctional ankylosis of the joints although this iscontroversial. In general, horses in continuous workor training are not candidates for PBZ therapy be-cause of the risks of prolonged use. Ideal candi-dates are occasional use performance horses. Rec-ommendations include 4.4mg/kg PBZ before theathletic activity and continued administration for1-2 days. Alternatively, it may be given on an on-off schedule – given for a few days and then stoppedfor a few days.

Hock lamenessBarrie EdwardsUniversity of Liverpool

147


147

Alternative or Complementary TherapiesThese include acupuncture, low energy light-therapylasers, magnetic therapy and therapeutic ultrasonog-raphy. The mechanism of action, efficacy and thera-peutic protocols have not been substantiated. Re-cently extracorporeal shock-wave therapy (ESWT)is a new treatment modality that has been investi-gated. The focussed shock waves are thought tostimulate bone remodelling, increase blood flowto bone-tendon interfaces, stimulate cellular me-tabolism and provide short-tem analgesia.

The horse is placed in lateral recumbency undergeneral anaesthesia. Under fluoroscopic guidancethe joint spaces and lesions are mapped on the skinsurface. Each joint is administered 2000 pulses at0.89 mJ/mm2 with the primary focus point at thesite or sites of the lesion.

Following treatment, the horse is stall-rested forone week. Then, before resuming full work, theyare restricted to walking in hand and ground workfor 4 more weeks. In one study, 80% of horses hadimproved at least 1 lameness grade 12 weeks fol-lowing treatment. Follow-up; radiographs 12weeks post-treatment did not show any consistentchanges compared to pre-treatment radiographs.Horses that responded to treatment continued toperform as expected without lameness returning.

Surgical Treatment

A variety of surgical treatments have been reported.

Cunean TenotomyCutting the cunean tendon is thought to relieve pres-sure over the ‘seat of spavin’ but its efficacy iscontroversial because lesions contributing toDTOA are predominantly intra-articular rather thanperi-articular. It is more likely to be effective intreatment cunean bursitis.

Intra-articular MedicationMost horses with DTOA benefit from intra-articu-lar medication of the distal tarsal joints with corti-costeroids or hyaluronan or a combination of thesedrugs. There has been concern about the detrimen-tal effects of corticosteroids on articular cartilagehowever these have primarily been demonstratedin high motion joints. Whether repeated intra-ar-ticular corticosteroid treatment hastens the progres-sion of OA in horses with DTOA remains contro-versial and unknown. Theoretically they shouldhelp promote clinical ankylosis of the distal tarsaljoints but repeated injections appear to rarely re-sult in ankylosis in most clinically affected horses.

The corticosteroid most frequently used is methyl-prednisolone acetate, although triamcinoloneacetonide and betamethasone acetate combinedwith sodium phosphate may also be effective.

Typically the dose of methylprednisolone acetateranges from 30-60mg/joint and that of triamcino-lone acetonide is 3-12mg/joint. In general the low-est dose that achieves clinical improvement shouldbe used.

5-10mg of hyaluronan are frequently combined withcorticosteroid and the combined intra-articularmedication is believed to produce a better clinicalresponse. Although some veterinarians treat onlythe TMT joint because injection of the DIT joint ismore difficult, because of the variability in jointcommunication a more consistent clinical responseis likely if the DIT and TMT joints are treated in-dividually.

Adjunctive Articular MedicationsAdditional articular medications which have beenused include oral glucosamine and chondroitin sul-phate products, i/v hyaluronan and i/m polysulfatedglycosamino-glycans. No specific study has evalu-ated these products. In general they are most ben-eficial in combination with other therapies.

148


148

Wamberg OperationA rhomboid incision is made through the periostealtissues to section the local nerve supply of the jointcapsule under the cunean tendon. The efficacy ofthis technique is equally controversial.

Tarsal ArthrodesisAs natural ankylosis of the distal tarsal joints isslow and often incomplete, several techniques, bothsurgical and chemical, have been developed fortarsal arthrodesis. Arthrodesis is fusion of a jointinvolving destruction of articular cartilage, withsubsequent intra-articular and peri-articular boneformation. This is thought to stabilise the joint andalleviate pain associated with OA.

Articular Drilling With or Without StabilisationSeveral variations of intra-articular drilling tech-niques have been reported for the distal intertarsaljoints. Most involve making a curvilinear incisionon the medial aspect of the hock over the cuneantendon which is usually cut to permit exposure ofthe TMT and DIT joints. The position and plane ofthe joints are identified using needles and their in-tra-articular position is confirmed using radiogra-phy or fluoroscopy. Initial surgical procedures de-scribed a drilling technique aimed at destroying60% of the articular cartilage of the two joints.

Good clinical results were obtained but concernsabout the severity of post-operative pain thought tobe possibly due to resultant instability has led tomodifications involving a less aggressive intra-ar-ticular drilling technique. Three drill holes each2-3 cm in depth, are made from the medial aspectof each of the distal two joints. The goal is to ‘spotweld’ the bones of the joints together without nec-essarily achieving complete joint arthrodesis. Us-ing a drilling technique combined with jointstabilisation with a small dynamic compressionplate may provide superior results.

Laser Facilitated ArthrodesisA technique using a ND:YAG laser to athrodese

the distal joints has recently been reported. Withthis technique a 600 micron conical tipped laserfibre ensheathed in a 16 gauge stainless steel can-nula is placed into the dorsomedial aspects of thejoint spaces under general anaesthesia. Egressneedles are placed in the joints 1cm from the laserfibre to evacuate the plume generated by the laser.Approximately 800-1000 joules of energy are de-livered to each joint. The goal of the procedure isto heat the articular cartilage and collagen in thesurrounding joint capsule by boiling the synovialfluid until it vaporises. Good success has beenreported in improving lameness and returning horsesto work with no major complications. In somecases horses become sound before radiographicevidence of joint arthorodesis is evident. Horseswith extensive periosteal bone formation aroundthe TMT and DIT joints may not be ideal candi-dates for laser facilitated arthrodesis because ofthe difficulty in placing the laser fibre intra-articularly in the affected joints.

Chemical ArthrodesisChemical fusion of the distal tarsal joints has beenperformed using sodium mono-iodoacetate (MIA).Sodium MIA is a chemical that causes a rapid de-crease in chondrocyte intracellular triphosphateconcentration resulting in inhibition of glycolysisand chondrocyte death. Tarsal fusion using MIAwas reported to occur within 24 weeks in normalhorses and was proposed as a relatively easy, in-expensive and non-invasive treatment for distal tar-sal OA.

Despite this advantage, there are many potentiallyserious complications. Most notably, horses maydevelop severe DIT and tarsocrural joint OA fol-lowing MIA injection, despite no obvious commu-nication between the TMT, DIT and proximal joints.The exact cause is not known. Early post-injectioncomplications include severe lameness, swelling,skin sloughing and infection. Additionally, MIAcannot be used in joints that are difficult to injector if the TMTand DIT are found to communicate

149


149

with the PIT or tarsocrural joints following con-trast arthrography. Because of these limitations andpotential complications, I would not recommendMIA. All of the distal tarsal arthrodesis proce-dures should be considered invasive, potentiallypainful procedures. Peri-operative analgesia is rec-ommended

Synovitis of the Tarsal Sheath(Thoroughpin)

The tendon of the deep digital flexor muscle(DDFT) traverses the groove formed at the back ofthe tarsus by the plantar surface of the sustentacu-lum tali and the medial surface of the tuber calcis.Its substance is extremely dense at this level and ispartially cartilaginous. The tarsal canal is boundedcranially in its proximal part by the caudal face ofthe common ligament of the tibiotarsal joint, andbelow by the tarso metatarsal ligament both of whichare intimately attached to the tarsal bones.

They are also in part cartilaginous and form asmooth surface over which runs the deep flexor ten-don. Laterally the canal is bounded by the groovedinner face of the tuber calcis, whilst caudally itsboundaries are completed by a fibrous arch whichstretches across the back of the os calcis to mergewith the medial collateral ligament.

The canal is lined by an extensive synovial mem-brane, the tarsal sheath, which covers the caudalsurface of the common ligament of the tibiotarsaljoint and envelops the tendon thus facilitating itsgliding movement. The sheath begins 5-7.5cmproximal to the level of the medial malleolus andextends downwards to the upper third of the meta-tarsus. Proximal to the sustentaculum the sheathoverlies the joint capsule of the tibiotarsal jointwhere the latter pouches plantar to the distal end ofthe tibia

Tarsal sheath distension is characterised by dis-tinct swellings either side of, and approximately

5cm cranial to the Achilles tendon and sometimesby a third swelling below the hock on the medialaspect at the level of the tarsometatarsal joint.

When the condition is unilateral, it is usually dueto trauma. Most frequently it is chronic with ab-sence of heat and no tenderness on palpation. Lame-ness is usually absent. In some horses, however,tarsal sheath distension is accompanied by moder-ate to severe lameness related to pathologicalchanges in the sustentaculum tali resulting from di-rect trauma.

In horses presenting with tarsal sheath distensionand lameness, the medial aspect of the hock shouldbe carefully examined for evidence of a kick orsimilar injury. In some there may be an open woundwhich may or may not communicate with the sheath.In others there may be little or no skin damage.

The radiographic examination should be directedat bringing the medial border of the sustentaculumtali into profile using a plantaro lateral dorsomedialoblique (PLDMO) projection.

This area is masked in the dorsoplantar plane bythe trochea of the tibiotarsal bone and a consider-able amount of dense new bone has to be presentbefore it can be seen on lateral-medial views. Ifthe horse will allow flexion of the hock, the dorsoflexed tangential projection is very useful.

Synoviocentesis will confirm or eliminate sepsisof the sheath. Contrast radiography is a valuableadjunct to investigation of changes within the sheathsuch as adhesions.

Arthroscopy or exploratory surgery on the sheathwill allow further assessment of any tendon dam-age, adhesion formation and the integrity of the sur-face of the sustentaculum tali over which the DDFTruns.

The radiographic findings reported in 37 horses

150


150

with tarsal sheath distension include:-

Sustentaculum tali Bony proliferations on medial border 13 Fracture 9 Destructive or mixed destructive 7 and proliferative changes

Calcaneus Bony proliferations on the medial surface 4

Tarsal Sheath Radiodensities involving the DDFT 4 Radiodensity involving the sheath 1

None 8

In the case of horses presented with acute onsettarsal sheath distension and lameness, evidence offracture of the medial border of the sustentaculumtali may be present. Small chip fractures are themost common. If accompanied by a communicat-ing wound into the sheath, these should be removedduring surgical exploration and lavage of the sheath.If there is no open wound, removal of fragments isstill indicated to try to minimise proliferativechanges which will subsequently cause severe ten-don abrasion.

The amount of new bone can vary from slight ir-regularity in outline to large proliferations depend-ing on the severity of the initial injury and the dura-tion of the problem. When these proliferativechanges are already established, irreparable dam-age to the DDFT will already have occurred.Arthroscopic or post mortem examination revealsgross fibrillation of the surface of the DDFT for adistance of 10cm where it has been abraded by con-tact with the damaged bone of the tarsal canal. Theextent of the tendon damage is not surprising in viewof the range of tendon movement within the tarsalcanal and its tension during flexion and extensionof the hock. The surface of the sustentaculum maybe found during exploratory surgery or at autopsyto be much smoother than might be expected from

the radiographic evidence because of fibrous tis-sue partially covering the pitted irregular surface.Irreparable damage may have occurred, however,before any irregularities in the surface of the tarsalcanal can be reduced by natural repair processes.Osteomyelitis of the sustentaculum often results ingross irregularities due to lysis of bone and these,together with proliferative new bone which accom-panies it, lead to very severe abrasive damage tothe DDFT. Abrasive damage to the tendon invari-ably leads to extensive fibrous adhesions of theDDFT to the thickened discoloured sheath.

In a small number of cases, horses with tarsal sheathdistension are found on X-ray to have dense calci-fied areas which involve the DDFT or, more rarely,the sheath itself. These may be associated withrepeated injections of corticosteroids into the sheath.Surgical removal has been attempted but the re-sidual tendon pathology usually results in chroniclameness.

Summary

The frequency with which chronic distension of thetarsal sheath accompanied by lameness is associ-ated with bony changes in the sustentaculum taliemphasises the importance of a careful radiographicexamination. Together with clinical and labora-tory findings, X-rays are of considerable help inassessing the prognosis and formulating appropri-ate treatment. A more favourable prognosis maybe given in cases of tarsal sheath effusion in whichthere is minimal lameness and absence of bonychanges affecting the sustentaculum tali. Horseswith established radiographic changes in the suste-ntaculum, particularly if associated with sepsis,carry a very poor prognosis and frequently requireeuthanasia.

Calcaneal Bursa Problems

Wounds to the plantar aspect of the tarsus present adiagnostic and treatment challenge. They frequentlyinvolve the calcaneal bursae and carry a guarded

151


151

prognosis.

The planteroproximal aspect of the tuber calcaneiis associated with several bursae including the po-tential subcutaneous bursa (SCB) which developssuperficial to the superficial digital flexor tendon(SDFT); the intertendinous calcaneal bursa (ICB)located between the SDFT and the gastrocnemiustendon (GNT) and the gastrocnemius bursa (GCB)located dorsal to the insertion of the GNT on thetuber calcanei. Traumatic wounds over the pointof the hock may result in sepsis of any of thesebursae. The injury may also involve the plantarligament, tarsal sheath, or tarsocrural joint. Thecomplex anatomy can make diagnosis and treatmentof cases of septic calcaneal bursitis difficult.

The clinical signs of septic calcaneal bursitis in-clude progressive lameness, a discharging woundand generalised swelling at the point of the hock.However clinical examination may fail to distin-guish the origin of the swellings in the plantar as-pect of the tarsus. Digital exploration provides lim-ited information about the extent of the injury.Synoviocentesis can be an effective diagnostic toolbut the technique can be difficult in cases withgeneralised swelling and open wounds. Diagnos-tic aids which can provide valuable informationinclude ultrasonography, plain and contrast radi-ography and endoscopy.

Early diagnosis and treatment of septic synovialstructure are essential to improve the prognosis forsurvival and return to work.

Ultrasonography is helpful in identifying ICB effu-sion, and tendinous or ligamentous abnormalitiesin many cases. Although mild fibrillation of theSDFT which is evident at surgery will not be pickedup on ultrasonography, more severe damage suchas necrotic areas in the SDFT, partial lacerationsof the SDFT, the SDFT retinaculum, or the gastroc-nemius tendon and hypoechoic areas in the plantalligament or gastrocnemius tendon can be identified.

RadiographyIn addition to standard radiographic projections,dorsoplantar, dorsal 45o latero-plantaromedial ob-lique, plantar 45o latero-dorsomedial oblique andlateromedial, numerous lesion-orientated obliqueprojections, with slight variation in angles are of-ten required to obtain a radiograph aligned to dem-onstrate an osseus lesion clearly. If the horse iswilling flex the tarsus, a plantaroproximal-plantarodistal projection should be taken of the cal-caneus. Radiographic changes of thetubercalcaneum are found in approximately 40%of cases and are associated with reduced survival.

The changes include poorly demarcated lysis, pro-liferative osteitis, sequestrum and proximal frag-mentation. The use of contrast radiography mayhelp to identify involvement of the ICB and GCB.

TreatmentSurgical treatment is recommended in all cases. Itincludes extension of the wound, aggressive debri-dement, lavage with several litres of polyionic fluidand partial wound closure under general anaesthe-sia. In any case showing radiographic abnormali-ties, the tuber calcanei should be exposed. Repeatsurgery may be necessary particularly in thosehorses with radiographic lysis.

Post-operative management should include box rest,parenteral and oral antibiotics, NSAIDS and ban-daging or casting. When available the decision re-garding the antibiotic of choice is based on bacte-rial culture and sensitivity. Systemic administra-tion of antibiotics is continued until the wound hashealed with a healthy bed of granulation tissue (av-erage 309 days).

The prognosis is excellent for horses with involve-ment of only the subcutaneous bursa but is signifi-cantly poorer for those with wounds involving theintertendinous calcaneal bursa. Horses with in-volvement of the tuber calcanei have only a fair toguarded prognosis.

152


152

Date post:	17-May-2020
Category:	Documents
Upload:	others
View:	1 times
Download:	0 times

· Table of Contents Scientific...

Documents