AUSTRALIAN AND NEW ZEALAND COLLEGE OF VETERINARY

SCIENTISTS

VETERINARY DENTISTRY CHAPTER SCIENCE WEEK PROGRAM

10 – 12 July 2014

Surfers Paradise

CONTENTS

Endodontics from the 1980’s until today – drill, fill and bill (David Clarke)

Mistakes and boo boos not to be repeated (Wayne Fitzgerald)

The teaching of Equine Dentistry in different countries (Shannon Lee)

Oops – where did that tooth go? / Intrusive luxation(Tara Cashman)

Teaching small animal dentistry in other countries (Elaine Cebuliak)

Emergency head trauma management in the Equine – dental perspective (Lizzi Tremayne)

Sedation / analgesia / anaesthesia of the equine head trauma patient (Chris Quinn)

The progression of equine dentistry from the 1980’s until today (Gary Wilson)

Intraoral radiography in the Equine (O Liyou and T Chinkangsadarn)

Anaesthesia and analgesia for head trauma patients (Jennifer Carter)

Emergency head trauma management – Traumatic Brain Injury (TBI) in small animals – ECC perspective (Melissa Claus)

Emergency head trauma management – Indications for direct pulp capping in traumatised teeth – pros and cons – Dental perspective (Winston Oakes)

Mandibular symphysis repair / Palatal injuries / Oral and tooth fractures (Dental perspective – Amanda Hulands – Nave); (ECC perspective – Eugene Buffa)

Discussion forum (Rebecca Tucker / Christine Hawke Co- chairs)

Dental Radiology Q and A (Tony Caiafa)

KEYNOTE PRESENTATION – Principles and Practice of Rotary Endodontics (Dr Ross Applegarth BDS, MDSc FICD MRACDS(Endo)

Endodontics from the 1980’s until today – drill, fill and bill (David Clarke)

No manuscript submitted

Mistakes and Boo Boos, Not To Be Repeated

Dr Wayne Fitzgerald, BVSc (Hons), MANZCVS (Vet Dentistry & Oral Surgery)Senior FellowVeterinary HospitalFaculty of Veterinary ScienceThe University of Melbourne250 Princes Highway, Werribee, VIC 3030

1. Analgesia: a. Renal damage from NSAIDsb. Inadvertent block of the lingual nerve c. Lignocaine toxicity

2. Facial nerve neuralgia3. TMJ inflammation4. Fracture repairs5. Iatrogenic jaw fractures6. Endo:

a. “Missed the canal!”b. Penetration of floor of PM4c. Bleach through the apexd. Vital pulpotomy failuree. Bonding problems

7. Root apex ‘disappeared’8. Orthodontics …KISS principle applies9. Imaging10.Procedure success but the patient died

Quote of the decade:“2/3rds of owners do not take care of their pet’s teeth.”

1. Analgesia By utilizing pre-emptive analgesia, anaesthesia may be shallower and smoother with the patient recovering well.

The classical mechanism of opioid analgesia is altered perception of the noxious stimulus. The ‘feeling’ of the painful stimulation is reduced but the location and intensity may remain, they are essentially CNS depressants and this significantly influences anaesthetic recovery. I rarely use these drugs in routine dentistry.

NSAIDs have some CNS analgesic effects but their effect is mainly to reduce inflammation at the surgical site and modulate the nerve pathways to the spinal dorsal horn synapses. Due to their potential adverse renal effects, they should always be given in conjunction with intravenous fluids (these are routine in all of my anaesthesia’s anyway). When the NSAID is given subcutaneously, and concurrently to the regional nerve block, it will not be effective for several hours but will become effective as the nerve block wears off.

Regional analgesia is truly pre-emptive, as when utilized appropriately the noxious stimulus does not leave the site and hence is not received by the central nervous system.

The distal mandibular block targets the inferior alveolar nerve as it enters the mandibular canal. Note that the lingual branch of the Trigeminal nerve branches off in this vicinity and may be inadvertently blocked; this unintended ‘negative’ may lead to self-trauma to the tongue upon recovery if the block remains effective. The lingual nerve is responsible for sensation to the rostral 2/3rds of the tongue.

Lignocaine has a fairly rapid onset (10-15 mins) and short duration (approximately 2 hours). Lignocaine’s toxic dose is considered to be 10 mg/kg. 2% solutions (20 mg/ml) are used, so 1 ml of this solution is toxic to a 2 kg animal. Lignocaine is recommended for all routine dental procedures because of its rapid onset and short duration of effect. This is of benefit in that animals are not waking up with numb or hypersensitive mouths that may worry them post-procedure.Toxic effects of lignocaine are mainly related to central nervous or cardiovascular signs: CNS ‘excitation’ to seizures may be followed by depression and apnoea; CV effects are related to hypotension, bradycardia, arrhythmias and cardiac arrest. It is always recommended to apply negative pressure to the syringe (‘draw-back’) to ensure the injection is not intravascular. Users must be aware of these toxic doses when utilizing nerve blocks – be aware of the total dose you are going to use. Remember to include the dose of local anaesthetic used to spray the larynx of your cat patients.

Bupivacaine has a slow onset (20-30 mins) and a long duration (4-6 hours). Bupivacaine’s toxic dose is considered to be 1-2 mg/kg. A common solution of Bupivacaine is 0.5% (5 mg/ml) so 1ml could be toxic in a 5-10 kg animal.

2. Facial nerve neuralgia The facial nerve (CN VII) can inadvertently be compressed as it crosses the face below the zygomatic arch as across the masseter muscle Padding should be used to pad and support the underside of the head over the table. Cases have occurred subsequent to forceful procedures such as extractions. The facial nerve innervates the superficial muscles of the head, face and ear muscles as well as the taste buds of the palate and rostral 2/3rd of the tongue, the result can be temporary or permanent facial paresis and eating disorders, such as seen with a stroke.Case report:

Seen as a second opinion: an 8-year old dog that just 4-weeks previously had tooth 409 extracted at another clinic. Her left face was ‘paralysed’; the owner observed this post-surgery when collected. The other clinic suggested she might have a brain tumour and suggested an MRI; the veterinarian had dispensed Metacam. I was told that any improvement had been very slow. Initially she had a dropped lip, inability to blink her left eyelid, had a slight left head tilt, abnormal sensation on the left side and some difficulty walking as she tended to fall to the left and wanted to lean on objects. These signs had improved, although she had some occasional balance issues, her gait was more normal now. There was reportedly less drooping of her left lip and the blink reflex was present although partial and sluggish. The PLR and menace reflexes were normal. The left face skin and nostril

showed no sensation, the left ear sat low and there was asymmetry of the masseter and temporal muscles. She allowed oral examination, no pain being elicited; and when eating, she would move food to her right mouth.The DDx included facial nerve neuritis secondary to compression, trauma / bruising or idiopathic. Steroids were initiated and the prognosis was for improvement but possibly not full recovery.Some 3-weeks later, she had recovered to about 80%; some 6-months later this had stabilized.

3. TMJ inflammation The most likely cause of this is the overuse of spring-loaded mouth gags. These should be used sparingly and for short durations only. The mouth can easily and softly be held open with appropriate cut sections of endotracheal tube fitted between the teeth.

4. Fracture repair Mandibular symphysis separation: I find most vets still follow the textbook directions and place the s/s circlage wire twist ventral to the chin. Remember that this is the cat’s mental organ and as it will rub its chin on furniture, legs etc there will be unhappy owners! The wire does not need to be heavier than 22g but it is possible to use an absorbable material such as PDS. Place the knot behind a canine tooth. To place the material, simply bend an 18g needle and use as a passer.

The primary aim of oral fracture repair is to regain function and occlusion. These tissues heal well and have great infection resistance, however nearly all fractures will be compound. These days we advise non-invasive techniques and rarely use pins, screws and plates. Comminuted oral fractures (mostly mandibular) may pose problems of stability and maintenance of occlusion, these are often solved by bonding the canines together and this is well described.Our biggest problem is getting orthopaedic surgeons to acknowledge that their understanding of the principles that we accept as basic, are foreign to them: we often do not need ridged immobilization, pins will often penetrate vital structures such as tooth roots and mandibular canals. These structures ARE significant are ‘out of bounds’. There are consequences in damaging them.

5. Iatrogenic jaw fractures How often do we say that dental radiology is essential to the practise of good dentistry? In fact, I would go so far as to suggest that is it now the “peer standard” just as veterinary radiology is in general practice.Periodontitis is, by definition, the loss of the supporting structures of the teeth: the periodontium. Oral radiographs often graphically demonstrate this and will give an indication as to the risk or ease of a proposed extraction.Although these fractures may be iatrogenic, they are most often secondary to pathology and hence have a guarded healing prognosis. It is always recommended to pre-warn owners of any obvious risk of jaw fracture.

6. Endodontics a. “Missed the canal!”

It is not too difficult to have a file slide down beside a tooth rather than into the canal, especially with oblique crown fractures in small teeth such as the incisors. Radiographs will tell the tale to be more careful in access and file placement.

b. Penetration of floor of PM4 pulp chamber Who hasn’t had problems locating the palatal root of 108 or 208 in small dogs? It is not difficult to penetrate the floor of the chamber by the file: indicated by bleeding and of course confirmed on radiograph. Although there are ways of saving the situation, it is easier to amputate the palatal root and complete the endo of the two buccal roots with a glass ionomer used to seal off the chamber at this level.It is also important not to remove too much crown in making access as this weakens the tooth structure significantly and dogs will break the remaining tooth crown quite easily if it is compromised.

c. Bleach through the apex Microorganisms and their by-products are considered to be the major cause of pulpal and peri-radicular pathosis. In order to reduce or eliminate bacteria and pulpal tissue remnants, use of various irrigation solutions have been suggested:

Bleach: Sodium hypochlorite. Debate over strength: full (5.25%) / ½ / etc… Still the best flush and removes the smear layer.

Saline: Safest, biocompatible but not antibacterial. Often used as the first and last flushes, large volumes are required.

H2O2 After the release of oxygen, only water is left. Chlorhexidine: 0.2% solution used, not as effective as a cleaner,

doesn’t touch the smear layer and NOT if using a resin based sealer. EDTA. Removes and softens inorganic tissues (smear layer) and

dentine. May increase the tubule diameter!

Sodium hypochlorite is an excellent non-specific proteolytic and antimicrobial agent and remains the most common irrigation solution used during root canal therapy. The major objective in root canal treatment is to disinfect the entire root canal system. This requires that the pulpal contents be eliminated as sources of infection. This goal may be accomplished using mechanical instrumentation and chemical irrigation, in conjunction with medication of the root canal between treatment sessions. It is effectively antimicrobial but also very tissue irritant, so side-exit endo needles are recommended. Accidental escape into the apical area will cause bone necrosis and (untreatable) intense pain.

d. Vital pulpotomy failure Use a steroid to reduce inflammation.MTA and the light-cured derivatives are now the ‘gold standard’ (similar pH to CaOH2: 12.5) and they have been shown to provide improved results over CaOH2.

Place a GI intermediate layer then the Composite restoration.Success rate: if traumatic and < 48 hours old, then less than 90%, but high 90s if elective. Failures may take years to detect and leakages are a significant issue.

e. Bonding problems a. Dr Ronald Perry, Tutts school of dental medicine (Notes from Dental Forum,

Boston, 2011)

Technique sensitive and enamel is vastly different to dentine!Dogs have 30% more dentinal tubules than humans (per mm2) therefore bonding strength is about 30% less (researched & published).

Human enamel is thicker, especially on occlusive surfaces; most veterinary bonding is to dentine. Bond strength of resins to dentine degrade over time: about 50% less over 6-12 months is not uncommon. Bonding to enamel is more durable.Prior to the 1980’s there was no bond, it has progressed since from 1st to 7th generation.

NB: Marketing departments often make material product decisions …and they have never done one! Vets rely on information from the human side.

Enamel: clean, pumice & etch no more than 30 seconds. Rinse thoroughly and air dry. Apply the ‘bond’ (adhesive, unfilled resin) and gently use air to spread, thin and evaporate the solvents before light curing. Apply the filled Composite in layers no thicker than 2mm and light cure.

Dentine: clean, pumice and etch (or condition) for only 10-15 seconds or the bond strength will be reduced. Rinse well and gently use the air to remove the excess water but leave the surface moist. This leaves the collagen fibres intact and suspended, not shrivelled and flattened. A Glass Ionomer can be applied at this time, or the ‘bond’ can be applied, with a rubbing motion, to allow its penetration around the exposed collagen. This can be repeated before the filled composite is applied.

What makes it stick? Resin enters the tubules and also encompasses the collagen fibre network that has been exposed by etching.What is done to the smear layer is critical and the etch / rinse / bond techniques still outperform the ‘self-etch’ systems.Contents: Conditioner (mild acid)

Primer (both hydrophilic & hydrophobic)Resin (penetrates into tubules & co-polymerises with primer.

Tubule density: pattern radiates out from the pulp; therefore outer dentine comprises about 30% tubules of its surface area.Live dentine: fluid moves in these tubules -> reduced strength of bond as it gets into the bond and disrupts it.

Operator technique accounts for 50% of the strength.

How to improve bond strength: Extra layer (x2) of Bond (resin agent). Increase curing time over the suggested time. Bond application: ‘scrub’ in when apply and don’t excessively air thin it

as flattens the collagen fibrils exposed when etched …cure and repeat. Use MMP inhibitors, apply 2% chlorhexidine for a few seconds after

etch and re-rinse, before applying Bond. Wet dentinal bond: still glistening, as will displace any water present. Store composites in a refrigerator. Use same company’s chemicals as they ‘match’ one another.

Flowable composites contain more Bond (resin) and less fill material, thus less strength. Newer composite chemistry is negating this however.Late 1990’s: 5th generation systems evolved, 2 steps -> high strength.Most recent: 7th generation (one step) -> low strength however!This is all designed to speed up procedures for the benefit of human dentists!

7. Root apex ‘disappeared’ I have received a number of calls for help from practitioners that have fractured the root apex and it has ‘disappeared’ when attempting to extract it.Not uncommonly these have gone into the mandibular canal but also into the retrobulbar space!What to do? Firstly, “do no harm”. It is up to you but my advice over the phone is to a) radiograph …most frequently not available, so working blind! and b) don’t create a more significant problem and this means leaving it alone and covering it with antibiotics etc. Note that I haven’t had a return call that suggests this has worked.

8. Orthodontics Alex Reiter (Notes from Dental Forum, Boston, 2011)Current classifications (AmVDS nomenclature Committee):

a. Class 0 = normalb. Class 1 = ‘neutrocclusion’c. Class 2 = mandibular distocclusion …descriptions now relate to

the mandibled. Class 3 = mandibular mesiocclusion e. Class 4 = asymmetric skeletal malocclusion

Always opt for the ‘KISS’ system as complex appliances or modalities tend not to be practical in our patients. Considering this, the maxillary plate with bite planes is the most robust and reliable (considering careful selection of patients and clients) and the use of masel chain to distally tip the maxillary canines is satisfactory but much more attention is required to maintain it.Nearly all veterinary orthodontic movements will tip teeth rather than bodily move them; the latter requires longer, controlled forces and complex devices that are often not practical in animals.

Linguoversed or Lingually displaced mandibular canine teeth (“base narrow”) is probably the most common of the significant malocclusions, treatment options include:

Gingivioplasty Passive orthodontics (passive force = by the patient) Active orthodontics (active force = by an elastic etc) Refer Extract (equivalent to ‘amputation’)

Direct’ incline plane = made on the animal.‘Indirect’ incline plane = made in a lab and fitted.Screw devices are almost impossible to adjust insitu without a GA! Thus not recommended.

9. Imaging: Pathology associated with dental diseases can be imaged with X-ray, CT or MRI.

X-rays: need >40% bone changes to see anything but dental radiology is accessible to the practitioner, cheap and not difficult to get diagnostic radiographs. It is considered not possible to perform professional veterinary dentistry without oral radiology whether using film or digital technology. I receive numerous calls from practices without any (dental) imaging facilities where procedures have gone awry and they don’t know what is happening or what to do next!

CT provides information on X-ray absorption, and is sensitive at detecting bone lysis and dental-associated lesions. While CT provides superior soft tissue contrast resolution compared to conventional radiography, CT is not as sensitive as MRI at detecting soft tissue lesions.

MRI images hydrogen content (cortical bone and hard dental tissue are hydrogen poor) and distribution within tissues, and is sensitive at detecting altered water content seen with many disease processes. Considerations restricting the choice of MRI include its high cost, the significant anaesthesia time taken to obtain images and the difficulties that may be encountered with small skulls to get signals.

10.Procedure success but the patient died There are many examples in both veterinary and human surgeries where the procedure was a success but the patient died during or after it. This is where a competent nurse is essential and is supported by mechanical monitoring equipment but not reliant on it as these machines are fallible. The surgeon will often be fully concentrating on the procedure and not paying attention to the anaesthesia, blood pressures, heart rate, oxygen saturation etc.

The teaching of Equine Dentistry in different countries (Shannon Lee)

No manuscript submitted

Intrusive Luxation of Canine Teeth

Dr Tara CashmanEurocoast Veterinary Centre

PO Box 3265Batehaven NSW 2536

An intrusive luxation is the displacement of the tooth along the axis of the tooth into the alveolar bone. It is associated with comminution or fracture of the alveolar socket, disruption to the gingival attachment, contusion of the periodontal ligament and damage to the pulpal structures. In immature teeth there is disruption to the Hertwig’s epithelial root sheath.

Due to the traumatic nature of intrusive luxation lesions, there may be a crown fracture with or without pulpal exposure. Bacterial plaque that covers the dentinal crown is forcibly displaced into the compromised wound site.

The incidence of intrusive injuries in humans varies between 0.3 to 1.9% of all traumatic injuries to the permanent teeth. Intrusive luxation injuries in humans are associated with a high complication rate and hence a grave long term prognosis for the intruded tooth. No data has been reported for dogs for either incidence or associated complication rates. The apparent rarity of intrusion injuries in dogs may relate to the fact that the alveolar bone of dogs is denser, associated with the filling up of the medullar spaces and extensive areas of hyalinization compared with humans.

The clinical presentation of intrusively luxated teeth varies with the time to presentation. Acute presenting signs may include:

tooth displacement into the alveolar socket which appears as a shortened tooth.

an apparently missing tooth if completely intruded into the alveolar socket. gingival bleeding and swelling. a high pitched metallic sound on percussion of the tooth – useful when

determining if the tooth is partially erupted due to young age. nasal bleeding if the root apex has been forced through the nasal cavity floor.

In more chronic cases, the clinical signs are usually related to the fact that the tooth is acting as a nasal foreign body. Nasal discharge, coughing, and difficulty breathing have been reported as presenting signs in dogs with chronic complete intrusive luxations.

The diagnosis of an intrusive luxation is straightforward and requires the visualisation of the affected tooth, directly or by diagnostic imaging techniques such as radiography and computed tomography (CT).

Initial trauma cases should have a thorough physical examination and any cardiovascular conditions, limb fractures and major body wounds stabilised. An oral examination especially noting any change to the number and position of the teeth, should be completed once the animal is stable.

Plain open mouth radiographs of the oral cavity are useful in identifying intrusively luxated teeth that have entered the nasal cavity. Intraoral dental radiographs provide greater definition once the tooth has been identified. The periodontal ligament space, pulp and root apex can be assessed from the dental radiographs. Radiographic signs evidence of intrusion include displacement of the tooth into the alveolar socket with

compression of the root apex and narrowing of the periodontal ligament space. Chronically affected teeth may show root resorption, radicular ankylosis and pulp widening relative to the surrounding teeth.

Clinical cases with presenting signs of chronic nasal/respiratory disease may be examined with additional diagnostic techniques such as CT scanning and rhinoscopy. Intranasal dental foreign bodies are evident on CT as radiodense masses of similar opacity to the cranium and hyoid bones. CT scanning is a non-invasive diagnostic technique, which has the advantage of removing the superimposition of overlying bony structures.

Rhinoscopy has been reported in identifiying the location of intranasal dental foreign bodies in dogs. The endoscope maybe placed retrograde or antegrade. Rhinoscopy has the added benefit of possibly allowing the removal of the tooth under direct visualisation. Some teeth however are so deeply embedded that a surgical approach is required.

There are 3 common treatment techniques for intrusively luxated teeth in humans being:

1. allowing spontaneous eruption2. surgical repositioning3. orthodontic extrusion

Spontaneous eruption is an option in children with incomplete root formation of their permanent teeth. The exception to this is if the incisal edge of the tooth is intruded below the gingiva. Complications such as ankylosis, pulp necrosis and inflammatory root resorption are still possible. No reports of intrusion in immature teeth have been identified in dogs. Spontaneous eruption may be an option in young dogs with careful radiographic follow up.

Surgical repositioning and orthodontic extrusion have been reported in research dogs where a controlled intrusive force has been applied to the affected tooth. Long term follow up has not been undertaken as the researchers were looking at acute histologic changes to the pulp, alveolar bone and the root morphology. In humans orthodontic extrusion of permanent teeth has been associated with improved marginal bone healing. It is the preferred treatment in adult teeth with minimal intrusion. Teeth with complete intrusion and in those cases with multiple tooth involvement, the preferred treatment option is surgical repositioning.

Extraction is used in those human cases where there is extensive trauma or the patient is not able to commit to ongoing monitoring and endodontic therapy. In dogs the only reported treatment in clinical cases of complete intrusion has been extraction. An oral approach can be made to access the nasal cavity.

Regardless of the treatment option the long term survival of intruded teeth in humans is poor. Approximately 30% of all intruded teeth are lost after 15 years irrespective of the degree of root development at the time of intrusion. This may not be an issue in dogs due to their reduced life span relative to humans.

Healing complications of treated intrusively luxated teeth are a direct result of the disruption to the periodontium and the pulp. Radicular ankylosis, pulp necrosis and inflammatory root resorption are routinely reported in the treatment of intrusive luxation in people. Endodontic treatment is required in nearly all cases initially with a long term calcium hydroxide dressing and followed with complete obuturation and coronal sealing of the affected tooth.

Intrusive luxation of canine teeth is rarely reported and of those cases reported most are associated with a chronic presentation. It is important at the initial presentation of head trauma in a dog that a thorough oral examination is conducted. Radiography is essential to confirm the absence or otherwise of any apparently missing tooth. Due to the need for regular monitoring, further endodontic treatments and the high incidence of healing complications, most clinicians will elect to extract the intrusively luxated tooth.

Teaching Small Animal Dentistry in Other Countries

Elaine Cebuliak MANZCVSc (dentistry)

This talk will be a visual experience sharing images from India, Fiji, Hawaii, Bali and the Cook Islands. The emphasis is on getting back to the

basics of dentistry and working with locals.

Dr Elaine Cebuliak has been fortunate to be involved in several overseas projects which has been a deeply enriching experience. One of her first volunteering exercises was in Bali before BARC or BAWA were formed. http://www.balidogrefuge.com/ This was the early 90’s when the Yudisthira foundation began. Following this street dog catch, desex and release training in Bali, I was approached to lead a team to India. Catherine Scheutze and I had an invitation to treat dogs at a buddhist retreat centre in Bodhgaya. The plans to start work on this project progressed with massive emails and discussions held late at night at my house in Brisbane. This eventually turned into VBB or http://www.vetsbeyondborders.org/

Whenever an animal is being examined – and especially if it is a street dog, an anaesthetic gives you an ideal time to consider dental health and extraction of any fractured teeth that might require removal. Because anaesthetics are generally done in the field without oxygen, the shorter the time to perform procedures the better for the animal. Prepare your assistants to help.

When one is asked to volunteer to teach some dental skills to local veterinarians, developing country Universities and vet techs, be prepared to improvise!Anaesthesia and instrumentation can be very limited, therefore it is a good idea to sit back, watch what protocols are presently being used and how they are working for them. Alpha 2 agonists are common, and although we in Australia shudder at the thought, the technique can be refined by improving intravenous access and fluid support. Many have donated “dead doctor” tools that are ineffective with poor mechanical torque which can cause great damage- for instance extracting forceps that are entirely inappropriate for removing small animal teeth.Basic skills are required, dog handling, safety, anaesthesia, analgesia, surgical technique, cleanliness. Use and adapt teaching methods regarding exodontia and periodontology, oral anatomy, instrumentation use and care, and preventative oral care. Many vets, vet students and volunteer workers from local veterinary clinics may choose to help and journey with you for an adventure. Your talk to locals can be altered from your previous lectures, or shared from other colleagues—just ask! Google translate your proposed speech while you have the internet (and it is surprising how little internet café’s exist in alleyways across the globe in the most out of the way even impoverished towns!).

When does a pet need dental care? "If it has teeth."

It is important to emphasise that good work can be done in whatever setting you find yourself, by remembering and using the basic principles and adapting whatever primitive or more advanced equipment you can find. The extraction principles can be boned down to these basic steps:1) Teach to Identify and recognise dental diseases that require extraction2) Show local anaesthetic blocks, and refine smallest diameter needle best

practice3) Use small blade (15) or whatever you can find aiming for sterility with any

tools-- to cut the periodontal ligament near the gingival border to gain purchase

4) Use curved elevator in horizontal fashion next to the tooth- bring a set from donated equipment and also show locals how to fashion one from what they have! Show how to sharpen it and how NOT to slip, especially useful to engage a swab between the tooth and instrument.

5) Divide and conquer- show furcation and sectioning the tooth- ask for jeweller’s drills, other things available: sometimes gigli wire (again stone craftsmen have this), sometimes chisel up and out- make sure you have adequate shock absorption on the other side and technique

6) Emphasise “slow” and turn ¼ and hold….hold, hold. (hati hati) tear periodontal ligament.

Go around the tooth in this fashion…until it “walks out of there.7) Collapse the socket and suture only if quick dissolving sutures are available,

burying knot

Local herbs such as garlic oil, aloe, and tumeric can be applied onto surgical sites if no antibiotic is available and it is felt necessary. Many street dogs are protein deficient so encouraging feeding with stews (no onions or cooked bones) is useful for healing.

Remember that there are many diseases to consider for your own health and for the animals safe recovery, leishmaniasis and rabies are particularly important to consider. Several blood parasites also will increase blood clotting time and may contribute to blood loss. Yunnan baio is a useful chinese herbal formula to carry.

Most important : SAVE FACE! Part of the Asian culture is to live with dignity and to not come in as “big white guy doing good because we are better”. All cultures have amazing qualities, be appreciative and heartfelt. Always sit, laugh and joke with the locals, try to learn a bit of their language, ask to be shown how to cook, prepare food, learn their medicines etc and bring some simple songs. Play soccer or other dancing games with the kids. Be friendly. When in Rome do as the Romans—learn their sport/song/language/game.

The concept of teaching locals to fish, rather than providing fish for a single meal is emphasised. That is, it is of greater good to teach local vets and veterinary allied staff how to identify dental disease, to empower them to recognise that there is something that can be done about it and reach the local pet population owners to do the same. Veterinary clinics around the world struggle to make a living, and cost constraints are common.

Understand that using local tools, drugs, equipment and anaesthetics will enable locals to proceed with caution. It helps to realise that we Aussie’s weren’t so far behind in the ‘70’s when all we had were some dremel tools to work with!Donations from Aussie suppliers (K-9 gums, Provet, Cenvet, Zebravet, IM3) has always been received with great enthusiasm and is welcome. Please ensure you send them a photo by email on your return of the good work their equipment/donations has provided. Also if you are going to a recognised charity there are now officialdom channels --- liase with them for paperwork and ensure you are not carrying ketamine or other drugs that might land you into trouble!

DENTAL CONSIDERATIONS IN EQUINE HEAD TRAUMAELIZABETH A. THOMPSON, BA (Hons.), DVM, MANZCVS, GradDipTeachBlue Mist Equine Veterinary Centre, Franklin Rd, RD 2, Waihi, 3682, New ZealandIntroductionHead and dental trauma is common in horses. Damage to dental or supporting tissues may go unnoticed in the absence of careful examination, allowing unnecessary pain and prolonged recovery or permanent dysfunction. This paper discusses evaluation of the mouth, sinuses and skull; dental eruption times; emergency methods of treating pulpar exposure, and stabilisation of rostral avulsions. Comments regarding iatrogenic dental injury are also included.

External evaluationObservation from a distance gives insight into the whole horse, assisting in maintaining perspective and not missing subtle problems, especially when confronted by an excited owner. As always, a thorough history and medical record are vital. Is the lower or upper lip drooping? Pulling in one particular direction? Tongue protruding from the mouth? As always, exercise caution with obtunded, twitching or seizuring patients and perform a baseline neural examination, including checking for pupillary light reflexes and retinal detachment. Assessment of cutaneous sensation near and distal to areas of damage is imperative.

Palpate skull and assess eyes, orbital sockets, sinuses and temporomandibular joints, observing for symmetry and penetrating wounds, keeping in mind location of underlying vascular, neural and osseous structures. Sinuses lie just beneath a thin layer of bone, as do teeth and their apices. Penetrating wounds to the sinuses must be fully evaluated, which may require creation of a bone flap or drilling a hole to admit a flexible endoscope. Be sure to note any presence of halitosis, difficulty or unwillingness to eat, ptyalism or misalignment of the incisors.

Even if no obvious rostral maxillary or mandibular fractures are evident, gentle manipulation of these areas prior to sedation and placement of a full mouth speculum helps ensure there is no fracture which may be exacerbated by a speculum.

Analgesia and sedationAnalgesia and minimal sedation necessary to perform further examination may be administered at this time. Rinsing of the mouth prior to placement of the speculum facilitates removal of feed material and clotted blood.

Speculum placementIf a rostral mandibular or maxillary fracture is present, a speculum may be used, but only if gum plates, or inverted and padded bite plates, can be placed caudally to the fracture site in the diastema to further evaluate the oral cavity. In an emergency, in the absence of an appropriate speculum, a 20 cm long piece of 5-6 cm diameter reinforced soft rubber/plastic vacuum tubing held in place at the commissures of the mouth with a bungee over the poll

may be utilized in the sedated horse to evaluate pathology rostral to this position.

Damage to soft tissue Any irregularities or asymmetry of the soft tissues of the mouth must be noted. Palates, buccal walls, tongue and frenulum may have sustained punctures or lacerations from objects gripped in the horse's teeth or from intraoral foreign bodies, pieces of which may lie beneath mucosa or within sinuses.

Fractures of mandible, maxilla and teeth Carefully evaluate the supporting bones of the teeth for fractures and check for tooth mobility and dental fractures, especially those resulting in pulp exposure. Pulp exposure will be discussed below in depth.

Avulsion fractures of the rostral mandible and maxilla, as well as those of the diastema are common, due to horses' penchant for pulling back while chewing on solid objects and becoming entrapped, while their teeth are still attached to these objects. Avulsion fractures of the rostral mandible and maxilla, with teeth 01-03 included, called "corner avulsions", may be repaired in the anaesthetised or standing horse with perineural anaesthesia and wire fixation. Wire fixation provides more stability and offers less risk of chronic osteomyelitis than internal fixation. 16-18 gauge steel wire may be inserted through 14 gauge needles hammered between incisive teeth or placed within small fenestrations drilled at the gingival margins. These wires may be secured into notches cut into the caudal aspects of teeth caudal to the fracture or to screws placed into the mandible or maxilla in the diastema and carefully tightened down with surgical wire twisters or sterilised fencing pliers, then the ends flattened to the gingiva and covered with PMMA or cold set hoof acrylic. Please see references (Knox, et. al., 2005) for details. Anti-inflammatories are indicated.

Teeth, both permanent and deciduous, lie just beneath the surface of the skull, and thus are at risk when the horse is kicked by another or when the horse runs into a solid object. When evaluating damage to the skull, surgically repairing fractures or otherwise invading the skull, it is wise to remember eruption sequences and placement of the teeth, both permanent and deciduous, as well as sinus locations.The top row indicates the Triadan number for the teeth of the 200 and 600 arcades, the second indicates approximate eruption times of the deciduous teeth, and the third shows approximate eruption times of the permanent teeth.

2/601 2/602 2/603 diastema 2/606 2/607 2/608 209 210 2112.5yr 3.5yr 4.5yr 2.5yr 3yr 4yr - - -decid decid decid decid decid decid 1yr 2yr 3.5yr

The danger in drilling or cutting into the skull behind the caudalmost cheek tooth in a two year old horse is that of encountering a soon-to-erupt 210 or 211!

Ancillary examinations

Endoscopy is useful in assessment of full-thickness defects of hard and soft palates, and in identification of pharyngeal foreign bodies. Their light and flush functions facilitate lavage of blood and debris from traumatized areas.

Radiography is essential to determine extent of trauma to the teeth and supporting bones, and helps identify foreign bodies in tongue, cheek or gums. Contrast radiography allows definitive diagnosis of oronasal fistulae.

Ultrasonography is helpful in determining extent of soft tissue damage and also aids in identification of foreign bodies in tongue, cheek or gums.

General oral trauma treatment and repairGeneral surgical repair considerations apply in oral pathology. Antimicrobial and non-steroidal anti-inflammatory drugs and tetanus prophylaxis are indicated. Considerations specifically useful in the mouth include:

Evaluation of lacerations inside the oral cavity may be best evaluated after thorough irrigation via water-pik with 0.01% povidone iodine or 0.05% chlorhexidine, followed by removal of loose bone fragments and foreign bodies and repeated flushing before stabilisation is attempted. Chlorhexidine has been found in human studies to be taken up by the oral mucosa and exhibit a prolonged antimicrobial effect.

Reducing the crown height of mobile teeth with a rotary grinding disc as well as the opposing tooth/teeth and the rostral and caudal edges of those adjacent to the opposing tooth/teeth to remove them from occlusion may assist in stabilization of the loosened ones.

Full thickness defects of the oral mucosa, muscle and cutaneous tissues must be repaired layer by layer to restore full function.

Pulp exposureA common sequella of dental fracture is pulpar exposure. Teeth thus damaged are in danger of pulpitis, which may result in pulpar necrosis and death of the tooth. Iatrogenic pulpar exposure by a veterinarian or dental technician may be caused by dental fracture from improper application of molar cutters or overzealous crown reduction via molar cutters, hand floats or motorised power floating instruments.

If a horse has recently undergone dentistry and owner reports discomfort, ptyalism or inability/ unwillingness to eat, check the teeth carefully. Pinkness, bleeding of an occlusal surface or extrusion of pulp tissue indicates obvious pulpar exposure and constitutes an emergency, requiring timely pulp capping. (Photo?)

Pulpar compromise and potential tooth death may also result from hyperthermia, via prolonged power grinding with inadequate water-cooling. Even crown reductions not displaying pinkness or redness may have removed the smear layer or the protective sclerotic layer of dentin and exposed the

sensitive odontoblast processes of the pulp or removed them from their tubules. These may be painful for the horse and initiate a pulpitis.

Due to their hypsodont dentition, equine teeth are designed to be ground down over time by the opposing arcades. A system has evolved in the species whereby the fine extensions of the pulp, the odontoblast processes, retreat deeper down the dentinal tubules into the pulp chamber in response to insults of exposure to the environment, heat, pressure, vibration, desiccation, chemical exposure and bacterial infection, and begin to form dentinal bridges.

Dentinal Bridge FormationIn response to the above pulpal insults, including normal, gradual attrition of teeth in horses, non-differentiated fibroblasts are induced to proliferate and differentiate into osteoblasts and odontoblasts. The odontoblasts adjacent to the noxious stimuli produce reparative dentin as they contract away from it to form a "dentinal bridge". In the normal attrition situation, this should be all that happens. In a sudden pulp insult/exposure, if the immune system in the pulp is able to allay impending infection long enough for the bridge to be formed, the pulpitis may be transient and tooth may live. Younger horses have larger apices, and therefore more blood supply to the tooth pulp, helping them fight pulpitis/infection. Conversely, in older horses, with smaller apices, the converse is true.

If the pulp exposure is too sudden and/or or the insult overwhelms the ability of the pulp to respond, exposed pulps hemorrhage, becoming oedematous and inflamed. Bacteria colonise first the superficial layers, then the deeper pulp, and the resulting inflammatory response causes pulpal (and therefore tooth) death, via the increased pressure in the essentially closed vessel of the pulp cavity. Subsequently, the bacterial flora changes to gram negatives and anaerobes, which may progress to periapical abscessation.

Whatever the cause of the exposure, in the case of sudden pulp exposure, pulp capping increases the chance of survival of the affected tooth/ teeth by enhancing dentinal bridge formation.

By virtue of its strongly alkaline pH, CaOH is bacteriostatic and creates a layer of sterile necrosis when it is applied to properly prepared, exposed pulp. By the dentinal bridge formation mechanism discussed above, the CaOH-induced dentinal bridge physically, as well chemically, prevents further contamination, which would encourage infection and pulpitis.

Pulp Capping Instructions

What you need High speed drill w/ new (and thus sharp), #4 round burr or small dental spoon curette or excavatorTriplex (Air/water syringe)Sterile paper points (#90 suitable)Sterile salineCalcium hydroxide (powder or paste)

Hard setting calcium hydroxide cement (eg: Dycal®)Small mixing spatulaGlass slab or mixing padPhosphoric acid etchantDental bonding agent (liquid unfilled resin)Composite restorative'Plastic' instrument (not necess made of plastic)Finishing burrs or discs optional. Can use cellophane on top instead.

Technique1-Take affected tooth out of occlusion. Perform a 'vital pulpotomy' by amputating exposed and bleeding pulp to approx. 10 mm depth from occlusal surface with drill or excavator, forming a cavity. 2-The blunt end of a paper point moistened with sterile saline is used to apply pressure to bleeding pulp and left for several minutes. Replace if bleeding still evident upon removal. Continue until bleeding stops. Dry paper points will remove the clot!3-Place layer of calcium hydroxide into the cavity and pack tightly with a paper point. Clean walls of cavity with spoon curette. Mix and apply (per manufacturer's instructions) a layer of hard setting calcium hydroxide cement. Clean walls again with spoon curette.4-When dry, acid etch the cavity and occlusal surface of the tooth. Apply acid and leave in place for 30 seconds, then thoroughly rinse (about 20 seconds) then dry the surface with a gentle stream of air. Check manufacturer's instructions to see if the bonding agent requires the surface to be completely dried.5-Apply bond per manufacturer's instructions. A gentle stream of air directed over it will dry the resin, as well as cover the surface in a thin layer of bond. If it is "chemical cure" product, it is allowed to set the required time. If "light cure" material is used, you'll need the curing light and use per product instructions. 6-Apply composite restorative with plastic instrument and cure according to manufacturer's instructions. Slightly overfill, then smooth surface with discs or finishing burrs.7-Radiograph in three months to assess the formation (or otherwise) of the dentinal bridge. If the bridge has not formed, the tooth has most likely died and a root canal or extraction is required.

References

Caldwell LA. Occlusal equilibration in horses—what is it and how do you do it? Retrieved from:

http://equinedentalvets.com/files/flip/20130206_occlusal_equilibration/files/asset s/basic -html/page1.html, 2014.

Dacre IT. Equine dental pathology. In: Equine dentistry, eds. GJ Baker, J Easley, Elsevier, Philadelphia, pp. 91-109, 2005

Dixon PM. Dental anatomy In: Proceedings of the American Association of Equine Practitioners: Focus on Dentistry, Albuquerque, 8-24, 2011

Greet TRC. The management of oral trauma. In: Equine Dentistry, eds. GJ Baker, J Easley, Elsevier, Philadelphia, pp. 79-86, 2005

Hall, M. Wounds to the skull, sinuses, incisive injuries…. Equine wound healing workshop, Ruakura, Hamilton, 1-2 May, 2014. Sponsors: Agresearch, Shoof, 3M, Kruuse, et. al., 2014

Knox PM, Crabill MR, Honnas CM. Mandibular and maxillary fracture osteosynthesis. In: Equine dentistry, eds. GJ Baker, J Easley, Elsevier, Philadelphia, pp. 313-324, 2005

Mohammadi Z, Abbott PV. The properties and applications of chlorhexidine in endodontics. International Endodontic Journal 42.4, 288-302, 2009

Pascoe JR. Complications of dental surgery. Proc. Am. Assoc. Equine Pract., 37, 141-150, 1991

Wilson GJ. Module 10. In: Equine dentistry, course notes. Post Graduate Foundation in Vet. Sci., University of Sydney, Sydney, 2004

Anaesthesia and Analgesia for Horses with Head TraumaChris Quinn

BSc(vet) BVSc MANZCVS DACVAASchool of Animal and Veterinary Sciences

Charles Sturt University

Traumatic injuries are relatively common in horses. Head trauma may occur due to self inflicted injuries, kicks from other horses, competition accidents or motor vehicle accidents (Feige et al 2000; Reed 2007; Rayner 2005; Atherton et al 2007). Successful treatment of head trauma can be challenging due to the delicate and vital nature of many of the structures within the skull (Reed 2007). Anaesthesia is often required to facilitate both surgery and diagnostic imaging in these cases. Careful anaesthetic management is essential for a good outcome especially in cases where central nervous system injury has occurred (Smith 2008; Armitage-Chan et al 2007; Rayner 2005).General considerations for anaesthesia of horses with head traumaA complete physical examination should precede administration of any anaesthetic and analgesic drugs. In cases of head trauma this is particularly important as vital structures of the head as well as other body regions may be impaired, increasing the risk of serious anaesthetic complications (Reed 2007; Smith 2008). Injuries such as facial lacerations and mandibular fractures are obvious and disturbing however focusing exclusively on obvious injuries may result in less prominent yet potentially life threatening problems being overlooked. This is particularly important after major accidents (eg collisions or vehicle accidents) where there may be thoracic injuries (eg Pneumo or Haemo thorax) that will complicate anaesthesia. Similarly limb injuries may be destabilised by anaesthetic induction or recovery (eg fractures or ruptured ligaments). When general anaesthesia is required, attempts should be made to stabilise other injuries and conditions as far as possible prior to induction of anaesthesia. Significant blood loss or dehydration should be treated with fluids. Analgesics administered to control pain and distress (see below). Limb injuries may need to be protected with bandaging and/or splints prior to induction. If thoracic or abdominal injury has occurred these cavities should be carefully evaluated and consideration given to removal of any fluid (blood and/or air) present. While many horses will tolerate significant accumulation of fluid within the pleural cavity, the additional compromise of the cardiopulmonary systems created by anaesthesia and recumbency can cause rapid de-compensation even with relatively small volumes of accumulated fluid.Trauma to the head can result in injury to several body systems that will complicate the provision of general anaesthesia. This includes injuries involving upper airways, eyes or brain. Although involvement of these systems may not be the reason why general anaesthesia is required; they must be carefully evaluated for any signs of injury or abnormality. Even relatively minor dysfunction within these systems may be exacerbated by general anaesthesia and recumbency.Anaesthetic considerations for horses with injury of the upper airways and mouthMaintenance of a patent airway is vital for successful anaesthetic outcomes. As horses are obligate nasal breathers, large fractures compressing the nasal cavities which are often accompanied by significant bleeding and swelling may compromise the upper airway. This problem will be exacerbated by muscle relaxation from sedative or anaesthetic drugs. In most cases this situation can be easily overcome by promptly inserting an endotracheal tube (ETT) immediately after induction. Cuffed tubes are essential to prevent aspiration of blood as bleeding often continues during surgery. In

cases of significant nasal swelling and/or epistaxis it is often necessary to leave an ETT in place during recovery until the horse is standing.In some cases dental injuries may preclude the placement of an ETT. In these situations either a nasotracheal tube (NTT) may be used or if nasal intubation is not possible a tracheotomy may be required. NTT are often a good option for maintaining patent upper airway during recovery.As bleeding from the nasal cavities, ethmoid turbinates and mouth can be profuse and difficult to control it is important to monitor blood loss in these cases. Monitoring of heart rate, blood pressure and systemic lactate are also useful in assessing the significance of acute blood loss and the need for fluids or transfusion. Intra-operatively, blood loss is most conveniently replaced with hypertonic (7%) saline and/or isotonic crystalloids such as Hartman’s solution. Blood transfusion must be considered in cases of blood loss in excess of 20% of blood volume. In adult horses replacement of clinically significant blood loss presents a logistical challenge. Large bore (10 SWG) IV catheters are useful, alternatively 2 (or more) smaller (14 SWG) catheters may be required. Large diameter fluid giving sets combined with pressure bags are also valuable for rapid administration of large volumes of fluids. There are several well described and effective nerve blocks that can be used in cases requiring dental, mandibular or maxillary surgery (Moyer et al 2011). Nerve blocks may be used in combination with sedation for standing surgery. During general anaesthesia, nerve blocks can be utilised to reduce the amount of anaesthetic agent/s required to maintain anaesthesia and thus reduce cardiovascular and respiratory depression. This reduction in anaesthetic dose is particularly important for maintaining cardiovascular stability when faced with significant blood loss or brain injuries and raised intra cranial pressure (see below). Detailed description of these nerve blocks is beyond the scope of this paper.Anaesthetic considerations for horses with ocular injuriesEye injuries can be very painful and require sedation and analgesia to permit further evaluation. In the absence of other injuries/conditions, most sedatives routinely used in equine practice (alpha-2 agonists, acepromazine and opioids) are suitable. However loss of vision after head trauma may also be the result of cerebral involvement and raised intra cranial pressure (Reppas et al 1995) which will warrant greater care in the selection of sedatives. When general anaesthesia is required major considerations include avoiding additional ocular injury and ensuring that the eye remains sufficiently immobile to facilitate delicate ophthalmic surgery. Further injury to the eyes may occur due to poor induction, inadvertent trauma during positioning and preparing the horse, violent recovery or increases in intra-ocular pressure. Further injury during induction can be minimised by premedication with a combination of agents (typically alpha-2 agonists + an opioid +/- acepromazine) to provide heavy sedation and induction with a combination of drugs likely to produce reliable anaesthesia. Ketamine combined with diazepam or low dose propofol generally produces reliable calm induction of anaesthesia when given to a well sedated horse (Hubbell et al 2000; Wagner et al 2002). However induction with ketamine can be unpredictable when sedation is insufficient or when it is used alone (i.e. without diazepam/propofol) (Hubbell et al 2000; Wagner et al 2002). The experience and skill of the handler during induction of general anaesthesia is also important in preventing injuries. Great care should be taken to protect the eyes during any surgery of the head. Anecdotally, chemical burns to the eyes commonly occur during surgical preparation of other structures on the head when surgical solutions (ethanol etc) inadvertently run into the eyes. Techniques to improve recovery quality

include provision of adequate analgesia, minimising stimulation (noise etc) and keeping total anaesthesia time as short as possible. Sedation with alpha-2 agonists (eg xylazine 0.2 mg/kg) at the start of recovery has been shown to improve recovery (Santos et al 2003).In a horse with a serious eye injury a sudden rise in intra-ocular pressure (IOP) could lead to rupture of the globe. Most anaesthetic and sedative agents reduce IOP. Ketamine is known to significantly increase IOP in horses (Ferreira et al 2013) and as such must be used with caution. The risk of further rising IOP must be balanced against the need to ensure calm induction and recovery from anaesthesia.Maintaining an immobile eye during ocular surgery can be difficult as even small changes in anaesthetic depth lead to eye movement. Use of constant rate infusions of analgesics\/sedatives assists in maintaining a more even plain of anaesthesia. Examples include xylazine (0.5 mg/kg/h) and ketamine (0.6 mg/kg/h). Complete paralysis of the eye can be achieved with the use of neuromuscular blocking agents (eg Atracurium 0.1 mg/kg IV). However use of these agents will also paralyse the muscles of respiration necessitating the use of a ventilator and extensive monitoring equipment. Equipment for monitoring neuromuscular function (eg peripheral nerve stimulator) and reversal drugs (eg neostigmine) are also essential if atracurium is used. Further discussion of this technique is beyond the scope of this paper.Anaesthetic considerations for horses with traumatic brain injuriesHead trauma is a common cause of neurological disease in horses (Reed 2007; Feige 2000). When evaluating a horse with head trauma prior to general anaesthesia, the possibility of central nervous system involvement must be considered. Obvious signs of brain injury may include loss of consciousness, recumbency, circling, altered mentation and seizures. Where brain injury is possible (even in the absence of obvious signs) a detailed neurological exam should be performed before planning anaesthesia if at all possible.The main consideration when preparing to anaesthetise a horse with a suspected brain injury is to maintain normal cerebral blood flow so as to prevent further neuronal injury. Cerebral blood flow is dependent on several key factors: the pressure driving blood flow (cerebral perfusion pressure CPP), which in turn is determined by mean arterial blood pressure (MAP) less the intra cranial pressure (ICP) and the relative resistance to blood flow within the cerebral blood vessels (CVR) (Armitage-Chan et al 2007; Raisis & Brearley 2004; Brosnan et al 2002 and 2004). This can be expressed in the following equation:

Cerebral Blood Flow = (MAP – ICP)/CVRConsequently any marked increase in ICP without accompanying increase in blood pressure will reduce cerebral perfusion and may cause further neuronal injury. Similarly reductions in MAP while ICP remains high will also result in decreased perfusion and neuronal injury.Head trauma may increase ICP by several mechanisms. These include depressed skull fractures, cerebral haemorrhage and swelling/oedema. Any of these may decrease cerebral perfusion especially where blood pressure may be reduced by cardiovascular depressant effects of general anaesthesia and/or hypovolaemia (eg from blood loss or dehydration). Where signs of raised ICP are present preoperatively, efforts should be made to reduce it prior to induction of anaesthesia. Horses at risk of rising ICP should be evaluated carefully and anaesthetised with techniques that will minimise further increases in ICP or reductions in MAP.Signs of raised ICP include altered mentation, anisocoria and strabismus. Patients with suspected significant elevations in ICP should be stabilised as far as possible

prior to anaesthesia. The osmotic diuretic mannitol (0.25 – 2.0 mg/kg IV) is effective in reducing elevated ICP and cerebral oedema (Nout 2008). If further reductions are required it may be combined with furosemide (1 mg/kg IV) (Nout 2008). As diuretics will result in significant fluid loss via urine, care must be taken to maintain normal hydration and correct any hypovolaemia with IV fluids. Consideration should also be given to the timing of general anaesthesia – in some cases surgical repair of facial/dental injuries may be safely postponed for a few days to permit cerebral swelling etc to resolve.Hypovolaemia should be treated promptly to optimise blood pressure which will assist in maintaining cerebral perfusion. Isotonic crystalloids (eg Hartman’s) may be used. Alternatively if there is significant hypovolaemia and cardiovascular compromise, hypertonic saline (7%) may provide faster resolution (Fielding and Magdesian 2011) and may also be beneficial in reducing cerebral oedema (Nout 2008; Raisis & Brearley 2004). Crystalloid fluids should be administered in controlled boluses aiming to rapidly correct hypovolaemia without excessive dilution of plasma proteins leading to reduced oncotic pressure which may exacerbate cerebral oedema. Hypertonic saline administration must be followed up with additional isotonic crystalloids; however the total volume of fluid required may be less than if isotonic boluses are used alone (Fielding and Magdesian 2011). Based on human studies it may be preferable to avoid colloids and plasma as IV fluids especially where the blood brain barrier is not intact. Glucose containing fluids should also be avoided except for treatment of documented hypoglycaemia (Armitage-Chan et al 2007). Occlusion of the jugular veins will increase ICP due to venous congestion, so placement of IV catheters needs to be done with great care.AnaesthesiaHorses should be pre-medicated with appropriate sedatives to facilitate calm controlled anaesthetic induction. In cases where brain injury has occurred there may be an exaggerated and disproportionate response to sedatives. In some cases even very low doses of sedatives may produce profound sedation and severe ataxia. Therefore sedation is often best achieved by use of small incremental doses until the desired effect is achieved. There are 4 classes of drugs in common use as sedatives in horses:

Alpha-2 adrenergic agonists (Xylazine, Romifidine and Detomidine) are probably the most widely used sedatives in horses. They produce reliable dose dependant sedation and analgesia. Alpha-2 agonists have been shown to reduce ICP in standing (Moore & Trim 1992) and anaesthetised horses (Moore & Trim 1993). As such they are suitable for use in head trauma cases however they have potent cardiovascular side-effects (Wagner et al 1991) and so should be used carefully. CVS effects may be minimised while maintaining good sedation by combining an alpha-2 agonist with an opioid (eg butorphanol or methadone) (Muir 2009). As noted above head trauma may lead to exaggerated ataxia and sedation.

Acepromazine is a phenothiazine tranquiliser. Other drugs in this class have been shown to increase the risk of seizures (Raisis & Brearley 2004). The effect of acepromazine on ICP in horses has not been evaluated. Acepromazine is a potent vasodilator and may increase the risk of intra-operative hypotension especially in hypovolaemic horses (Parry, Anderson,

Gay 1982). Although acepromazine may be beneficial in routine equine anaesthetic cases it is probably best avoided in head trauma patients.

Benzodiazepines (Diazepam and Midazolam) produce dose dependant reductions in cerebral activity, ICP and reduce the risk of seizures (Raisis & Brearley 2004). In horses they may be useful in the acute management of seizures (Nout 2008). However in adult horses marked ataxia and dysphoria restrict their use to adjuncts to general anaesthetics. They are useful sedatives in young foals, where the absence of cardiovascular and respiratory side effects makes them attractive alternatives to alpha-2 agonists (Muir 2009).

Opioids (butorphanol, methadone and morphine) are highly effective analgesics (especially methadone/morphine). Used alone they do not produce effective sedation in adult horses; however they exhibit strong synergism with all of the above classes of sedatives (Muir 2009). This synergism can be exploited to produce reliable heavy sedation with less CVS effects than would occur if a high dose of single sedative were used alone.

As calm controlled induction is important to avoid exacerbating any injuries, anaesthesia should be induced in a quiet environment with minimal disturbances. The horse should be supported during induction preferably with a swing gate/door and held by an experienced handler if possible. As hypoxaemia and hypercapnia can both exacerbate raised ICP and poor cerebral perfusion, preparations should be made for rapid intubation, administration of oxygen and if necessary controlled ventilation immediately after induction.Intravenous anaesthetic agents:

Ketamine is the most commonly used induction agent in horses. However the use of ketamine in head trauma patients has not been widely recommended (Raisis & Brearley 2004; Armitage-Chan et al 2007; Smith 2008). Ketamine increases cerebral blood flow, metabolic rate and risk of seizures (Smith 2008; Raisis & Brearley 2004). In some species, ketamine has been shown to increase ICP (Raisis & Brearley 2004) however this has not been studied in the horse. Recent human studies have suggested that ketamine may not be as problematic in patients with brain injuries as previously thought (Zeiler et al 2014). However all patients in these studies were already treated with either benzodiazepines or barbiturates and were mechanically ventilated (Zeiler et al 2014). Furthermore ketamine was primarily evaluated at analgesic/sedative doses rather than in the context where it is commonly used in horses, as a high dose given as a rapid bolus. Without further evaluation in horses it remains difficult to recommend ketamine as an induction agent in the context for horses with head trauma.

Thiopentone like all barbiturates reduces ICP, cerebral metabolic rate and seizure activity (Smith 2008; Raisis & Brearley 2004). Consequently it is the agent of choice for induction of anaesthesia in horses with head trauma and risk of raised ICP (Smith 2008). Thiopentone is not suitable for maintenance of anaesthesia as it is cumulative and leads to poor recoveries (Wagner et al 2002). Induction of anaesthesia with thiopentone is optimised by the use of

effective sedative premedication and induction in combination with guaiphenesin and/or midazolam.

Propofol can be used to induce anaesthesia in horses and produces similar reductions in ICP, cerebral metabolic rate and seizure activity to thiopentone (Smith 2008; Raisis & Brearley 2004). The volume required (>200 ml for a 500kg horse) and very short duration of action make it less practical to use compared to thiopentone. Unlike thiopentone, propofol can be infused to maintain general anaesthesia in the horse and may produce acceptable recoveries when used in combination with alpha-2 agonists.

Alfaxalone has not been evaluated in the context of head trauma and brain injury.

Maintenance of general anaesthesia:Volatile anaesthetic agents are the most practical option for maintaining anaesthesia in horses with head trauma. All of the commonly used agents (Halothane, isoflurane and sevoflurane) decrease cerebral metabolic rate and the risk of seizures (Raisis & Brearley 2004). Unlike in small animals, general anaesthesia and recumbency dramatically increases ICP in horses (Brosnan et al 2003 and 2004). This places horses with head trauma at much greater risk of serious reductions in cerebral perfusion and subsequent complications. There are several factors that will further affect ICP during anaesthesia:

Positioning: Dorsal recumbency increases ICP, however when the head is kept level with the thoracic inlet the effect on ICP and cerebral perfusion pressure is not significantly different compared to lateral recumbency (Brosnan et al 2002b). Positioning with the head down will markedly increase ICP leading to reduced cerebral blood flow (Brosnan et al 2002b and 2008). Therefore every effort should be made to keep the head at the level of the thoracic inlet at all times during positioning of the horse and where possible dorsal recumbency should be avoided.

Duration: ICP increases with duration of general anaesthesia resulting in decreased cerebral perfusion (Cullen et al 1990; Brosnan et al 2003). General anaesthesia time should therefore be minimised as far as possible.

Hypercapnia will substantially increase ICP (Cullen et al 1990; Brosnan et al 2003b) and in cases where ICP may already be high, this further increase is likely to result in reduction in cerebral blood flow. It is essential that normocapnia be maintained throughout maintenance of general anaesthesia with volatile anaesthetic agents. As end-tidal CO2 (ETCO2) is normally 5 to 10 mmHg lower than arterial CO2 (PaCO2) in anaesthetised horses (Taylor & Clarke 2007), horses should be maintained with an ETCO2 of 30 to 40 mmHg (typically corresponding to PaCO2 40-45 mmHg). However accurate measurement of PaCO2 via arterial blood gas analysis is always preferable (if possible). In virtually all cases achieving these CO2 goals will require intermittent positive pressure ventilation (IPPV) for the duration of general anaesthesia and early recovery period. IPPV may be accomplished with either

an anaesthetic machine & ventilator or if volatile anaesthesia is not used an oxygen demand valve.

Hypocapnia (PaCO2 30 to 35 mmHg) may be induced to cause a rapid reduction in ICP in the event of an acute rise in ICP (Smith 2008; Raisis & Brearley 2004). As Hypocapnia causes cerebral vasoconstriction which may limit blood flow this technique should only be utilised for short periods of time.

Mean arterial blood pressure MAP: maintaining MAP over 70 mmHg is equally essential to ensuring adequate cerebral perfusion. Fluid therapy should be continued during general anaesthesia and hypovolaemia aggressively treated with hypertonic and/or isotonic crystalloid boluses. If required dobutamine should be infused to maintain MAP > 70 to 80 mmHg (Taylor & Clarke 2007). MAP will be more easily maintained if the dose of volatile anaesthetic agent is minimised. This dose reduction is best facilitated by either local anaesthetics (especially for dental or jaw surgery) or administration of adjunctive sedatives such as alpha-2 agonists (Xylazine/Romifidine or Midazolam).

Oxygenation: supplemental oxygen should be administered throughout the general anaesthetic as inadequate oxygenation will be as harmful as reduced blood flow. IPPV may assist in maintaining oxygenation.

During recovery from general anaesthesia supportive care and monitoring should be continued as far as it is practicable and safe. In particular IPPV should be maintained until strong respiratory efforts are made by the horse and oxygen supplementation given at least until the horse is in sternal recumbency. It is not uncommon for horses with head trauma to have recovery times far longer than average. This should be tolerated so long as the horse shows progressive signs of return of consciousness even if the signs are returning slower than usual. Prompting the horse to move prematurely is likely to lead to a highly ataxic horse making repeated unsuccessful attempts to stand.AnalgesiaOcular and dental injuries may be very painful and warrant prompt treatment with analgesics. Uncontrolled oral pain can lead to anorexia and dehydration with subsequent gastrointestinal complications. Non steroidal anti-inflammatories (NSAIDs) are suitable first line analgesics for almost all horses with head trauma including those with raised ICP and brain injury. Other analgesics that may be considered include morphine (0.2 mg/kg IM) or alpha-2 agonists however both of these classes of drugs should be used with care if repeated doses are required due to gastrointestinal side effects. Nerve blocks with long acting local anaesthetics (bupivacaine) may also be considered for the initial management of some injuries.

ReferencesArmitage-Chan EA et al (2007) Anaesthetic management of the head trauma patient. JVECC 17: 5-14Atherton RP et al (2007) Traumatic fracture of the basiphenoid and secondary bacterial meningitis in a Thoroughbred gelding. EVE 19: 359-364Cullen LK et al (1990) Effect of high PaCO2 and time on cerebrospinal fluid and intraocular pressure in halothane-anaesthetised horses. AJVR 51: 300-304Brosnan RJ et al (2002) Direct measurement of intracranial pressure in adult horses. AJVR 63: 1252-1256

Brosnan RJ et al (2002b) Effects of body position on intracranial and cerebral perfusion pressures in isoflurane-anaesthetised horses. J Appl Physiol 92: 2542-2546Brosnan RJ et al (2003) Effects of duration of isoflurane anaesthesia and mode of ventilation on intracranial and cerebral perfusion pressures in horses. AJVR 64: 1444-1448Brosnan RJ et al (2003b) Effects of ventilation and isoflurane end-tidal concentration on intracranial and cerebral perfusion pressures in horses. AJVR 64: 21-25Brosnan RJ et al (2004) Intracranial elastance in isoflurane-anaesthetised horses. AJVR 65: 1042-1046Brosnan RJ et al (2008) Effects of head-down positioning on regional central nervous system perfusion in isoflurane-anaesthetised horses. AJVR 69: 737-743Feige K et al (2000) Traumatic injury to the central nervous system in horses: occurrence, diagnosis and outcome. EVE 12: 220-224Fielding CL & Magdesian KG (2011) A comparison of Hypertonic (7.2%) and Isotonic (0.9%) Saline for fluid resuscitation in Horses: A randomised, double-blinded, controlled trial. JVIM 25: 1138-1143.Ferreira TH et al (2013) Effects of ketamine, propofol, or thiopental administration on intraocular pressure and qualities of induction of and recovery from anaesthesia in horses. AJVR 74: 1070-1077Hubbell JAE et al (2000) Anesthetic, cardiorespiratory and metabolic effects of four intravenous anesthetic regimens induced in horses immediately after maximal exercise. AJVR 61: 1545-1552Moore RM & Trim CM (1992) Effect of xylazine on cerebrospinal fluid pressure in conscious horses. AJVR 53: 1558-1561Moore RM & Trim CM (1993) Effect of Hypercapnia or Xylazine on lateral ventricle and lumbosacral cerebrospinal fluid pressure in pentobarbital-anaesthetised horses Vet Surg. 22: 151-158Moyer W et al (2011) Equine joint injection and regional anesthesia. Academic Veterinary Solutions, Chads Ford, PA, USA.Muir WW (2009) Anxiolytics, nonopioid sedative-analgesics, and opioid analgesics. In: Muir WW, Hubbell JAE, editors: Equine Anaesthesia – Monitoring and Emergency Therapy, St. Louis, Saunders Elsevier.Nout Y (2008) Central nervous system trauma. In: Equine Neurology, ed. Furr M & Reed SM, pp 305-328. Blackwell Publishing, Iowa, USA.Parry PW, et al (1982) Hypotension in the horse induced by acepromazine maleate. Aust Vet J 59: 148-151Raisis AL & Brearley JC (2004) Anaesthesia, analgesia and supportive care. In: BSAVA manual of canine and feline neurology, ed. Platt SR & Olby NJ, pp 337-354. British Small Animal Veterinary Association, England.Rayner SG (2005) Traumatic cerebral partial lobotomy in a Thoroughbred stallion. AVJ 83: 674-677Reed SM (2007) Head Trauma: A neurological emergency. EVE 19: 365-367Reppas GP et al (1995) Trauma-induced blindness in two horses. AVJ 72: 270-272Santos M et al (2003) Effects of alpha-2 adrenoceptor agonists during recovery from isoflurane anaesthesia in horses. EVJ 35: 170-175Smith AA (2008) Anaesthetic considerations for horses with neurologic disease. In: Equine Neurology, ed. Furr M & Reed SM, pp 305-328. Blackwell Publishing, Iowa, USA.Taylor PM, Clarke KW (2007) Handbook of equine anaesthesia 2nd Ed, Saunders Elsevier, USA.Wagner AE, Muir WW, Hinchcliff KW (1991) Cardiovascular effects of xylazine and detomidine in horses. AJVR 52: 651-657Wagner AE et al (2002) Behavioral responses following eight anesthetic induction protocols in horses. VAA 29: 207-211Zeiler FA et al (2014) The ketamine effect on ICP in traumatic brain injury. Neurocrit Care, doi: 10.1007/s12028-013-9950-y

The progression of equine dentistry from the 80’s until today

Gary Wilson

This will be a more relevant discussion if we look at the changes from the 1880’s until today.

Equine dentistry has been practiced as long as man has domesticated horses. Little changed over those early centuries and Captain M. Horace Hayes in his book “Veterinary Notes for Horse Owners” 1877 states this basic approach: “If the defective mastication be due to imperfect teeth, they should be carefully attended to by filing them down, &c.” p. 207. This could really have been stated in 1977 as that was the approach to dentistry when I graduated. Hayes was disturbed by the standard of veterinary examination for soundness especially when it came to assessing the age of the horse that in 1887 he wrote a second text titled “Soundness and Age of horses. A Veterinary and Legal Guide to the Examination of Horses for Soundness.”As this is an Australian lecture, it is most appropriate to start our dateline in the 1880’s with the production of Sydney Galvayne’s book “Horse Dentition: Showing how to tell exactly the age of a horse up to thirty years.” Sydney refers to himself as “The Australian Horse Tamer and Lecturer on Horse Dentition.” Interestingly, in his later years, he refers to himself as Professor Sydney Galvayne. Perhaps the first textbook that could be said to raise the standards of equine dentistry was that by L.A. (Louis) Merillat first published in 1906 titled “Animal Dentistry and Diseases of the Mouth.” This book was Volume 1 of three volumes in his Veterinary Surgery series and by far the largest (261 pages in all). His opinion of the others in his profession was scathing as regards dentistry and is best summed up with this quote: “The veterinarian consigns dental operations to others because it is rather beneath the dignity of the learned veterinarian to float the teeth of horses; not because it is difficult, tedious or dangerous, but because animal dentistry is regarded as a trifling accomplishment that the uneducated can master.” No wonder it has taken the profession so long to master the skills and knowledge required.He goes on to say “The intimate relation of the condition of the teeth to the general health is becoming more recognized, and when the value and importance of veterinary dentistry is universally recognized by the veterinary profession and lay public, and when it becomes more generally admitted on all sides that the veterinary patient receives the same relative benefits from dental operations as the human subject, animal dentistry will then take its place among the useful branches of veterinary science.” Have we reached this point yet?The next major advance in veterinary dentistry came with Erwin Becker (1898 – 1978). Becker was induced to study veterinary science by his uncle Helmar Dun (a veterinarian). He was pursuing a career in engineering prior to this which explains his many inventions that progressed veterinary dentistry. Becker’s understanding of the pathophysiology of dental conditions led to his many treatment options which would rival the human dentists of the day. Becker ran an equine dental hospital prior to the outbreak of WWII as well as having a set of

portable stocks towed by his car. He invented many dental instruments such as a horse speculum with removable plates and an air-driven, water-cooled equine dental unit which was manufactured commercially by Hauptner. He performed restorations, made stone models of equine cheek teeth before and after treatment, had cast metal crowns made and fitted to restore equine incisors to function and conducted a large amount of research. This was all in the 1930s!In 1938 he published a textbook which documented his findings and treatment protocols – Neuzeitliche Zahnbehandlung beim Pferd. After the war Becker trained American veterinarians serving in the army. Following this he taught at the Berlin Free University and became Head of the Veterinary School, Head of the School of Photography and Head of the Radiology Institute whilst all of the time remaining Chair of Veterinary Orthopedics and Chair of Veterinary Dentistry. He retired in 1968.The middle of the 20th century was a time of increased mechanization and the horse lost its place as a beast of burden in the western world. Simultaneously, veterinarians “found” better anaesthesia and developed an increasing interest in invasive surgical procedures and equine dentistry became a little too mundane for the equine surgeons. It was “only teeth” after all. Most veterinary practices had dental equipment which consisted of a full-mouth speculum, a Swayles gag (spool speculum) and an upper and lower tooth rasp. Some veterinarians also had molar extraction forceps but extraction was usually done surgically by trephine and punch. Sedation for dentistry was unheard of and, indeed, clients regarded the vet who needed to sedate to be a poor horseman. The tooth rasps had a basic steel blade which rusted (and therefore blunted) quickly and dentistry was hard physical work for little reward.In the late 1970s tungsten carbide chip blades were introduced. These were a massive improvement on the steel blades. They did not rust and would also cut in both directions. Most veterinarians would still only have the same basic instrumentation though.In 1979, Gordon Baker completed his PhD titled “A study of dental disease in the horse” at Glasgow. The study and papers from it were largely ignored by the veterinary profession.During the 1980s equine sedation with alpha agonists became common. This allowed relative safe standing procedures to be performed in horses and rapidly became accepted for equine dentistry. Suddenly the twitch and restraint by holding the tongue were only done by “old school” veterinarians and lay dentists. The ability to perform good oral examination under safer conditions stimulated an interest in the development of better instrumentation. Powered equipment started to appear initially with rotary die grinders modified for dentistry. These were all designed to remove tooth material easily without the fatigue factor of hand rasping. Techniques performed, however, had not changed since the 1800s. Only now could iatrogenic damage become a potential issue especially the rapid removal of excessive amounts of tooth.In the early 1990s some veterinarians became worried by the incorrect usage of power instrumentation. A resurgence in the use of hand floating occurred with the introduction of tungsten carbide blades. These allowed relatively easy removal of tooth material by hand. The blades were very sharp but easily damaged with care in transport and storage. Power instruments continued to be developed. Research into equine dentistry started with Edinburgh University

leading the way through Professor Padraic Dixon and his team setting the standard. This was one of the few veterinary schools that considered dentistry of value to teach, let alone research. Since this time research and scientific papers have proliferated from around the world and the majority of North American veterinary schools have veterinary dental departments and dentistry is an integral part of undergraduate training. Many “known facts” of equine dentistry have been challenged with this research most notably the accuracy of ageing horses by their dentition.The 21st century has seen an “explosion” of research and development of new techniques and procedures in equine dentistry. Multiple textbooks have been published and scientific papers are common in most veterinary journals. Instrumentation has continued to be developed and refined and procedures used in other species are beginning to be performed regularly in the equine. These techniques such as endodontics, restorative dentistry, orthodontics and periodontal disease therapy are being researched and refined for use in the horse.Postgraduate training in equine dentistry for veterinarians has become readily available with programs at most equine veterinary association meetings such as the AAEP. Specific courses and workshops have been held in multiple venues worldwide. This has, to a large extent, been driven by the rise in political activity of lay equine dental associations.In 2001, the Academy of Veterinary Dentistry established an equine pathway (no longer available) allowing for advanced training in equine dentistry. In 2009 the International College of Equine Veterinary Odontology was formed in Canada and the first Diplomates were examined in 2010. In 2013, the inaugural examinations were held for the American Veterinary Dental College equine speciality and 12 candidates (7 from USA; 1 each from South Africa, UK, Austria, Canada and Australia) were successful at this examination to become the Founding Diplomates. Equine dentistry has moved from “its only teeth, why bother” to a veterinary speciality.Instrumentation for use in the equine is rapidly moving toward that used by Becker.

Intra-Oral Radiography in the Horse

O Liyou and T Chinkangsadarn

As the levels of education and care for equine dentistry increase, so do the numbers of questions as to the best way to handle some pathologies detected in the mouths of horses upon thorough oral examination. Common examples of such pathologies include pulp exposures, periapical disease and periodontal disease. An obvious suggestion to help decision making is to gather more information about the tooth and supporting structures involved. Radiology is the most effective and available way to do this for most practitioners, and can be done in clinic or in the field on a sedated horse. CT and MRI may be more sensitive in gaining accurate diagnostic information at times, but their significant expense and lack of availability restricts their use. Extra-oral radiography, both closed and open mouth has been the cornerstone to achieving useful radiographic findings in the past. Intra-oral radiography was being trialled and suggested 5-10 years ago, but has been largely dismissed by many equine practitioners as not being justifiable, especially in light of the high quality of images that can be achieved with DR radiography. In this paper, we are revisiting Intra-Oral Radiography, in light of how easy and highly sensitive images can be achieved, when done correctly, using the right equipment! Only CR digital machines have plates small enough to be used for I-O radiography of cheek teeth. Both DR and CR plates can be used for incisors and canines. Reports of sensitivity of 76% for detecting apical infection in cheek teeth was reported by Townsend et al in 2010, when using extra oral radiography. Intra-oral radiography has the potential to increase this sensitivity, by largely eliminating the superimposition of the other arcade and structures of the head, and giving far superior detail of the apical and periapical anatomy.Intra-oral radiology is the easiest and effective method for assessing the coronal and periodontal structures of mandibular cheek teeth. By gaining increased sensitivity for detecting significant dental diseases, it will be easier to decide whether to extract a tooth or not, when it is suspected to be causing pain to a horse. It will also be easier to demonstrate the pathology to the untrained eye of the owner. Intra-oral radiology will never replace the need for extra oral radiography, but definitely complements it well and serves to increase sensitivity for detecting pathology of equine teeth.

Anaesthesia and Analgesia for Head Trauma PatientsJennifer E. Carter, DVM, MANZCVS, DACVAA

Registered Specialist in Veterinary Anaesthesia (Victoria)University of Melbourne

Basic Brain PhysiologyIn the normal brain, cerebral blood flow is influenced by blood carbon dioxide and oxygen levels as well as systemic blood pressure; however it remains constant over a wide range of normal physiologic changes in those variables due to auto-regulation of vascular tone. Cerebral blood flow is proportional to cerebral perfusion pressure and inversely proportional to cerebral vascular resistance. It is difficult to measure cerebral perfusion pressure directly but it is calculated by subtracting the intracranial pressure from the systemic mean arterial pressure. The Monroe-Kellie doctrine states that the skull cannot be stretched and, as a result, the volume of the contents of the skull (brain, CSF, blood) must remain fixed. An increase in one must result in a decrease of another in order to maintain a normal intracranial pressure. The auto-regulation of cerebral blood flow over a wide range of physiologic changes helps to minimise changes in intracranial volume. Finally, under normal states the brain is subject to flow-metabolism coupling, meaning that vasomotor tone is subject to the metabolic oxygen needs of the brain. If cerebral metabolic oxygen demand decreases, cerebral blood flow will decrease and intracranial pressure will decrease.Brain Pathophysiology with Traumatic Brain InjuryIn the traumatised brain, many of the protective mechanisms are diminished or lost completely. Loss of auto-regulation leads to significant changes in cerebral blood flow from changes in ventilation, oxygenation, and systemic blood pressure which are all variables that may be disturbed with traumatic injury. Hypoventilation leads to cerebral vasodilation and increases in intracranial pressure where as severe hypoxemia or hypotension can cause decreased cerebral blood flow and potentially cerebral ischemia. In addition, as intracranial pressure is often increased in the head trauma patient, systemic mean arterial pressure must also increase to maintain cerebral perfusion pressure. If the flow-metabolic coupling is also disrupted and cerebral metabolic oxygen demand is not decreased due to the vasoconstriction then the risk of cerebral hypoxia increases. Lastly, injury to the brain and cranial nerves can result in abnormalities in nerve function, increases in metabolic oxygen demand, and neuronal cell death.Effects of Anaesthetics and Analgesics on Brain PhysiologyOpioids have minimal direct effects on cerebral blood flow and intracranial pressure making them an excellent option for provision of analgesia to the head trauma patient. Opioids are also anaesthetic sparing drugs and reduce the doses of other drugs necessary to achieve and maintain general anaesthesia. All opioids have the potential to cause bradycardia which, in theory, could influence mean arterial blood pressure however this is easily controlled by administration of an anticholinergic drug such as glycopyrrolate if needed. Unfortunately opioids also have the potential to cause hypoventilation and subsequent vasodilation in the head trauma patient. As such, ventilation should be monitored closely and provisions for mechanical or manual ventilation should be available. Partial mu agonists such as buprenorphine may be less likely to cause derangements in cardiorespiratory function and may be preferable for analgesia in patients where ventilation cannot be measured or controlled.Alpha-2 agonist drugs such as medetomidine or dexmedetomidine have no inherent effect on intracranial pressure however they cause a significant decrease in cardiac

output with even small doses which could cause decreased cerebral perfusion and ischemia in the head trauma patient. Alpha-2 agonist drugs do provide sedation and analgesia and reduce the doses of other drugs necessary to maintain general anaesthesia. Their potential benefit should be weighed against the possibility of alterations in cerebral perfusion in the head trauma patient. In addition, medetomidine and dexmedetomidine are reversed by administration of atipamezole. Atipamezole has been shown to temporarily inhibit cerebral blood flow which may exacerbate cerebral ischemia.Benzodiazepine drugs such as diazepam and midazolam can be used to provide sedation in the brain trauma patient as they cause no meaningful changes to the cardiopulmonary system or to intracranial pressure. Benzodiazepines reduce the doses of other agents necessary to induce and maintain general anaesthesia and have been reported to induce mild decreases in cerebral metabolic oxygen demand. These qualities suggest that benzodiazepines should be included in the induction or maintenance of general anaesthesia for brain injury patients.Barbiturate drugs such as thiopental can be used for anaesthetic induction and maintenance of the head trauma patient. Barbiturates are actually neuroprotective because they reduce cerebral metabolic oxygen demand and intracranial pressure as well as providing protection from neuronal damage and providing antioxidant effects. Unfortunately even ultra-short acting barbiturate drugs like thiopental have a long duration of action when compared to propofol, accumulate in the body when used as an infusion, and can prolong anaesthetic recovery. In addition, barbiturates can cause hypotension and hypoventilation which can exacerbate existing cerebral blood flow issues in the brain injury patient. The use of barbiturates in head trauma patients should be coupled with cardioventilatory support for the patient.Propofol provides many of the same benefits as barbiturates with reduction of cerebral metabolic oxygen demand and antioxidant properties as well as a potential decrease in intracranial pressure. Propofol is advantageous when compared to barbiturates as it can be easily titrated to effect, has a short duration of action, does not accumulate significantly when used as an infusion, and provides a smooth anaesthetic recovery. Propofol and barbiturates have similar cardiorespiratory effects and care should be used to maintain systemic blood pressure and ventilation when using propofol in the head trauma patient. Finally, some controversy exists regarding the effect of propofol on flow-metabolism coupling and some reports state that propofol use can actually disrupt this process leading to a greater decrease in cerebral perfusion than expected from decreased metabolic oxygen demand alone.Inhalant anaesthetics can be used in the head trauma patient in low doses. Isoflurane and sevoflurane reduce cerebral metabolic oxygen demand when used at or below their MAC values (approximately 1.3% and 2.4% respectively) which can lead to decreased perfusion and a reduction of intracranial pressure when flow-metabolism coupling is intact. Unfortunately inhalant anaesthetics are potent vasodilators and at doses higher than MAC, the decrease in systemic blood pressure causes decreased cerebral perfusion and increased intracranial pressure. Inhalant anaesthetics also cause dose dependent decreases in ventilation which can worsen cerebral perfusion due to hypercapnia. In addition, high concentrations of inhalant anaesthetics will disrupt cerebral auto-regulation even if it is intact. Isoflurane and sevoflurane in concentrations lower than MAC may be beneficial for the head trauma patient without increases in intracranial pressure by improving cerebral perfusion however mechanical ventilation should be provided.

The use of ketamine for brain trauma patients is controversial due to the fact that ketamine acts as an indirect sympathomimetic agent and can increase systemic blood pressure leading to increases in intracranial pressure and cerebral oxygen consumption. However ketamine has also been demonstrated to decrease intracranial pressure when administered with propofol. In addition, ketamine is thought to possess neuroprotective activity owing to its inhibitory effects on the NMDA receptor. The NMDA receptor plays a key function in the pathophysiology of neuronal ischemic injury and antagonism by ketamine could help guard against this. Lastly, ketamine provides antihyperalgesic activity which could be beneficial in a multimodal analgesic therapeutic regimine. Although ketamine is not widely used in the treatment of head trauma patients, its use could be considered as a part of a multi-agent approach to anaesthesia and analgesia.Supportive Care for Anaesthesia of the Head Trauma PatientPeri-operative support of the head trauma patient is the same as care of any other anaesthetic patient in many ways. Systemic blood pressure should be supported to maintain mean arterial pressure within normal physiologic ranges and ideally greater than 90 mmHg to improve oxygenation of cerebral tissues. Positive inotropic and vasopressor drugs can be used to assist in maintenance of blood pressure. Intravenous fluid support should be provided and care should be exercised to avoid over- or under-hydration. Balanced replacement fluids such as Hartmann’s solution are appropriate for intravenous fluid support and glucose containing fluids should be avoided as they have been negatively correlated with outcome. Hypertonic saline can be used for volume resuscitation and may also be beneficial in reducing cerebral oedema. Positive pressure ventilation should be provided to maintain eucapnia and reduce intracranial pressure. Capnograph readings between 35-40 mmHg are ideal. Hyperventilation can be used for short-term, rapid reduction in intracranial pressure however it increases the risk of cerebral ischemia and is not recommended for maintenance of anaesthesia. Body temperature should be supported however efforts should be made to prevent hyperthermia via active cooling if necessary as hyperthermia increases cerebral oxygen demand and potentially intracranial pressure.Additional basic measures should be used in the head trauma patient. Gagging or retching on anaesthetic induction or recovery will cause increases in intracranial pressure and efforts should be made to achieve smooth induction with premedication and recovery with sedation if needed. Elevation of the head can help to reduce intracranial pressure and care to avoid occlusion of the jugular veins can help to promote good venous drainage and avoid potential increases in intracranial pressure. Lastly, in patients with increased intracranial pressure, administration of mannitol or hypertonic saline can diurese the brain and reduce cerebral oedema.

Selected References:1. Sande A, West C. Traumatic brain injury: a review of pathophysiology and management. J Vet Emerg Crit Care 20(2), 2010, 177-190.2. Armitage-Chan EA, Wetmore LA, Chan DL. Anaesthetic management of the head trauma patient. J Vet Emerg Crit Care 17(1), 2007, 5-14.3. DiFazio J, Fletcher DJ. Updates in the management of the small animal patient with neurologic trauma. Vet Clin Small Animal 43, 2013, 915-940.

Emergency head trauma management – Traumatic Brain Injury (TBI) in small animals – ECC perspective

Melissa A. Claus, DVM, DACVECCMurdoch University, Murdoch, WA, Australia

PathophysiologyTraumatic brain injury (TBI) occurs with direct impact of the head or with rapid acceleration-deceleration of the head. There are two types of brain injury that occur when the brain is involved in a traumatic event. Primary injury is the direct physical damage that occurs immediately at the time of the injury. It is due to the variety of forces that act upon the head and brain during the event. The forces involved in primary injury include concussive, compressive, stretching, and shearing forces. Concussive forces to the calvarium can cause skull fractures and contusions within the brain parenchyma. Shearing forces occur during acceleration-deceleration events. Shearing forces can cause blood vessels and axons to stretch and tear. Torn or severely damaged axons will lead to neuronal dysfunction and death. Torn blood vessels will result in parenchymal contusions, or parenchymal or meningeal haematomas. Pooling of blood within the confines of the skull will lead to increased intracranial pressure (ICP), compression of the brain tissue, and in severe cases, brain herniation. Rarely, a primary injury should be addressed surgically. If the patient has a growing haematoma or depressive skull fractures, decompression surgery can be attempted to alleviate the increased ICP and prevent brain herniation. No standard therapy is directed toward primary brain injuries. Instead, all therapy is directed toward decreasing the severity of the secondary brain injury that will develop in the subsequent hours to days after the primary injury has been sustained. Secondary brain injury occurs due to a variety of physiological responses that are set in motion once the brain has been damaged. Though there are many different inflammatory pathways with multiple mediators, the ultimate outcome is an increase in ICP secondary to cerebral oedema. Neuronal death due to ischemia, oxidative damage, and excessive neural stimulation from the release of excitatory neurotransmitters are additional sequelae. To decrease the severity of secondary brain injury, the goal is to promote optimal oxygenated blood flow to the brain. This is accomplished by stabilizing and optimizing the patent’s pulmonary and cardiovascular system, and administering medications to decrease cerebral oedema and promote normal ICP. Cerebral perfusion pressure (CPP), the blood pressure required to perfuse the brain, is equal to the difference between the mean arterial pressure (MAP) and the ICP. Intracranial pressure is the pressure within the skull and is applied to all of the intracranial tissues, including brain parenchyma, cerebrospinal fluid, and blood. The Monroe-Kellie Doctrine describes the directly proportional relationship between the volume of the intracranial tissues and the ICP. The sum of the intracranial tissues must remain constant as they exist within a non-distensible structure, the calvarium. If one tissue increases in volume, the other tissues must decrease in volume in order to maintain a constant ICP. Intracranial compliance is the change in intracranial volume via increased outflow and decreased inflow of cerebrospinal fluid, blood, and interstitial fluid to maintain the ICP at ≤ 10 mmHg. Compensation to maintain a constant ICP is only possible to a certain extent. Once the limits are reached, small increases in intracranial volume will lead to profound increases in ICP (Figure 1).

As ICP climbs, CPP falls. The Cushing’s reflex is a physiologic response to a decreasing CPP that consists clinically of systemic hypertension coupled with profound bradycardia. When brain perfusion is compromised, local carbon dioxide levels increase. This triggers a large spike in sympathetic output, which increases systemic blood pressure. The baroreceptors in the carotid body and aortic arch sense the elevated pressure and increase vagal input to the heart to induce a reflex bradycardia. The Cushing’s reflex is a dire sign in a patient with TBI as it signifies a potentially fatal increase in ICP.

Figure 1: ICP-volume relationship and the limitations of intracranial compliance

Intracranial Volume

ICP

Cerebral perfusion pressure is not only compromised as ICP increases, but it can be negatively impacted by hypotension. In the non-traumatized brain, CPP is regulated locally by constriction and dilation of arteries feeding the brain to ensure maintenance of constant perfusion to the brain over a range of arterial pressures between ~50-150 mmHg. This local perfusion pressure control is known as autoregulation. A patient in severe hypovolaemic shock may experience a marked decrease in MAP. Autoregulation ensures that unless the MAP drops below 50 mmHg, CPP will be maintained, and cerebral ischemia will not occur. Patients sustaining head trauma, however, often lose the ability to locally regulate CPP. With loss of autoregulation, minor drops in MAP will lead to decreased cerebral perfusion and secondary ischemia, further perpetuating secondary brain injury. Thus, it is of the utmost importance to achieve and maintain normal blood pressure in TBI patients.

Assessment of neurological statusSerial monitoring of the patient’s neurological status over time is critical. It is the only way to determine the success of directed therapy to decrease ICP. It is important to record and compare results over time using a consistent series of neurological tests. The Modified Glasgow Coma Scale (MGCS) is one objective measure to serially monitor a patient in a repeatable and consistent manner. This scale (Table 1) includes evaluation of body posture, brainstem function, and consciousness. It allows the assignment of a score to each patient for comparison over time to assess severity and progression of neurological disease. A retrospective study of 38 dogs with TBI by Platt et al. in 2001 demonstrated that the MGCS score reflected probability for survival within the first 48 hours following injury, where a MGCS score of 8 was correlated with a 50% probability for survival.1

Evaluation of body posture and motor function can provide information on severity of brain injury. Abnormalities can range from mild weakness on one side of the body to opisthotonus and extensor rigidity of all four limbs to absent muscle tone and spinal reflexes. Unilateral postural abnormalities reflect damage to the contralateral aspect of the brain or ipsilateral aspect of the cervical spinal cord. Decorticate posturing involves flexion of the forelimbs and extension of the pelvic limbs and results from damage to or compression of the corticospinal tract in the midbrain. Decerebrate posturing involves extension of the forelimbs, pelvic limbs, and neck and results from damage to or compression of the brain stem. In humans, both of these postures indicate significant brain disease, but decerebrate posturing carries a more guarded prognosis than decorticate posturing. Decorticate posturing can progress to decerebrate posturing when these postures arise due to brain herniation.

Serial evaluation of cranial nerve function is crucial to determine severity of brain injury. Level of consciousness should be evaluated and graded alert, mildly to moderately obtunded, stuporous, or comatose, based on the patient’s responsiveness to its environment. Consciousness should be frequently re-evaluated for deterioration until the patient is deemed to be more stable.

Diagnostics

Table 1: Modified Glasgow Coma Scale

Motor Activity Score Normal gait, normal reflexes 6 Paresis or decerebrate activity 5 Recumbent, intermittent extensor rigidity 4 Recumbent, constant extensor rigidity 3 Recumbent, constant rigidity and opisthotonus 2 Recumbent, hypotonia, decreased or absent reflexes 1

Brain stem reflexes Normal PLR and OCR 6 Slow PLR and normal to slow OCR 5 Bilateral unresponsive miosis and normal to slow OCR 4 Pinpoint pupils and slow to absent OCR 3 Unilateral unresponsive mydriasis and slow to absent OCR 2 Bilateral unresponsive mydriasis and slow to absent OCR 1

Level of consciousness Occasional periods of being alert and responsive 6 Obtundation to delirium, capable of responding though

may be inappropriate 5 Obtunded but responsive to visual stimuli 4 Obtunded but responsive to auditory stimuli 3 Stuporous – only responsive to noxious stimuli 2 Comatose – unresponsive to repeated noxious stimuli 1

PLR: pupillary light reflex, OCR: oculocephalic reflex

Blood Glucose:Studies in humans with TBI have demonstrated that hyperglycaemia on presentation and persistent hyperglycaemia are poor prognostic indicators for survival.2 There are two schools of thought as to why hyperglycaemia is linked to decreased survival. One view is that hyperglycaemia provides the damaged and depolarizing brain a substrate for energy production in a hypoxic environment, and thus perpetuates the formation and build-up of lactic acid. An acidic environment promotes cerebral vasodilation. An increase in cerebral blood volume further increases ICP, which decreases cerebral perfusion, perpetuates neuronal injury and death, and increases the risk of brain herniation. An alternative view is that hyperglycaemia is not a direct contributor to progressive brain injury, but merely indicates that severe brain injury is present. Hyperglycaemia occurs in traumatized patients due to insulin resistance resulting from the massive catecholamine and glucocorticoid release as a response to bodily injury. Hyperglycaemia in cats and dogs with TBI was evaluated in a retrospective study by Syring et al. in 2001. This study showed hyperglycaemia was correlated with more severe injuries based on MGCS score and longer hospitalizations, but it had no effect on mortality.3 At this time, there is not enough evidence in veterinary literature to recommend glycaemic regulation using insulin in patients with head trauma. Additionally, there is a risk of inducing hypoglycaemic seizures with insulin therapy. Thus, the blood glucose level is important to consider, but it is not currently a piece of information at which therapy is directed.

Imaging:Skull radiographs require manipulation of the patient’s head and neck, and may require positioning devices to ensure appropriate, symmetrical images. Even the most ideal radiographic view of the skull can be difficult to interpret for evidence of skull fractures. Additionally, severe brain injury can be present in the absence of any skull fractures, and skull fractures can be present that are not necessarily associated with brain injury. Thus, in light of the low sensitivity of radiographs to demonstrate fractures, the poor correlation of skull fractures with severity of brain trauma, as well as the harm that can be inflicted while manipulating the patient, radiographs of the skull are not recommended at this time.

Computed tomography (CT) of the skull will demonstrate skull fractures as well as acute haemorrhage within the calvarium. Computed tomography can be costly, is not always readily available, and requires general anaesthesia in non-comatose patients. Thus, CT is mainly indicated in patients with moderate to severe head trauma, in patients that have deteriorating neurological signs, and in patients with more severe unilateral neurological deficits (e.g. hemiparesis). Lateralizing neurological deficits most often occur with depressive skull fractures, or with subdural haematomas, which are uncommon in dogs and cats.

TreatmentsExtracranial stabilization:Patients with TBI usually present in hypovolaemic shock and often have multi-systemic injuries. Good emergency practices necessitate following the ABCs. Airway assessment should be made for haemorrhage, fluid, or other debris that may have entered during the traumatic event. Intubation is essential for the patient without a swallow or gag response. Assess the respiration quality and rate. Hypoventilation may indicate brainstem trauma or compression. Hypoventilation causes hypercapnia which leads to increased cerebral blood volume via cerebral vasodilation. Increasing the cerebral blood volume will contribute to increasing ICP. Ideally, venous, arterial, or end-tidal carbon dioxide (CO 2) should be monitored. The partial pressure of CO2 should be maintained around 35-40 mmHg, corresponding to an end-tidal CO2 of around 30-35 mmHg.

Oxygenation should be monitored in a head trauma patient and supplemental oxygen should be provided to promote optimal oxygen saturation of hemoglobin. Patients with head trauma often have suffered thoracic trauma as well, and may have pulmonary contusions or pleural space disease impairing gas exchange. Oxygen supplementation should be provided to ideally achieve oxygen saturation (SpO2) ≥ 95%.

Fluid resuscitation should be initiated for patients in shock. Hypertonic saline (7.2-7.5%) will not only help restore blood volume in a patient in hypovolaemic shock, it can also facilitate a decrease in cerebral oedema and ICP, an improvement in blood rheology, and the induction of immunomodulatory and anti-inflammatory effects.6 Hypertonic saline additionally has direct effects on the myocardium to increase cardiac contractility, and thus improves cardiac output.7 The dose of 7.0-7.5% hypertonic

saline to use is 4-6 ml/kg (dogs) or 2-4 ml/kg (cats) intravenously. This dose must be given over a period of 10 minutes to avoid profound, though transient, vasodilation.8 This dose will only transiently improve perfusion and further fluid therapy may be required. Be cautious of hypernatraemia with repeated doses.

With a mildly supraphysiologic sodium concentration of 154 mmol/L, 0.9% NaCl is the isotonic crystalloid of choice when resuscitating a patient with potential TBI. Administer ¼ to ½ of a blood volume rapidly and reassess perfusion parameters to determine if more fluids are required. Other isotonic crystalloids including lactated ringers solution, Hartmann’s solution, and Plasmalyte 148 are also acceptable resuscitation solutions. Crystalloids that should be avoided when treating shock include hypotonic solutions like 0.45% NaCl with 2.5% dextrose and 5% dextrose in water. These fluids rapidly redistribute out of the intravascular space and into the intracellular compartment. Thus, they are poor at restoring blood volume and can contribute to cell swelling and increasing ICP.

Synthetic colloid solutions like hydroxyethylstarch (Voluven) can be used to resuscitate a patient in hypovolaemic shock. The dose of colloid needed to restore blood volume is less than that required with a crystalloid because, unlike with crystalloids, the volume of colloid administered will be retained in the intravascular space rather than redistributed to the interstitial space. This is due to the presence of starch molecules in the solution adding an oncotic pressure to the solution. Unlike hypertonic saline, they do not decrease cerebral oedema, and thus do not decrease ICP. In dogs, boluses of 5 ml/kg over 10-15 minutes can be administered up to a volume of 20 mL/kg during the treatment of shock. In cats, boluses of 2-3 mL/kg can be administered to a total volume of 10 mL/kg. Perfusion parameters should be assessed at the end of each bolus to determine if further volume will be required.

Perfusion parameters need to be monitored to assess for appropriate end points of resuscitation. Appropriate end-resuscitation perfusion parameters include pink mucous membranes, normal heart rate, good pulse quality, warm extremities, capillary refill time < 2 sec, and possibly improved mentation. Blood pressure should also be monitored and systolic blood pressure ≥ 90 mmHg should be maintained.

Intracranial stabilization:The main goal for intracranial stabilization is to decrease the severity of secondary brain injury. The clinician’s goal is to optimize cerebral oxygen delivery and uptake by maintaining CPP and cerebral blood flow, and to minimize cerebral metabolic rate.

Cerebral oedema can be treated by administering hypertonic solutions to promote water loss from the brain tissue. The hypertonic solutions typically used to decrease cerebral swelling include mannitol and hypertonic saline.

Mannitol is a low-molecular weight, poorly-metabolized sugar suspended in water. 20% and 25% solutions have osmolarities of 1100 and 1370 mOsm/L, respectively. Administration of a bolus of mannitol induces an increase in serum osmolarity due to the addition of the small mannitol molecules that do not cross cell membranes or the intact blood-brain barrier. Increased serum osmolarity induces movement of water from the brain parenchyma into the intravascular space. Mannitol also induces an osmotic diuresis, as it is freely filtered in the glomeruli and is not reabsorbed in the tubules. Risks associated with its use include a potential for worsening cerebral oedema if there is major blood-brain barrier disruption, as well as a potential to cause hypovolaemia if the volume of fluid lost in the urine is not replaced. There is also a possibility for inducing circulatory overload immediately after administration in patients with heart disease. Acute renal failure is rarely reported in humans administered multiple doses. The dose of mannitol to administer is 0.25-1.0 g/kg intravenously over a 15-20 minute period. Administering frusemide with mannitol is not recommended. Frusemide administered at clinically relevant doses in conjunction with mannitol does not significantly decrease cerebral oedema from TBI.9 Additionally, inducing a further diuresis by adding a loop diuretic greatly increases the risk of the patient

developing hypovolaemia and hypotension.

Hypertonic saline 7.5% has an osmolarity of 2500 mOsm/L. It decreases cerebral oedema and ICP by increasing the serum osmolarity to draw water across the blood brain barrier and into the intravascular space. By this mechanism, it also expands intravascular volume and decreases blood viscosity. Because the expansion of intravascular volume persists (no osmotic diuresis is induced), blood viscosity remains decreased and blood rheology is improved as compared to mannitol.6 Hypertonic saline can

improve cardiac output by directly increasing cardiac contractility. In regions where the blood brain barrier is disrupted, it can enter the interstitial space and help restore neuronal resting membrane potential, as well as decrease parenchymal inflammation. Finally, hypertonic saline promotes blood-brain barrier health by osmotically drawing water from injured oedematous blood-brain barrier cells and endothelial cells.7 Risks associated with administration of this hypertonic agent include hypernatraemia with multiple doses, and circulatory overload in patients with heart disease. Serum sodium should be monitored prior to re-dosing to assess for development of hypernatraemia. The dose of 7.0-7.5% hypertonic saline to use is 4-6 ml/kg (dogs) or 2-4 ml/kg (cats) intravenously over a 10 minute period, as discussed above.

ICP will be elevated if the patient is hypoventilating for the reasons mentioned above. Manual hyperventilation is contraindicated as it will cause cerebral vasoconstriction, decreased cerebral blood flow, and cerebral ischemia. One study in people with TBI showed that even with mild hypoventilation (PaCO2 < 34 mmHg), global cerebral blood flow decreased and areas of critically underperfused brain tissue were present despite significant decreases in ICP and increases in CPP.10 Hyperventilation can be used as an acute intervention to decrease ICP urgently when the patient shows signs of imminent brain herniation (decorticate or decerebrate posturing) or rapid decline in MGCS score or neurological status.11

Cerebral blood flow and blood volume can be optimized by elevating the head above the heart by 30 degrees. In people, 30 degree elevation of the head has been shown to optimize cerebral venous outflow while preserving CPP and cerebral oxygenation.12 It is important to place the patient on a board to achieve this elevation so as to avoid kinking the neck and thus obstructing the jugular veins. Additionally, it is very important to avoid occlusion of the jugular veins for venipuncture or intravenous catheterization, as these are the main routes of venous outflow from the brain.

Attempts should be made to minimize elevations in cerebral metabolic rate by decreasing risk of seizures, preventing iatrogenic hyperglycaemia, and preventing hyperthermia. With increases in cerebral metabolic rate, oxygen consumption increases. When oxygen delivery to the brain is compromised by globally decreased cerebral blood flow, cerebral ischemia and perpetuation of secondary brain injury result.

Seizure activity consumes large amounts of cerebral oxygen and nutrients. Seizures should be immediately controlled with diazepam or midazolam. An intravenous constant rate infusion of midazolam should be considered if seizures are occurring frequently (2-3 seizures/24 hours). Seizures developing within 1 week of injury are considered early post-traumatic seizures, whereas seizures developing after 1 week are considered late post-traumatic seizures. Human head trauma patients that have had a seizure within the first 24 hours after injury, have as high as an 86% chance of having another seizure within the next 2 years.13 In these patients, daily antiepileptic medications are recommended. Prophylactic administration of anti-epileptic medications to prevent early and late development of post-traumatic seizures has been evaluated in people. These studies are conflicting on the ability of prophylactic anti-epileptics to reduce the development of early seizures, but they clearly show there is no reduction in the development of late post-traumatic seizures with the administration of anti-epileptic medications. Thus, it is not recommended to use prophylactic anti-epileptic medications beyond 1 week of the traumatic insult.14 At this time, there are no studies in dogs or cats on which to base similar recommendations regarding the use of prophylactic anti-epileptic medications. It is certainly recommended to begin a regimen of anticonvulsants in a patient that has already had a seizure, but there is no data to suggest when would be appropriate to discontinue this medication.

It is essential avoid inducing hyperglycaemia in head trauma patients. As discussed above, it is unclear as to whether the development of elevated serum glucose directly contributes to a poor prognosis, or merely reflects the severity of injury. It is unadvisable to administer any dextrose-containing fluids unless the patient is hypoglycaemic. At this time, it is not recommended to treat hyperglycaemia with insulin therapy unless the patient is diabetic and requires daily exogenous insulin to maintain euglycaemia.

In people with TBI, the jury is still out on whether therapeutic hypothermia has any benefit in terms of survival or improved long-term neurological outcome.15,16 Additionally, therapeutic hypothermia has been associated with an increased incidence of pneumonia and sepsis in patients with TBI.17 Inducing and maintaining hypothermia in people is a fairly intensive intervention, and is not readily applicable to

our veterinary patients. There is presently only one report of the use of therapeutic hypothermia in the veterinary literature. It was used in a dog with TBI to successfully control post-traumatic status epilepticus.18 At this time, the recommendation is to maintain the body temperature in the low-normal range. Do not aggressively warm these patients as overshooting the mark and inducing hyperthermia can contribute to an increased metabolic rate.

Information on the use of steroids in head trauma patientsGlucocorticoids are not recommended in the treatment of TBI. They promote hyperglycaemia, suppress the immune system, delay tissue healing, perpetuate a catabolic state, and can cause gastrointestinal ulcerations. They are not part of the recommended TBI therapy. The CRASH trial in humans compared the effects of glucocorticoid versus placebo administration on death and disability in a population of 10,008 adults with TBI. This study demonstrated a significant increase in mortality and severe disability in the patients who received the glucocorticoid compared with those who received the placebo.19 This is very strong evidence supporting the recommendation against glucocorticoid administration in patients with TBI.REFERENCES

1. Platt SR, Radaelli ST, McDonnell JJ: The Prognostic Value of the Modified Glasgow Coma Scale in Head Trauma in Dogs. Journal of Veterinary Internal Medicine 15:581-584, 2001.

2. Jeremitsky E, Omert LA, Dunham CM, et al: The Impact of Hyperglycaemia on Patients With Severe Brain Injury. Journal of Trauma and Acute Care Surgery 58:47-50, 2005.

3. Syring RS, Otto CM, Drobatz KJ: Hyperglycemia in dogs and cats with head trauma: 122 cases (1997–1999). Journal of the American Veterinary Medical Association 218:1124-1129, 2001.

4. Efrati S, Ben-Jacob E: Reflections on the neurotherapeutic effects of hyperbaric oxygen. Expert Review of Neurotherapeutics 14:233-236, 2014.

5. Bennett M, Trytko B, Jonker B: Hyperbaric oxygen therapy for the adjunctive treatment of traumatic brain injury. The Cochrane Database of Systematic Reviews:CD004609, 2012.

6. Cottenceau V, Masson F, Mahamid E, et al: Comparison of Effects of Equiosmolar Doses of Mannitol and Hypertonic Saline on Cerebral Blood Flow and Metabolism in Traumatic Brain Injury. Journal of Neurotrauma 28:2003-2012, 2011.

7. Doyle JA, Davis DP, Hoyt, et al: The Use of Hypertonic Saline in the Treatment of Traumatic Brain Injury. Journal of Trauma and Acute Care Surgery 50:367-383, 2001.

8. Ken ND, Kramer GC, White DA: Acute Hypotension Caused by Rapid Hypertonic Saline Infusion in Anesthetized Dogs. Anaesthesia & Analgesia 73:597-602, 1991.

9. Todd MM, Cutkomp J, Brian JE: Influence of Mannitol and Furosemide, Alone and in Combination, on Brain Water Content after Fluid Percussion Injury. Anesthesiology 105:1176-1181, 2006.

10. Coles JP, Minhas PS, Fryer TD, et al: Effect of hyperventilation on cerebral blood flow in traumatic head injury: Clinical relevance and monitoring correlates*. Critical Care Medicine 30:1950-1959, 2002.

11. Bratton SL, Chestnut RM, Ghajar J, et al: Guidelines for the management of severe traumatic brain injury. XIV. Hyperventilation. Journal of Neurotrauma 24:S87-S90, 2007.

12. Ng I, Lim J, Wong HB: Effects of Head Posture on Cerebral Hemodynamics: Its Influences on ICP, CPP, and Cerebral Oxygenation. Neurosurgery 54:593-598 510.1227/1201.NEU.0000108639.0000116783.0000108639, 2004.

13. Frey LC: Epidemiology of Posttraumatic Epilepsy: A Critical Review. Epilepsia 44:11-17, 2003.14. Bratton SL, Chestnut RM, Ghajar J, et al: Guidelines for the management of severe traumatic brain

injury. XIII. Antiseizure prophylaxis. Journal of Neurotrauma 24:S83-S86, 2007.15. Sandestig A, Romner B, Grände P-O: Therapeutic hypothermia in children and adults with severe

traumatic brain injury. Therapeutic Hypothermia and Temperature Management 4:10-20, 2014.

16. Crossley S, Reid J, McLatchie R, et al: A systematic review of therapeutic hypothermia for adult patients following traumatic brain injury. Critical Care 18, 2014.

17. Geurts M, Macleod MR, Kollmar R, et al: Therapeutic Hypothermia and the Risk of Infection: A Systematic Review and Meta-Analysis*. Critical Care Medicine 42:231-242 210.1097/CCM.1090b1013e3182a1276e1098, 2014.

18. Hayes GM: Severe seizures associated with traumatic brain injury managed by controlled hypothermia, pharmacologic coma, and mechanical ventilation in a dog. Journal of Veterinary Emergency and Critical Care 19:629-634, 2009.

19. Edwards P, Arango M, Balica L, et al: Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet 365:1957-1959, 2005.

Emergency head trauma management – indications for direct pulp capping in traumatised teeth – pros and cons – dental

perspectiveWinston Oakes BVSc, BSc(vet), MANCVS, MACVSc (small animal dentistry

and oral surgery)Northside Veterinary Centre

43 Limestone Ave Braddon, ACT 2612

IntroductionTooth trauma is very common in small animals. Falls, fights, motor vehicle accidents and other causes of head trauma are all likely to result in damage to the teeth. Addressing dental trauma is important to prevent both acute and chronic dental pain. Trauma to dental structures is not life-threatening, so it is important to address critical organ damage before the teeth.

Trauma to the head can result in several types of tooth trauma including- fracture- avulsion- blunt trauma (pulp necrosis)

Of these, fracture is the most common and will be discussed here.

Classification of tooth traumaMany systems have been devised to categorise tooth fractures, but the commonly used systems are based on which parts of the tooth are affected. The crown of the tooth is composed of an outermost layer of mineralised enamel surrounding the mineralized dentin, which contains dentinal tubules communicating with the central soft-tissue component of the tooth, the pulp.

Figure 1: diagram of the structure of a single rooted tooth. The image on the left shows the relationship of the enamel, dentin and pulp. The image on the right shows the tip of the tooth with dentinal tubules radiating out from the pulp towards the enamel.

Classification of fractures usually revolves around the following schema:1. Enamel infraction: a tooth injury where the enamel is cracked but the structure is not compromised.2. Enamel fracture: a tooth injury where the enamel is fractured, but the dentin is not involved (uncomplicated crown fracture).3. Enamel-dentin fracture: a fracture involving the enamel and dentin, but not involving the pulp (uncomplicated crown fracture).4. Complicated crown fracture: a fracture where the pulp is exposed.5. Uncomplicated crown-root fracture.6. Complicated crown-root fracture.7. Root fracture.

Pathophysiology of tooth traumaBecause the tooth is composed of a vital tissue encased in hard structures, the usual inflammatory response of haemorrhage and oedema can have dire consequences for the pulp. Increased pressure inside the tooth results in compression of the blood supply to the pulp and subsequent avascular necrosis. This is analogous to brain trauma with subsequent elevations in intracranial pressure. Additionally, bacterial contamination of the pulp is a particularly significant issue as there is no facility for normal wound drainage inside the tooth. Consequently, the pulp is acutely sensitive to trauma and bacterial contamination. When dentin is involved in the fracture, 20,000-90,000 dentinal tubules are exposed per square millimeter of dentin. Each of these tubules is 0.9 to 2.5µm in diameter and these can provide a route for bacterial contamination of the pulp even if there is no direct pulp exposure

Emergency Management of Tooth FractureEnamel infraction and uncomplicated enamel fractures require no emergency management. It is worth noting, however, that such damage can occur in combinations with pulpal inflammation from concussive trauma. The subsequent pulp necrosis will necessitate subsequent treatment. If there is pulp exposure, pulpal inflammation, infection and necrosis will always develop, and such teeth always require treatment. There are only three treatment options for teeth with pulp exposure:

1) exodontics (removal of the entire tooth and root)2) root canal treatment (removal of the vital structures of the tooth and

replacement with an inert filling material)3) pulp capping (removal of contaminated pulp and the placement of a “cap”

to stimulate the production of a reparative dentin “bridge” to seal the pulp chamber)

Of these three, only the pulp capping procedure is time critical as this is the only procedure that leaves a vital pulp, where infection or irreversible pulpitis will cause failure of the procedure. Extraction and root canal treatments can be done at a later time, and the only time critical component of these therapies is pain management.

Pulp Capping The term pulp capping refers to a procedure whereby the exposed pulp is covered with a layer of material to protect the pulp and encourage the pulp to produce new dentin to form a “bridge” to seal the pulp chamber. The capping layer is most often calcium hydroxide with a restoration placed over the top. In the setting of a tooth fracture, the superficial exposed pulp is removed and haemorrhage controlled prior to the calcium hydroxide and restoration being placed. With progressive inflammation, haemorrhagee is harder and harder to control, and there is increased bacterial contamination of the pulp, both of which are likely to cause subsequent pulp necrosis and failure of the procedure. Therefore, the sooner the procedure is performed after the tooth injury, the less likely it is to fail (Clarke, 2001, Niemiec, 2001, Murray et al, 2002). In a retrospective study (Clarke, 2001), the success of the treatment was 88.2% for cases where pulp capping was performed within 48 hours of the tooth injury, but fell to 23.5% for those teeth treated within 3 weeks. A smaller retrospective study (Niemiec, 2001) demonstrated 100% failure for teeth treated greater than 7 days post trauma. This study also looked at the ability of owners to detect failure and found poor correlation between the subjective owner impression and tooth vitality following this procedure. Therefore, a critical component of this procedure is the reevaluate pulp vitality with intraoral radiography six months post operatively, and semi-annually for at least two years following this.

If pulp capping fails, the pulp becomes irreversibly inflamed, or necrotic. Both of these situations result in chronic pain for the animal. Therefore, owners need to be counseled as to the risks of failure and need for radiographic follow-up prior to referral, and referral for the procedure needs to be arranged as soon as the animal is a suitable candidate for a general anaesthetic.

References:Clarke, DE Vital pulp therapy for complicated crown fracture of permanent canine teeth in dogs: a three-year retrospective study. J Vet Dent 2001 Sep;18(3):117-21

Murray PE, Fafez AA, Smith AJ, Cox CF Hierarchy of pulp capping and repair activities responsible for dentin bridge formation. Am J Dent 2002 Aug;15(4):236-43

Niemiec, BA Assessment of vital pulp therapy for nine complicated crown fractures and fifty-four crown reductions in dogs and cats. J Vet Dent 2001 Sep;18(3):122-5

Mandibular symphysis repair / Palatal injuries / Oral and tooth fractures (Dental perspective – Amanda Hulands – Nave); (ECC perspective – Eugene Buffa)

ANZCVS 2014 Proceedings Paper – Dental and Emergency & Critical Care Chapters Joint SessionDr Eugene Buffa BVSC M.MED.VET(surgery)Eastside Veterinary Emergency and Specialists (EVES), Rosebay, Sydney Dr Amanda Hulands-Nave BVSc(Hons) MVSt MACVSc (SA Med) MANZCVS (SA Dent)Bellarine Veterinary Practice, Geelong

MAXILLOFACIAL AND MANDIBULAR FRACTURESThe fractures that will be discussed in this presentation will be limited to those bones that contain teeth – the mandible and the maxilla. These fractures can be the result of trauma, but may also be pathologic, secondary to periodontal disease or neoplasia. As this is a joint session between the dentists and the emergency vets, we will concentrate predominantly on the traumatic injuries to the mandible and maxilla, but will discuss briefly periodontal pathologic fractures where they complicate the repair of traumatic fractures.Animals that are the victims of trauma will often present with multiple issues – shock, haemorrhage, internal injuries of abdomen and/or thorax, fractures of limbs or other bones, head injuries/brain injuries and skin wounds – in addition to fractures of the mandible and/or maxilla. This topic has been discussed by other presenters in this session, and so refer to those notes for that relevant information. CNS, cardiovascular and airways need to be considered along with soft tissue damage. Local anaesthesia with maxillary and mandibular nerve blocks can help control pain and windup. These two blocks used together will provide local anaesthesia to the entire region rostral to the blocks, both labially and palatally/linguially, compared with blocks further rostral (eg palatal, infraorbital or mental). Care needs to be taken with volume in small animals. Local anaesthetics can be administered quickly with very short neuroleptic anaesthesia or short general anaesthesia. Comprehensive oral examination requires a general anaesthetic. The maxilla, mandible and the temporomandibular joint all need to be palpated intraorally and extraorally to assess for alterations to normal anatomy. It is important to remember that fractures can be multiple. Four view survey radiographs will need to be taken ( DV, VD, standard and oblique laterals). Intraoral radiographs have more benefit in the mouth as it limits the amount of superimposition that is seen with extraoral skull radiographs. The caudal mandible can be difficult to radiograph adequately using intraoral techniques. If there is ready access to CT, this can be the most efficient technique, as it is quick and also gives a three dimensional image of all the injuries.There are essentially ten “commandments” of oral fracture repair. They are:

1. Restoration of occlusion2. Neutralisation of forces on fracture site3. Preservation of blood supply4. Rapid restoration of function

5. Avoidance of further soft tissue detachment from bone6. Avoidance of soft tissue entrapment7. Removal of diseased teeth within the fracture8. Proper assessment of tissue viability9. Avoidance of further dental trauma10. Aim to achieve primary bone healing by anatomic fracture reduction and

stable fixation.

The most critical of the ten commandments are restoration of occlusion and the consideration of forces on the fracture site, followed by preservation of blood supply and attachment and restoration of function.Consideration of major anatomical structures to avoid should also be given. These are the parotid duct, trigeminal nerve branches, mandibular canal and oral cavity foramens. Local anaesthesia of local nerves is essential for pain control and prevention of windup in these patients. Mandibular nerve blocks via the extra oral route can be done in conscious animals to provide adjunctive pain relief to control shock.There are many described techniques for oral fracture repair. The best technique for a given fracture can be made by weighing up the pros and cons of each technique. Many of the traditional surgical techniques have morbidities that far outweigh the minimally invasive dental repairs.Maxillofacial and mandibular fracture repair differ from long bones in many respects. The mandible does not have a medullary canal and about 50 % of its volume is filled by tooth roots. The maxillofacial skeleton consists of a thin lamina of bone with greater vascularity and rapid bone healing. Fracture of the mandible is painful because of concurrent trauma to the inferior alveolar nerve in the mandibular canal. The mandible cannot be rested when traumatised because drinking, eating, swallowing and panting cause continuous movement of the fracture site and traction on the nerve. This fracture stabilisation and repair should occur as soon as possible. The repair techniques will be discussed along with pros and cons of each technique with reference to the ten commandments above.

Dental techniques Interdental composite fixation

Protemp Garant used on teeth to secure fracture

Composite can break if used alone as not very strong

Interdental wiring

Wire can slip if used alone

Can use a needle to guide wire under gum between teeth

Creating gouges in teeth to allow the wire to sit better is contraindicated as the enamel cannot regenerate

Interdental reinforced composite fixaton

Combination of wire and composite allows for extra strength and stabilisation like reinforced concrete

For fractures where there are minimal teeth in the mandibular arcade, the vertical ramus can have soft tissue dissected off the bone, a hole drilled through the bone and the wire passed for the caudal anchoring point and then the rostral teeth used as normal

Interdental arcade composite fixation

Upper and lower canines are bonded together

Stronger light fixed acrylic required, a maxillomandibular suture can be added for extra stabilisation more caudally

This is good for multiple fractures

Can use coloured composites which aid in differentiation of the tooth enamel and the composite when removing the composite

Fractured teeth Fractured teeth are painful and a source of infection and need to

be addressed

Fractured teeth can be repaired with vital pulpotomy or root canal therapy if they meet the criteria for those procedures

Fractured teeth can be hemisected and treated endodontically if multirooted and one root is ok but the other is not

These teeth may be able to be salvaged long term, but in some cases may need to be removed after the fracture has healed

Surgical techniquesINDIRECT SURGICAL STABILISATION: These offer a biological approach to fracture repair with the advantage of non disturbance of the fracture site and preservation of the blood supply.

Tape Muzzle

Useful for caudal mandibular fractures, relatively stable fractures, temporomandibular joint (TMJ) fractures and luxations and for use in animals with deciduous teeth.

Disadvantages include patient compliance (cats do not tolerate them), difficulty in keeping clean and irritation to the skin.

Proprietary Muzzle

Indications as for tape muzzle

Involves having 2-3 proprietary muzzles in a size that still allows drinking and panting

Rotate muzzles so there is always one on the pet and one being cleaned +/- another spare

BI – gnathic encircling and retaining devise (BEARD)

A strong suture encircling the mandible and maxilla, crimped ventrally (Nicholson et al VCOT 2/2010)

Good to stabilise caudal mandibular fractures and TMJ fractures or luxations

Does not require the presence of 4 intact canine teeth.

Cannot be used with concurrent maxillary fractures unless they are simultaneously rigidly repaired.

Complications relate to swelling and discharge associated with suture irritation, especially over the dorsum of the nasal bone.

Mandibulomaxillary suture

To avoid the complications associated with suture irritation over the dorsum of the nose, the mandibular maxillary fixation suture is secured with two buttons placed on the dorso lateral aspect of the upper lips. This technique is particularly valuable in cats.

DIRECT SURGICAL STABILISATION:

Perimandibular (circumferential) wiring

Indicated for repair of mandibular symphysis separation – effectively a cerclage wire around the mandibles immediately caudal to the canine teeth with the twist positioned ventrally

Consideration should be given to using a heavy gauge nylon instead of wire for these repairs as there is less soft tissue injury to both the cat and Grandma when the cat rubs its face on her fragile arms

Suture rather than wire can also prevent the external rotation of the lower canine teeth from a wire repair that is too tight

The wire or suture is removed after 6 weeks.

Intraosseus wiring

Effectively interfragmentary wires placed through drill holes in adjacent fracture fragment. They rely on the static frictional forces generated by the tension in the wire to stabilise the fractures.

Require anatomical reduction of the fractures and do not neutralise rotation or bending forces.

In the mandible, the wires should be placed along the alveolar margin (tension side) and combined with a second wire along the ventral bone margin to neutralise shear and rotation.

In the maxilla, they are frequently combined with a skewer pin to prevent overriding of the fragments.

There is danger with this technique in damaging tooth roots and entering the mandibular canal

Soft tissues in the mouth can also be damaged and become infected, especially if the wire twist penetrates the mucosa.

Intramedullary pins

There is a lot of danger with this technique in damaging the neurovascular structures in the mandibular canal as well as the tooth roots.

This method cannot be recommended.

External fixation

This method provides semi-rigid fixation of the mandible. It works very well if combined with other methods of stabilisation (e.g. Intraosseus wiring) and in fractures with severe soft tissue injury (e.g. gun shot trauma)

Pin placement should be aimed at the alveolar margin (tension side), avoidance of the tooth roots is important. The use of an acrylic cementing bar simplifies the application.

Strength of the fixation can be improved by using multiple, positive profile pins, engaging both mandibles with the pins, using multiple connecting bars and employing a type 2 (bilateral) frame design.

Pin loosening and sepsis can be a problem, especially in the caudal part of the mandible

Requires significant post operative attention and there is a danger to owners of injury

Plate fixation

Miniplates (Low profile, Titanium plate and screws) have proven to be very efficacious in maxillofacial and caudal mandibular fracture repair in the dog where they provide three dimensional buttress support

Due to their small size, they must be placed along the tension side of the fracture. This requires that they be positioned along the alveolar border of the mandible body and that the tooth roots be avoided by directing the screws between the roots.

Similarly, they should be positioned along the coronoid and condylar crest of the mandibular ramus.

They should always be used in pairs on the mandible – one on the alveolar margin and one on the ventral margin to address shearing and torsional loads.

Require fairly extensive soft tissue exposure and sometimes there can be difficulty closing the soft tissues over the plate. Plate exposure may require the use of a buccal mucosa advancement flap to cover it, or removal of part of the exposed plate.

Resections

Resection of part of the mandible or maxilla may be required if the bone is so badly damaged or pathological that repair is impossible

The bone is removed and soft tissues closed over the top.

Most patients seem to cope very well with the loss of part of the maxilla or mandible.

Other injuriesPalatal defects

These can be acquired or congenital. These defects can be primarily repaired by direct apposition, or by use of

flaps (the latter are more successful) Double layer closure with the suture line away from the defect is ideal.

Flaps can be harvested and repositioned from the cheeks, lips and soft palate (mucosal), from the hard palate and gingiva (mucoperiosteal) and with attached afferent blood vessels (axial pattern flaps - angularis oris flap or island palatal flaps).

All attempts should be made to preserve maximum vascularity to the flaps, including extraction of interfering teeth if necessary

Patient should receive nil by mouth for 10-14 days, nutrition can be provided via a tube feeding. The flap beds are allowed to heal by second intention.

Surgical repair of congenital defects is usually delayed until the patients are 16 weeks of age. Palatoplasty preformed prior to this can hinder maxillofacial growth and development.

TMJ luxations Occur as a result of head trauma. May be uni or bilateral. Most commonly

the mandibular condyles displace craniodorsally. These animals usually have an open mouth and are reluctant to close it. Diagnosis is by careful palpation under GA and by imaging (4 view

radiographs or CT) – check for a widening of the TMJ space. Closed reduction with a dowel rod to act as a fulcrum is usually

successful, followed by maxillo-mandibular fixation for 10-14 days. Open surgical reduction is described for irreducible luxations TMJ luxations should be differentiated from TMJ dysplasia which

produces open jaw locking (treatment of the latter involves partial Zygomatic arch resection or mandibular condylectomy)

High Rise Syndrome Falls from at least 2 stories, especially cats. They usually sustain the following injures:

o Soft tissue facial abrasions and avulsion of the lower lipo Dental fractureso Mandibular fractures – particularly symphyseal separation and

condylar fractureso Midline palatal fracture or separation.

Adjunctive therapiesMultimodal analgesia and fluid therapy are very important in the postoperative period. It is important to allow adequate nutrition to be gained by these animals as there are often multiple injuries. Facial injuries can often cause significant swelling to the oral regions. As such, consideration should be given to the need for a

tracheostomy if there is significant compromise to the airways, and the provision of a oesphagostomy tube to provide nutrition.Cats often have a poorer prognosis than dogs with these types of injuries, so I am very aggressive with placing an oesophagostomy tube in cats at the time of initial anaesthetic at which diagnosis and repair takes place. Tubes can always be removed at a later time if not needed, but it is a relatively easy procedure to do and with the risk of hepatic lipidosis, deciding to put in a tube later may be after the horse has bolted and the risks increase.Frequent oral rinses with tap water or a suitable anti septic solution to prevent food and plaque accumulation that occur with intraoral and external fixation. Antibiotic therapy is valuable, typically a 5-7 day course .Most oral fractures will heal in 3-6 weeks. Non-unions are deemed to be those fractures which have not healed in 6 weeks.

Discussion forum (Rebecca Tucker / Christine Hawke Co- chairs)

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Dental Radiology Q and A (Tony Caiafa)

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KEYNOTE PRESENTATION

Principles and Practice of Rotary EndodonticsDr Ross Applegarth BDS, MDSc FICD MRACDS(Endo)

Dr Ross Applegarth has been a registered specialist endodontist since 1993. He joined the Endodontic Group in Brisbane after completing his Master of Endodontics at the University of Queensland. Prior to studying endodontics, Ross enjoyed eight years in general dentistry and travelled extensively throughout the United Kingdom and Europe. Ross has held executive positions with the Australian Society of Endodontology at State and Federal levels, serving as Federal President between 2005 and 2007. He has lectured extensively throughout Queensland and also Internationally. He has most recently been active in delivery of rotary instrumentation lectures and workshops. Ross has been involved with the endodontic teaching programs at all Queensland dental schools, and currently lectures and demonstrates for undergraduate endodontic programs at Griffith University in Queensland. Ross has also acted as external examiner for the Queensland University post graduate endodontic program. Ross has been inducted into the International College of dentists, and is a member of the Royal Australasian College of Dental Surgeons. Ross has a special interest in endodontic retreatment outcomes and endodontic rotary instrumentation.