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Lung ultrasound and confirming pericardial effusion

Lecture Time
09:25 AM - 09:50 AM
Authors
Room
Hall 711
Date
07/16/19, Tuesday
Time
09:25 AM - 10:15 AM

Abstract

Abstract Body

See proceedings co-authored and submitted with Dr Chalhoub for this session

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Rock & roll, turn and dance in circles - Work-up and manage vestibular diseases successfully

Lecture Time
08:00 AM - 08:50 AM
Authors
Room
Hall 714
Date
07/19/19, Friday
Time
08:00 AM - 08:50 AM

Abstract

Abstract Body


Rock & roll, turn and dance in circles - Work-up and manage vestibular diseases successfully

Prof. Holger A. Volk, DVM, PhD, PGCAP, DipECVN

University of Veterinary Medicine Hannover, Germany

The vestibular system main function is to maintain an animal’s equilibrium during movement and orientation against gravity. It is divided into two main sections, the peripheral and the central. The peripheral one is composed of cranial nerve VIII (CNVIII; vestibulocochlear nerve) and sensory receptors contained within the petrosal bone. The central one is that part of the vestibular system held within the cranial vault, i.e., the vestibular nuclei of CNVIII. The peripheral system detects linear acceleration and rotation movement of the head. It is responsible to maintain the position of the eyes, neck, trunk and limbs in reference to the position of the head.

The sensory receptors of the vestibular system are located in the inner ear. The sacculus and the utriculus are located in the vestibule and detect linear acceleration and head positioning against gravity. The semicircular ducts with their ampullae detect rotational acceleration. There are three semicircular ducts, which are orientated in each dimensional direction.

The vestibular nerve fibres travel in CNVIII, terminate mainly in one of the four vestibular nuclei, but also in the cerebellum. A pathway (medial longitudinal fasciculus) connects the medial vestibular nucleus with the nuclei of III (N. occulomotorius), IV (N. trochlearis) and VI (N. abducens) to control eye movements. Other pathways connect the vestibular nuclei with the cerebellum, cerebrum, other brainstem centre (e.g. vomiting centre) and the spinal cord. The vestibular system is mainly unilateral. The lateral vestibular nucleus give rise to a pathway to the spinal cord ventral grey matter and is facilitatory to the extensor muscle (inhibiting the contralateral extensor tone and the ipsilateral flexor muscle).

Keeping this in mind, it is logically that a head tilt and a reduced extensor tone of the limbs are on the side of the lesion. “It looks like the animal is running around a curve”. The jerk nystagmus develops from the dysfunction of the pathways connecting the vestibular nuclei with the cranial nerve nuclei responsible for the eye movement. When the head moves, no / uncoordinated eye movements can be seen. The slow phase of the jerk nystagmus goes into the direction of the lesion; the fast phase is the compensatory one. Vision and proprioception can help to compensate the vestibular dysfunction. This can be often observed in clinics as vestibular disease can progressively improve.

Clinical signs of dysfunction of the vestibular system are: loss of balance, head tilt, leaning, rolling, circling, nystagmus, strabismus, and depending on the type of vestibular disease, other cranial nerve deficits, Horner's Syndrome, cerebellar signs, mental depression and hemiparesis with postural reaction deficits. By defining the clinical signs present the clinician will be able to determine central vs. peripheral vestibular disease. Because the list of differentials depends on the location of the lesion, this determination is most important (see below).

Nystagmus -There is the "normal" physiological nystagmus that we can elicit performing the occulovestibular test or by spinning the animal (together with the clinician) around its on axis. Another type of "normal" nystagmus would be the pendulous nystagmus of particular cat breeds (Siamese, Birman and Himalayan), which is caused by a larger numbre of fibres crossing at the optic chiasm. The pendulous nystagmus is characterised by equal speed of eye movement to both sides. There is also a searching type nystagmus described in animals, which have been born blind.

Abnormal types of nystagmus would be the jerk nystagmus with a slow and a fast phase with varied directions; horizontal, rotatory or vertical. These may be conjugate or disconjugate, they may also be positional. Positional nystagmus will vary with the patient depending on its head position. The direction of the nystagmus is always defined by the fast phase, even if the slow phase is to the side of the lesion.

Strabismus -Certain cat breeds (Siamese) may have congenital divergent strabismus. A divergent strabismus may also be seen in severe cases of hydrocephalus. The strabismus seen with vestibular disease is ventrolateral (unilateral) and is not responsive to the occulovestibular test. It is seen in the eye ipsilateral to the lesion. This does not differentiate central from peripheral vestibular disease.

Leaning, falling, circling - The patient tends to lean or fall toward the affected side because the vestibular system facilitates the extensors of the ipsilateral side (see also above). The patient also tends to circle toward the affected side as with lesions of the forebrain. However, the circles of vestibular disease tend to be closer and tighter rather than the large roaming circles of forebrain disease. The patient with central vestibular disease is more likely to be non-ambulatory.

The head tiltis on the side ipsilateral to the lesion, unless, the lesion is in the flocculonodular lobe of the cerebellum or the cerebellomedullary pontine angle; then the patient may have aparadoxical head tilt. In this case, the head tilts to the contralateral side. Because the lesion involves the cerebellar projections to the vestibular nuclei, and because the cerebellum is predominantly inhibitory in effect, the side of the lesion becomes overactive, giving excessive tone to the extensors of that side and causing the patient to lean and tilt away from the lesion. However, the side of the lesion can be determined by testing the proprioception, especially paw positioning which are reduced to absent on the side of the lesion.

Horner’s syndromeis characterised by the loss of sympathetic innervation to the eye. In dogs and cats fibres of the postganglionic sympathetic fibres travel through the middle ear before following the ophthalmic nerve of the trigeminal nerve. A damage at this site can cause a Horner’s syndrome. The postganglionic sympathetic fibres innervate the smooth muscle of the periorbit and eyelids (also third eyelid in the cat). Furthermore, they innervate the dilator pupillaris and iris muscle. Therefore, the cardinal signs decribed by Dr. Horner were: 1. Enophthalmos; 2. Third eyelid protrusion; 3. Ptosis; 4. Miosis. As the sympathetic system also controls the smooth muscles in blood vessel, a failure of the system results in congested vessels. This can be best appreciated on the sclera and the ear.

Sometimes the patient may present with bilateral vestibular disease. One typically sees wide excursions of the head, symmetrical ataxia, no head tilt and the patient may not demonstrate a "normal" physiological nystagmus. Examples would be aminoglycoside toxicity, bilateral otitis media/interna in cats, and congenital bilateral vestibular disease in young Doberman Pinchers.

Differentials to consider for peripheral vestibular disorders

Category

Acute nonprogressive

Acute progressive

Chronic progressive

Degenerative

Congenital vestibular syndrome

Metabolic

(Diabetes mellitus; indirect)

Hypothyroidism

Neoplastic

Metastatic

Soft tissue tumours

Nerve sheath tumour

Inflammatory / infectious

Otitis media/interna (bacterial)

Protozoal

Otitis media/interna (bacterial)

Protozoal

Idiopathic

Idiopathic (vascular?)

Traumatic

Fracture

Toxic

Streptomycin

Gentamycin

Streptomycin

Gentamycin

Vascular

Infarction

Septic emboli

Hemmorrhage

The diagnostic work-up may vary greatly between central versus peripheral disease but all patients should have a complete blood count, biochemistries, thyroid screening and blood pressure evaluation. Even if it is only a geriatric with idiopathic vestibular syndrome, there may be an underlying renal deficiency and the nausea/vertigo may be enough to keep the patient from drinking adequately, precipitating renal failure.

Given a peripheral vestibular location, radiography of the skull with oblique views and open mouth can be considered, but the main investigation will be an otoscopic examination of the external ear canal and the tympanic membrane. If the potential for otitis media exists then myringotomy is simple and quick. It does necessitate some form of short acting sedation. Cultures and cytology may be obtained from within the bullae. Take note that the bullae of the canine are different from the cat. The feline has two compartments in the bulla. Myringotomy is done in the ventrocaudal aspect of the tympanic membrane. The resultant puncture in the membrane is quick to heal.

Central vestibular disease will almost always require advanced imaging. This is the most important reason to localise as it will change the way how you work up the case. It is generally believed that it has to do with determining the prognosis. But the prognosis is determined by the diagnosed disease process and not by the location of the lesion. We have diagnosed many animals with soft tissue sarcomas invading the middle ear (poor prognosis) and vice versa have diagnosed dogs with cerebellar infarcts (usually good prognosis).

Differentials to consider for central vestibular disorders

Category

Acute nonprogressive

Acute progressive

Chronic progressive

Anomalous

(Hydrocephalus)

Degenerative

Neurodegenerative diseases

Storage diseases

Metabolic

Hypoglycaemia

Neoplastic

Metastatic

Primary: Choroid plexus papilloma,Glioma,

Meningioma or secondary such as lymphoma

Nutritional

Thiamine def. (usually bilateral)

Inflammatory / infectious

FIP

Protozoal

FIP

Protozoal

Toxic

Lead

Hexachlorophene

Metronidazole (usually bilateral)

Lead

Hexachlorophene

Traumatic

Fracture/bleed

Vascular

Infarction

Septic emboli

Haemmorrhage

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Oral Pathology

Lecture Time
08:30 AM - 09:20 AM
Room
Hall 701
Date
07/16/19, Tuesday
Time
08:30 AM - 09:20 AM

Abstract

Abstract Body

ORAL PATHOLOGY

Brook A. Niemiec, DVM, DAVDC, DEVDC, FAVD

Southern California Veterinary Dental Specialties & Oral Surgery

San Diego, CA USA

Kymberley Stewart DVM

Idexx laboratories

Toronto, ON, Canada

Orthodontic (bite) problems

Orthodontic problems may be purely cosmetic or can result in trauma to the lips, gums, palate, or teeth. By far, the most common cause of malocclusions is hereditary. Additional genetic causes include tongue size as well as lip and cheek tension.

These patients often do not show any overt clinical signs other than the jaws or teeth being out of alignment. Depending on the type and severity of the problem, oral trauma may be present and can result in bleeding, oral pain, gum disease, tooth death and even nasal infection.

Therapy for malocclusions is relative to type and severity of the disease process. Options include:

• No therapy (if purely cosmetic).

• Extraction of the offending tooth or teeth.

• Orthodontic correction using appliances.

• Lowering the tooth and then protecting the root canal (Coronal amputation and vital pulp therapy)

Persistent deciduous teeth

Persistent deciduous teeth are very common, especially in small and toy breed dogs. However, they can occur in any breed as well as cats. They create both orthodontic and periodontal problems if not treated promptly. It used to be believed that the persistent deciduous caused the permanent tooth to become malocclused. Studies have shown, however, that it is the permanent tooth erupting incorrectly that causes the deciduous to be persistent.

It has been reported that orthodontic problems begin within two weeks of the permanent canines starting to erupt. This is due to the deciduous tooth being in the place that the adult wishes to occupy.

The periodontal issues occur due to a disruption of the normal maturation of the periodontium. When there is a persistent deciduous tooth, one area of the periodontium is not attaching to the permanent, therefore the periodontal attachment in that location will not be normal. It has been reported that the damage begins within 48 hours of the permanent teeth starting to erupt!

Therefore, the adult tooth does not need to be completely erupted for these problems to occur, and they should be extracted as early as possible, do not wait until six months of age to perform the extractions along with neutering. In fact, we recommend that the owners of breeds prone to retain their teeth be instructed to watch for eruption of the permanent teeth and to present the patient for therapy as soon as this occurs.

Fractured teeth

The two main types of crown fracture seen in veterinary medicine are complicated and uncomplicated. Both types require therapy; however treatment for each is often different.

All teeth with direct pulp exposure (complicated crown fractures) should be treated with endodontic or exodontic therapy; ignoring them is NOT an option. Prior to tooth necrosis, the viable nerve is excruciatingly painful. Following tooth death, the root canal system will act as a bacterial super-highway creating not only local infection, but also a bacteraemia which has been linked to more serious systemic diseases (see the article on periodontal disease for further information). The owners of these patients will be reluctant to pursue therapy as “It does not seem to bother the dog”. Fractured and/or infected teeth do bother the pet and they will act better following therapy. Veterinary patients are known for being stoic, and therefore lack of outward signs of oral pain should not be misinterpreted as a benign state. Therefore, you must be a patient advocate and recommend therapy.

Uncomplicated crown fractures are also a very common finding on oral exam, particularly in large breed dogs. These fractures will result in direct dentinal exposure. The exposed dentinal tubules will create significant pain for the patient. The currently accepted means by which this sensitivity is created is via the theory of fluid dynamics. In addition, some of these teeth will become non-vital due to the traumatic incident, pulpal inflammation, or direct pulpal invasion via the dentinal tubules. For these reasons, it is recommended that these teeth be radiographed to ensure vitality. If the teeth are non-vital (evidenced by periapical rarefaction or a widened root canal) endodontic or exodontic therapy is required. If the teeth appear vital, the application of a bonded composite is recommended to decrease sensitivity.

Intrinsically stained teeth: Endodontic disease is also manifested by intrinsic staining. This can appear as pink, purple, yellow, or grey. A study by Hale showed that only 40% of intrinsically stained teeth had radiographic signs of endodontic disease, however 92.7% are non-vital. Non-vital teeth lose their natural defence ability and are often infected via the bloodstream, which is known as anachorisis. Therefore, do not rely on radiographic appearance to determine vitality; all teeth should be definitively treated via root canal therapy or extraction.

Enamel hypocalcification (hypoplasia)

Areas of enamel hypocalcification will generally appear stained a tan to dark brown (rarely black) color, and may appear pitted and rough. The tooth surface is hard however, as opposed to the soft/sticky surface of a caries lesion. The areas of weakened enamel are easily exfoliated which will expose the underlying dentin, resulting in staining. Dentin exposure will result in significant discomfort for the patient.

The roughness of the teeth will also result in increased plaque and calculus retention, which in turn leads to early onset of periodontal disease.

Treatment is aimed at removing sensitivity, avoiding endodontic infection by occluding the dentinal tubules, and smoothing the tooth to decrease plaque accumulation. The most efficient and effective way to accomplish these goals is placement of a bonded sealant or composite restoration.

Feline Tooth Resorption (TR):

The best diagnostic tool for differentiating between types is dental radiology. With type 1 lesions, there is no replacement of the lost root structure by bone, whereas with type 2 there is generally marked replacement of the lost tooth structure.

Type 1 TRs are typically associated with inflammation such as caudal stomatitis or periodontal disease. In these cases, it is thought that the soft tissue inflammation has activated the odontoclasts. Type 2 lesions are generally seen in otherwise healthy mouths; however the lesions will create local gingivitis. The etiology of type 2 TRs remains unproven.

Recently, crown amputation has been suggested as an acceptable treatment option for advanced type 2 lesions as it results in significantly less trauma and faster healing than complete extraction. This procedure, although widely accepted, is still controversial. Most veterinary dentists employ this technique, however in widely varying frequency. Veterinary dentists typically employ this treatment option only when there is significant or complete root replacement by bone. Unfortunately, the majority of general practitioners use this technique far too often. Crown amputation should only be performed on teeth with radiographically confirmed advanced type 2 TRs which show no peri-apical or periodontal bone loss. Crown amputation should not be performed on teeth with: type 1 TRs, radiographic or clinical evidence of endodontic or periodontal pathology, inflammation, or infection; or in patients with caudal stomatitis. Those practitioners without dental radiology capability SHOULD NOT perform crown amputation. In these cases, the teeth should either be fully extracted or the patient referred to a facility with dental radiology.

Missing teeth

There are several reasons that teeth may be missing. These reasons include: congenitally missing, previously extracted, fractured (or extracted) with retained roots, or impacted. The first two scenarios do not require therapy, where as the latter two may necessitate intervention. Therefore, dental radiographs are indicated in all cases of “missing teeth”.

If dental radiographs reveal retained roots and evidence of inflammation or infection (clinical or radiographic), the teeth should be surgically extracted. If they are “quiet”, the owners should be informed and given the option of having the teeth surgically extracted.

Impactions occur most commonly in the maxillary cuspid and premolar teeth (especially PM1). They also occur most often in toy and small breeds as well as brachycephalic dogs.

These patients generally have no overt clinical signs other than a missing tooth in a young animal. Alternatively, there may be a persistent deciduous tooth present.

On occasion, an unerupted tooth may lead to the development of a dentigerous cyst. Pathologic changes were noted in 29% of cases in one veterinary study. Consequently, the presenting complaint or oral examination finding may be a swelling in the area of a “missing” tooth.

A dentigerous cyst is a fluid filled structure which develops from the enamel forming organ, of an unerupted tooth. Small dentigerous cysts are generally asymptomatic, and often go undiagnosed without dental radiology. Dentigerous cysts can become quite large and disfiguring, requiring major surgical correction. Dental radiographs are generally diagnostic, revealing a unilocular radiolucent area that is associated with the crown of an unerupted tooth.

Surgical removal of the offending tooth and careful debridement of the cystic lining will prove curative. It is important to avoid leaving any of the cystic lining behind, as this could allow the cyst to reform. Early surgical intervention will result in the least invasive surgery possible.

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Use of ultrasound in emergency medicine: indications, benefits, and pitfalls

Lecture Time
08:55 AM - 09:20 AM
Authors
Room
Hall 711
Date
07/16/19, Tuesday
Time
08:30 AM - 09:20 AM

Abstract

Abstract Body

See proceedings co-authored and submitted with Dr Chalhoub for this session

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Water quality in Koi practice

Lecture Time
08:30 AM - 09:20 AM
Authors
Room
Hall 705
Date
07/16/19, Tuesday
Time
08:30 AM - 09:20 AM

Abstract

Abstract Body

WATER QUALITY IN KOI PRACTICE

Nick Saint-Erne, DVM, CertAqV

Certified Aquatic Veterinarian

Phoenix, Arizona, USA.

nsainterne@gmail.com

With any animal, environmental conditions can affect their overall health, but with aquatic animals such as fish, proper water quality is an important part of keeping them healthy. Without clean water, the fish will be stressed and more susceptible to diseases and parasites. This lecture will provide veterinarians with information regarding how to test pond water and what the various water chemistry characteristics mean for the health of the fish. Correcting water quality problems is also included in the discussion.

Water quality can be measured with test kits available through pet stores or pond supply companies, or from many aquaculture suppliers. The simplest tests are small plastic strips with chemical pads attached that are dipped into the water to be tested. The pads change color which, when compared to a color chart, indicates the level of that substance in the water. These are fast, easy to use, inexpensive, and relatively accurate (they indicate a range rather than a precise measurement). Dry tablet tests are also available where a small tablet is dissolved into a test tube containing the water sample. Its color is then compared to a chart to determine the results. Some test kits have liquids that are mixed with the water to produce the color reactions. More expensive test kits use a spectrophotometer to electronically compare colors and these give more accurate results. Effective electronic meters are also available for some water tests.

Temperature:

Koi (Cyprinus carpio) have a preferred optimum temperature range of 18-25 degrees Celsius (65-77 degrees Fahrenheit), but are able to survive at temperatures below or above this range. Gradual changes in water temperature within a fish’s optimum range seldom cause health problems. Ideally, water temperature fluctuations should be no more than 3°C change per day. Temperature shock can occur with rapid changes, especially from warmer water to cooler water. Increasing the water temperature will lower the saturation point of dissolved oxygen (warmer water holds less oxygen than cooler water). It will also increase the toxicity of dissolved substances such as ammonia, chlorine, and heavy metals.

Chlorine and Chloramine:

Chlorine and chloramine are used by water municipalities to make the water supply safe for human consumption. These compounds are extremely toxic to aquatic organisms and no amount can be tolerated by fish. There should never be any chlorine detectable in aquarium or pond water! Add sodium thiosulfate or other dechlorinator to the koi pond whenever adding tap water of if chlorine is detected.

Ammonia:

Ammonia in the water reduces the ability of the fish to excrete nitrogenous wastes from their blood through the gills. As ammonia increases in the water, so do nitrogenous waste products increase in the fish’s blood, causing toxicity, gill damage, and death. Ammonia is mostly converted to nontoxic ammonium at a pH level below 6.5, but above 6.5 ammonia can become toxic very quickly if allowed to accumulate. The higher the pH and temperature of the water, the more toxic ammonia becomes. The ammonia in the pond water is broken down by aerobic nitrifying bacteria into nitrite and then into nitrate. Properly operating biological filtration systems (after they have been cycled) should keep ammonia levels at 0.0 mg/L in the water.

In the event of a filtration system problem that creates high ammonia levels (>0.25 mg/L), Ammonia Neutralizing products can be added to the pond to bind the ammonia in a nontoxic form until water changes can be used to bring the ammonia level down. Failure to eliminate the ammonia through water changes will result in elevated nitrite levels a few days later.

Note: Some municipalities add chloramine to the water to make the tap water safe for human consumption. Contact the local water service if unsure of the chemicals being used in the tap water. Fish keepers in areas that have chloramine added to the tap water need to use an ammonia neutralizer as well as a chlorine remover to make the tap water safe for use in their aquarium or pond.

Nitrite:

Nitrite is produced by the aerobic bacterial nitrification of ammonia. It should also be maintained at a level of 0.0 mg/L. Nitrite reduces the ability of the fish’s blood to carry oxygen. Salt in the water at 0.1-0.3% salinity will block the absorption of nitrite by the fish’s gills. Remove any nitrite from the system by performing a partial water change. Nitrite will also be converted to nitrate by a different species of aerobic nitrifying bacteria.

Nitrate:

Nitrate is produced by the aerobic bacterial nitrification of nitrite. While high nitrate levels are dangerous to saltwater fish and invertebrates, freshwater fish are very tolerant of high nitrate levels. Most freshwater fish can tolerate levels of 100 mg/L for short periods of time without significant problems. It is preferable to maintain nitrate below 10-20 mg/L, and periodic water changes in the pond should keep the nitrate level down. If nitrate levels exceed 20 mg/L, additional water changes can be used to lower the concentration. High levels of nitrate also promote algae growth.

pH:

The potentia Hydrogenii, or power of Hydrogen, is the acid-base balance in water. Most freshwater fish are highly adaptable to slow changes in the pH as long as it is not too extreme (less than 5.5 or above 8.5). Rapid changes in pH are more detrimental to fish, and it is very important that the pond water has a stable pH. The stability of the pH is related to water Alkalinity and Hardness. If there are extremes of pH, or rapid fluctuations, it is likely because the alkalinity is too low.

Alkalinity:

Alkalinity is a measurement of the negative ions (e.g., Hydroxide, Carbonate, Bicarbonate) in the water that buffer against pH shifts. Ideal alkalinity for koi is in the 100-250 mg/L range. As the alkalinity falls, the water in a pond may experience sudden, and deadly, pH shifts. If it happens in your system you can increase the buffering capacity of the water to stabilize the low pH by adding supplements such as sodium bicarbonate or calcium carbonate to raise the alkalinity.

Hardness:

Hardness is the measurement of metallic positive ions (e.g., Calcium, Magnesium) in the water. Water with high hardness usually also has a high pH. Softening the water will lower the mineral content and the pH. Hardness in koi ponds is best at 100-250 mg/L. Most fish will adapt to existing hardness as long as it is not too extreme of a change.

Summary:

Water testing is one of the most important aspects of maintenance for your filtration systems. It is an important key in determining how the biological filters are functioning. Keep a log book of the water test results, to monitor changes in the water parameters. Water testing is not something to be taken lightly.

Periodic partial water changes using dechlorinated tap water will keep pond water values normal. The frequency of changes will depend on the water test results, but normally once per month in established ponds is sufficient. Examples of incidents requiring increased water changes include toxin contamination, abnormal pH or alkalinity values, high ammonia, nitrite or nitrate levels, or over-medication. Test the water after performing a partial water change; if necessary, repeat partial water change to correct water quality parameters. Test the source water (tap water) to ensure it has the correct water parameters fo the fish, and adjust with chemicals as necessary.

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Basic diagnostic techniques for fish

Lecture Time
09:25 AM - 10:15 AM
Authors
Room
Hall 705
Date
07/16/19, Tuesday
Time
09:25 AM - 10:15 AM

Abstract

Abstract Body

BASIC DIAGNOSTIC TECHNIQUES FOR FISH

Julius M. Tepper

Long Island Fish Hospital

1 Saddlebrook Lane, Manorville, NY 11949

cypcarpio@aol.com

As with all our diagnostic protocols for different species in veterinary medicine, the first step is to observe the patient (or patients) in their natural environment. In fish medicine, this means slowly approaching the pond or tank to note the movements and interactions of the fish. Stressors, such as water quality and temperature issues, parasites, feeding behavior abnormalities and cohort interactions may manifest themselves in gross or subtle changes in fish behavior. The direct physical exam can then be done after capture and before microscopic exam sampling. Many species are sedated for this sampling. The general condition of the skin, eyes, mouth and fins are noted. A small sample of peripheral gill tissue is excised (gill snip) and placed on a glass slide. A drop of tank water is applied and covered with a coverslip. These will then be examined to determine the microscopic condition of the gill tissue and check for the presence of parasites. Small samples of gill tissue, obtained non-lethally in this way, can also be submitted to the lab for histopathology and viral antigen identification. Similarly, several samples of skin mucus are obtained by gently but firmly scraping craniocaudally with a coverslip (preferably plastic) in high- probability areas. These are typically areas of minimal water movement, such as behind the pectoral fins. Scrapings should also be done at the periphery of any skin lesions found. A fin clip at the tip of any fin can be useful to identify bacterial, fungal and/or parasitic lesions. Blood analysis can be useful to identify internal disease conditions, though less so than in homeotherms. This is because parameters will vary depending on water temperatures, making standardized norms harder to establish. In some species, important viral screening can be done via blood tests. Many different locations are sampled, depending on the species and size of the patient. In typical pet fish species, such as koi and goldfish, the caudal vein is accessed via a ventrodorsal puncture, similar to the technique used for reptiles. In large specimens, the lateral cutaneous vein can also be sampled via an anterolateral needle insertion. Fecal exams are often done to identify parasites or ova. Radiology can be useful to visualize internal abnormalities. Of particular interest is the condition of the swimbladder, which may be affected when buoyancy disorders occur. A horizontal beam lateral x-ray, with or without sedation, is useful to visualize fluid in the swimbladder. Ultrasound is also a beneficial diagnostic procedure to identify solid masses and when fluid is found to be present in the swimbladder, to help guide the aspiration procedure.

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Water biology for healthy freshwater aquasystem

Lecture Time
11:15 AM - 12:05 PM
Authors
Room
Hall 705
Date
07/16/19, Tuesday
Time
11:15 AM - 12:05 PM

Abstract

Abstract Body

WATER BIOLOGY FOR HEALTHY FRESHWATER AQUASYSTEMS

Julius M. Tepper

Long Island Fish Hospital

1 Saddlebrook Lane, Manorville, NY 11949

cypcarpio@aol.com

In natural bodies of freshwater, the purification of pathogens from the water column occurs primarily in wetlands. Four processes have been identified in achieving this end, being: aggregation (floc formation) and sedimentation; adsorption on suspended inorganic matter; competitive inhibition and ingestion by beneficial micro-organisms; and the presence of antibiotics and biocides produced by beneficial micro-organisms and plants. Despite the absence of inorganic matter, it is possible to identify and utilize both floc formation and sedimentation and competitive inhibition and ingestion in purifying artificial freshwater aquasystems. It is also likely that antibiotics and biocides produced by algae and higher plants may play a role in purifying artificial systems.

Aggregation of suspended organic matter and pathogens into settleable solids (floc) is primarily due to the presence of mucopolysaccharides in the water column. These have been highly exploited in treating storm runoff water and sewage water. Many commercial preparations of bacterial origin are used to this end. Of interest to aquaculture is the presence of nematodes in the substrate which produce these mucopolysaccharides. as well as those of bacterial origin. Once floc formation has occurred, upflow filtration provides excellent separation of settleable solids via sedimentation for removal from the aquasystem.

Competitive inhibition and ingestion by beneficial micro-organisms is an important function which occurs primarily in the microstructure of the periphyton. Many of the rotifers of natural bodies of freshwater can be present in artificial aquasystems. They require a suitable substrate on which to attach and a steady gentle flow of highly oxygenated water. Many of these sessile rotifers, such as stentor, vorticella and epistylis may take months or years to develop their potential in a given aquasystem. Of particular interest is the motile rotifer Philodina, which can swim through the water column or crawl along the microstructure to a desirable location. These rotifers possess the ability to process large quantities of organics and bacteria under ideal conditions. They can reproduce and mobilize rapidly when conditions warrant. They are also capable of anhydrobiosis, thus not killed through desiccation. A suitable substrate microstructure, which supports these rotifers and nematodes, while facilitating the transit of highly oxygenated water will maximize the purification process in filtering artificial aquasystems.

The antibiotic and biocidal effects of both algae and higher plants has yet to be studied, but their presence in the aquasystem, where possible, is desirable for the removal of iron, nitrates and phosphates from the system.

Based on these processes, a phytoremedial device was developed for use in artificial aquasystems. When combined with an upflow refugium, a synthetic wetlands filter was produced. Once biologically activated and planted with a terrestrial plant, excellent control of ammonia, nitrite and nitrate was achieved. Lower turbidity levels were measured compared to the inert control setup.[1],[2] Further testing for the control of a pathogenic strain of Aeromonas sobria introduced into the aquasystem proved the synthetic wetlands filter to be highly effective.[3] Additional testing in an aquasystem housing a painted turtle Chrysemys picta for an extended period showed excellent control of total coliforms.[4]

[1] A PHYTOREMEDIAL DEVICE FOR KOI PONDS; Julius M. Tepper, Proceedings of the IAAAM, 2000

[2] THE USE OF AN UPFLOW REFUGIUM AND PHYTOREMEDIAL DEVICE FOR WATER PURIFICATION IN CLINICAL PET FISH PRACTICE Julius M. Tepper Proceedings of the IAAAM, 2004

[3] TESTING A REFUGIUM AND PHYTOREMEDIAL DEVICE FOR THE CONTROL OF A PATHOGENIC STRAIN OF Aeromonas sobria; Julius M. Tepper* and Tirath S. Sandhu Proceedings of the IAAAM, 2005

[4] TESTING A REFUGIUM AND PHYTOREMEDIAL DEVICE FOR THE CONTROL OF TOTAL COLIFORMS IN AN AQUATIC REPTILE HABITAT Julius M. Tepper and Tirath S. Sandhu Proceedings of the IAAAM, 2007

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Update on Insulin Therapy: What’s available and when to use it

Lecture Time
08:30 AM - 09:20 AM
Authors
Room
Hall 717
Date
07/16/19, Tuesday
Time
08:30 AM - 09:20 AM

Abstract

Abstract Body

UPDATE ON INSULIN THERAPY:

WHAT’S AVAILABLE AND WHEN TO USE IT

Jon M. Fletcher, DVM, DACVIM

Louisiana State University, Baton Rouge, LA, USA

jmfletcher@lsu.edu

OVERVIEW AND CLASSIFICATION OF INSULIN

Insulin is classified by source, duration of action, and preparation. Today, the majority of available insulin preparations are human recombinant or synthetic insulin. In fact, Vetsulin® is the only remaining animal source (porcine) insulin in use today. When classified by onset and duration of action, insulin preparations are classified as rapid-acting, short-acting, intermediate-acting, or long-acting. The rapid-acting and majority of the long-acting insulin preparations are human insulin analogs, which are created by modifying the amino acid structure of recombinant human insulin. In general, these alterations make absorption and duration of action more consistent and predictable. This has led to an overall decrease in the occurrence of hypoglycemic episodes in human diabetics. This is in comparison to crystalline insulin preparations (e.g. NPH, Vetsulin®, PZI) where the addition of protamine and/or zinc promotes the formation of insulin hexamers leading to a slower onset and longer duration of action. Hexamer dissociation is associated with greater variability in absorption and duration of action, and increases the risk of hypoglycemic events.

CURRENTLY AVAILABLE INSULIN PREPARATIONS

Rapid-acting: Insulin lispro (Humalog®)

Insulin aspart (NovoLog®)

Insulin glulisine (Apidra®)

Short-acting: Regular insulin (Humulin® R, Novolin® R)

Intermediate-acting: NPH (Humulin® N, Novolin® N)

Lente insulin- 30% semilente + 70% ultralente (Vetsulin®)

Long-acting: Insulin glargine- 100 U/ml (Lantus®, Basaglar®)

Insulin glargine- 300 U/ml (Toujeo®)

Insulin detemir- 100 U/ml (Levemir®)

Protamine Zinc Insulin (ProZinc®)

INSULIN THERAPY IN DOGS

Intermediate-acting insulin formulations continue to be the most commonly used and recommended insulin preparations for the management of canine diabetics. The two currently available intermediate-acting insulin formulations are NPH and Vetsulin®. The starting dose is 0.25-0.5 U/kg every 12 hours with acceptable glycemic control being achieved in most dogs with a dose of 0.5-1 U/kg every 12 hours. The long-acting insulin formulations have been evaluated in dogs, and there does not appear to be a clear benefit to using insulin glargine (Lantus®) or PZI (ProZinc®) in the management of dogs. Insulin detemir (Levemir®) results in improved glycemic control in some dogs but the potency (Levemir® starting dose: 0.1-0.2 U/kg) of the formulation limits its use in small dogs. The low potency of Lantus® and Toujeo® make these formulations useful in small dogs that are unregulated but have recurrent hypoglycemia with small doses (1-3 U) of NPH or Vetsulin®. Long-acting insulin analogs are an option for dogs in which acceptable glycemic control cannot be achieved with NPH or Vetsulin®.

The use of a rapid-acting insulin analog administered concurrently with NPH has been investigated in a small group of dogs. This protocol (i.e., administration of a rapid-acting insulin with an intermediate-acting maintenance insulin) is similar to protocols commonly used to manage human diabetics. In the trial, insulin lispro was administered with NPH at mealtime in six dogs that were considered to have well-regulated diabetes while receiving NPH, but continued to have a profound postprandial spike in blood glucose. Subcutaneous insulin lispro at a dose of 0.1 U/kg was well tolerated and blunted the postprandial spike (decreased the blood glucose at 60 and 90 minutes). Although this approach may prove beneficial in dogs that have unacceptable glycemic control related to postprandial hyperglycemia, this combination protocol is likely not necessary for the majority of canine diabetics and increases the risk of hypoglycemia. When initiating this protocol, it is recommended that the maintenance insulin dose be reduced by at least as many units as the number of units of rapid-acting insulin being added (i.e., total units of insulin being administered is the same or less). This will hopefully decrease the potential for hypoglycemic complications.

INSULIN THERAPY IN CATS

It is possible to achieve ideal glycemic control in most cats with twice daily administration of long-acting insulin formulations. The time-action profile of these insulins is more appropriate in cats than intermediate-acting insulins and higher remission rates are reported in cats receiving long-acting insulin preparations. Currently available formulations that are routinely used in cats include insulin glargine (Lantus®), PZI (ProZinc®), and insulin detemir (Levemir®). The recommended starting dose for these long acting formulations is 1-2 U/cat every 12 hours. The majority of cats will have acceptable glycemic control at a dose of 1-6 U/cat every 12 hours. Twice daily insulin administration is recommended and is more likely to result in good glycemic control. If it is not possible to administer insulin twice daily, once daily administration of Levemir® or Toujeo® (starting dose: 1-2 U/cat) may provide acceptable control of clinical signs and decrease the occurrence of complications associated with untreated diabetes mellitus. Toujeo® has been studied in healthy cats, but there is limited information about clinical use available.

INSULIN THERAPY FOR DIABETIC KETOACIDOSIS (DKA)

The three protocols for the treatment of DKA that have been described in veterinary medicine include administration of human regular insulin via intravenous constant rate infusion (CRI), hourly intramuscular (IM) insulin, and IM insulin administered every 4 to 6 hours. Many clinicians consider intravenous CRI the standard of care although the ideal route of administration remains a matter of debate. More recently, insulin lispro and insulin aspart administered as an intravenous CRI have been successfully used to treat DKA in dogs. It was concluded that these rapid-acting analogs are a safe and effective alternative to regular insulin although a clinically significant benefit was not identified.

To the author’s knowledge, subcutaneous administration of rapid-acting insulin analogs for the treatment of DKA in dogs and cats has not yet been investigated. This treatment may provide an alternative to CRI and IM regular insulin protocols in cats and dogs, and may have advantages when compared to traditional protocols. Results obtained in the author’s research laboratory in healthy cats combined with the clinical data obtained in people suggests that a subcutaneous insulin aspart protocol could be an effective treatment for cats with DKA. This type of intermittent treatment protocol could be a better option for intermediate care wards or veterinary facilities that do not have an intensive care unit or access to numerous intravenous fluid pumps. The ability to use rapid-acting analogs to treat dogs and cats with DKA may be of greater importance in the future if regular insulin becomes unavailable due to decreasing demand for the management of human diabetics.

REFERENCES

Brunton S, Heile M, Schneider D, Meneghini L, Reid T, King A. Update on insulin management in type 2 diabetes. The Journal of Family Practice. 2012;61:S4-S12.

Fleeman L, Rand JS (2013). Canine Diabetes Mellitus. In J. Rand (Ed.), Clinical endocrinology of companion animals. Ames, Iowa: John Wiley & Sons, Inc.

Gilor C, Graves TK. Synthetic insulin analogs and their use in dogs and cats. Vet Clin N Am Small Anim Pract. 2010;40:297-307

Marshall RD, Rand JS, Morton JM. Treatment of newly diagnosed diabetic cats with glargine insulin improves diabetic control and results in higher probability of remission than protamine zinc and lente insulins. J Feline Med Surg. 2009;11L683-689.

Rand JS (2013). Feline Diabetes Mellitus. In J. Rand (Ed.), Clinical endocrinology of companion animals. Ames, Iowa: John Wiley & Sons, Inc.

Roomp K, Rand JS. Management of diabetic cats with long-acting insulin. Vet Clin N Am Small Anim Pract. 2013;43:251-266.

Sako T, Mori A, Lee P, et al. Time action profiles of insulin detemir in normal and diabetic dogs. Res Vet Sci. 2011;90:396-403.

Bertalan AV, Drobatz KJ, Hess RS. NPH and lispro insulin for treatment of dogs with diabetes mellitus [abstract]. J Vet Intern Med 2014;28:1026.

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How to Deal with Problem Diabetics

Lecture Time
09:25 AM - 10:15 AM
Authors
Room
Hall 717
Date
07/16/19, Tuesday
Time
09:25 AM - 10:15 AM

Abstract

Abstract Body

HOW TO DEAL WITH PROBLEM DIABETICS

Jon M. Fletcher, DVM, DACVIM
Louisiana State University, Baton Rouge, LA, USA
jmfletcher@lsu.edu


MAINTENANCE INSULIN THERAPY IN DOGS

Intermediate-acting insulin preparations continue to be the most commonly used and recommended preparations for the management of canine diabetics. The two currently available intermediate-acting insulin preparations are NPH (Humulin® N, Novolin® N) and Vetsulin®.

Dosing Recommendations

NPH and Vetsulin®
-0.25 – 0.5 U/kg subcutaneously every 12 hours
-Acceptable glycemic control achieved with 0.5 – 1 U/kg every 12 hours in most dogs
-Begin suspecting and evaluating for causes of insulin resistance when dose is ≥ 1.5 U/kg
-Consider changing insulin formulation if dose ≥ 2 U/kg and no cause of resistance or lack of acceptable glycemic control identified
-Insulin should be administered at the time of feeding to avoid hypoglycemia and minimize postprandial hyperglycemia

DIETARY RECOMMENDATIONS

It is most important that the type and amount of food remain consistent and that all or most of the calories (including treats) be consumed at or near the time of insulin administration. Ideally, food consumption would coincide with maximal insulin activity, but this could be challenging to predict, create unnecessary stress for the pet owner, and increase the risk of hypoglycemia because of variability in the onset of action. It is possible to achieve acceptable glycemic control in most dogs that consume a balanced maintenance diet at the time of insulin administration. It is also worth noting that it has not been possible to identify a clear benefit to feeding high-fiber, moderate-carbohydrate, and moderate-fat diets. High-fiber, calorie restricted diet formulations should not be fed to dogs that are underweight and/or have decreased lean body mass.

GOALS OF THERAPY

-Resolution of clinical signs
-Normal activity level and good quality of life
-Stable body weight
-Avoidance of hypoglycemic episodes
-Ideal glycemic control (BG < 250 mg/dL for majority of the day) is nice but not always necessary to achieve the above goals




REASONS FOR POOR REGULATION

Insulin therapy
-Underdosing (common cause)
-Insulin time-action profile not appropriate
-Handling issues and/or inactivation
-Administration issues
Treatment regimen
-Inconsistent feeding and/or insulin administration time
-Access to food and/or treats throughout the day
-Increased activity/exercise
Insulin resistance
-Urinary tract infection
-Pancreatitis
-Cardiac disease
-Renal disease
-Diestrus
-Hyperlipidemia
-Hyperadrenocorticism
-Hypothyroidism

MONITORING AND INSULIN DOSAGE ADJUSTMENT

Changes in the insulin dose should be based on clinical assessment combined with some assessment of glycemic control (blood glucose curves or continuous glucose monitoring). The parameters that are considered when determining how much the insulin dosage should be increased include the degree of hyperglycemia, the size of the dog, and the current insulin dose (U/kg). Although dependent on the degree of hyperglycemia, the dose is typically increased by 1-2 units per dose in small dogs and 2-3 units per dose in larger dogs.

Continuous Glucose Monitoring (dogs and cats)

The FreeStyle Libre continuous glucose monitoring system provides a readily available, cost-effective way to continuously assess glycemic control over a 14-day period. This system does not require calibration so the owner does not have to obtain blood samples from the pet to check the blood glucose concentration. Continuous glucose monitoring is the recommended assessment method for any challenging diabetic and could replace the blood glucose curve in most diabetics.

Home Blood Glucose Curve Protocol (dogs and cats)

-Use a hand-held glucometer that has been designed and validated for use in dogs and cats
-Blood glucose before food and insulin administration
-Feed and administer insulin
-Blood glucose 1 hour after food and insulin, then every 2 hours (every 4 hours in cats receiving long-acting preparations) until the next dose of insulin


Despite substantial day-to-day variation in BG curves, a complete 12-hour BG curve can provide useful information when evaluating a poorly regulated diabetic, especially if continuous glucose monitoring is not an option. Blood glucose curves may provide more accurate information when performed in the home environment. It is recommended that BG curve data from multiple days during a 2-3 week period be evaluated prior to recommending significant changes such as a change in the insulin formulation. This will allow the clinician to evaluate trends rather than basing the decision on a single BG curve that may not be an accurate representation of the overall glycemic control. Routine blood glucose monitoring also plays an important role in detecting subclinical hypoglycemia.

DIETARY MANAGEMENT OF UNREGULATED DIABETIC DOGS

Consider a moderately to markedly carbohydrate-restricted diet (15-30% metabolizable energy from carbohydrate) in dogs with unacceptable glycemic control that appears to be associated with postprandial hyperglycemia. Dietary fat restriction is recommended for diabetic dogs that have persistent hypertriglyceridemia and/or recurrent pancreatitis.

USING LONG-ACTING INSULIN FORMULATIONS IN DOGS

Based on the currently available clinical data, there does not appear to be an obvious benefit to using long-acting insulin analogs in most dogs. The low potency of Lantus® (insulin glargine 100 U/ml) and Toujeo® (insulin glargine 300 U/ml) make them useful in small dogs that are unregulated but have recurrent hypoglycemia with small doses of NPH or Vetsulin®. These formulations have a slower onset of action and a more gradual glucose lowering effect. Levemir® (insulin detemir 100 U/ml) is an option for dogs in which acceptable glycemic control cannot be achieved with NPH or Vetsulin®. The author has observed improved glycemic control when switching to Levemir® even if a short duration of action is not the cause of poor regulation. Levemir® is a potent insulin formulation and a dosage reduction is necessary when switching from NPH or Vetsulin®. The recommended starting dose for insulin detemir is 0.1-0.2 U/kg, which limits the use of this insulin in small dogs. The long-acting insulin analogs are substantially more expensive than NPH and Vetsulin®. For this reason, the use of long-acting analogs is often reserved for cases in which acceptable glycemic control cannot be achieved with standard therapy.

USING RAPID-ACTING INSULIN ANALOGS AT MEALTIME

It is standard practice to use two insulin formulations in the management of human diabetics. One preparation is a short or rapid-acting insulin that is administered at mealtime (bolus), while the other has an intermediate or long duration of action (basal insulin) and maintains the BG during periods of fasting. This is not commonly recommended in diabetic dogs because it increases the risk of hypoglycemia and because it is often possible to achieve acceptable glycemic control with a single insulin preparation administered twice daily.

The use of a rapid-acting insulin analog administered concurrently with NPH was investigated in a small group of dogs. Insulin lispro (Humalog®) was administered with NPH at mealtime in six dogs that were considered to have well-regulated diabetes while receiving NPH, but continued to have a profound postprandial spike in blood glucose. Subcutaneous insulin lispro at a dose of 0.1 U/kg was well tolerated and blunted the postprandial spike (decreased the blood glucose 60 and 90 minutes after eating). Although this approach may prove beneficial in dogs that have unacceptable glycemic control related to postprandial hyperglycemia, this combination protocol is likely not necessary for the majority of canine diabetics and could increase the risk of hypoglycemia. When initiating this protocol, it is recommended that the maintenance insulin dose be reduced by at least as many units as the number of units of rapid-acting insulin being added (i.e., total units of insulin being administered is the same or less). This will hopefully decrease the potential for hypoglycemic complications. It is not appropriate to substitute regular insulin for a rapid-acting analog in this protocol. Regular insulin has a slower onset of action, longer duration of effect, and will increase the risk of hypoglycemia.

Case example: 20 kg dog receiving 30 units of NPH every 12 hours but continues to have profound postprandial hyperglycemia associated with unacceptable glycemic control.

Recommendation: Add insulin lispro at the starting dose of 0.1 U/kg = 2 units

New insulin dosing protocol: 25-28 units NPH (dosage reduction) + 2 units insulin lispro every 12 hours.

Recommend performing a blood glucose curve (or using a continuous glucose monitor) following the first administration of the rapid-acting analog to confirm that hypoglycemia is not an immediate concern.

MAINTENANCE INSULIN THERAPY IN CATS

It is possible to achieve ideal glycemic control in most cats with twice daily administration of long-acting insulin formulations. The time-action profile of these insulins is more appropriate in cats than intermediate-acting insulin formulations and higher remission rates are reported in cats receiving long-acting insulin preparations. Currently available formulations that are routinely used in cats include insulin glargine (Lantus®), PZI (ProZinc®), and insulin detemir (Levemir®). The recommended starting dose for these long acting formulations is 1-2 U/cat every 12 hours. The majority of cats will have acceptable glycemic control at a dose of 1-6 U/cat every 12 hours. Twice daily insulin administration is recommended and is likely to result in better glycemic control than once daily administration. If it is not possible to administer insulin twice daily, once daily administration of Levemir® or Toujeo® (starting dose: 1-2 U/cat) may provide acceptable control of clinical signs and decrease the occurrence of complications associated with untreated diabetes mellitus. Toujeo® has been studied in healthy cats, but there is limited information about clinical use available.

DIETARY RECOMMENDATIONS

-Low carbohydrate diet (Purina DM, Hill’s Prescription Diet m/d)
---Associated with better clinical control, reduce insulin requirements, and increased remission rates
-Meal feeding is ideal, but eating does not need to be coordinated with insulin administration (grazing is allowed)
-Recommend weight loss in obese cats
---1-2% loss of body weight per week
-Have had success with Hill’s Prescription Diet Metabolic when cats gain weight or fail to lose weight with classic high protein/low carbohydrate diets.

GOALS OF THERAPY

-Resolution of clinical signs
-Normal activity level and good quality of life
-Stable body weight
-Possible to achieve ideal glycemic control in most cats with long-acting insulin
-Diabetic remission

REASONS FOR POOR REGULATION

Insulin therapy
-Underdosing
-Time-action profile is not appropriate (use of intermediate-acting insulin)
-Handling issues and/or inactivation
-Administration issues

Insulin resistance
-Hypersomatotropism / Acromegaly- recommend screening (measure IGF-1 concentration) all diabetic cats 6-8 weeks after initiating insulin therapy
-Urinary tract infection
-Pancreatitis
-Renal disease
-Hyperthyroidism
-Hyperadrenocorticism

MONITORING AND INSULIN DOSAGE ADJUSTMENT

Increases in the insulin dosage should be based on the presence of clinical signs combined with an objective assessment of glycemic control (see above- continuous glucose monitoring [FreeStyle Libre], home blood glucose curves, fructosamine concentration, HbA1c, +/- urine glucose monitoring). Routine blood glucose monitoring allows for assessment of glycemic control as well as detection of subclinical hypoglycemia. This is especially important in cats because of the possibility of diabetic remission (return to a noninsulin-dependent state). The insulin dose in cats is typically increased by 1-2 U per dose.

REFERENCES

1. Brunton S, Heile M, Schneider D, Meneghini L, Reid T, King A. Update on insulin management in type 2 diabetes. The Journal of Family Practice. 2012;61:S4-S12.
2. Fleeman L, Rand JS (2013). Canine Diabetes Mellitus. In J. Rand (Ed.), Clinical endocrinology of companion animals. Ames, Iowa: John Wiley & Sons, Inc.
3. Gilor C, Graves TK. Synthetic insulin analogs and their use in dogs and cats. Vet Clin N Am Small Anim Pract. 2010;40:297-307
4. Marshall RD, Rand JS, Morton JM. Treatment of newly diagnosed diabetic cats with glargine insulin improves diabetic control and results in higher probability of remission than protamine zinc and lente insulins. J Feline Med Surg. 2009;11L683-689.
5. Rand JS (2013). Feline Diabetes Mellitus. In J. Rand (Ed.), Clinical endocrinology of companion animals. Ames, Iowa: John Wiley & Sons, Inc.
6. Roomp K, Rand JS. Management of diabetic cats with long-acting insulin. Vet Clin N Am Small Anim Pract. 2013;43:251-266.
7. Sako T, Mori A, Lee P, et al. Time action profiles of insulin detemir in normal and diabetic dogs. Res Vet Sci. 2011;90:396-403.
8. Bertalan AV, Drobatz KJ, Hess RS. NPH and lispro insulin for treatment of dogs with diabetes mellitus [abstract]. J Vet Intern Med 2014;28:1026.
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But it has to be Cushing’s… Challenges in diagnosing canine hyperadrenocorticism

Lecture Time
11:15 AM - 12:05 PM
Authors
Room
Hall 717
Date
07/16/19, Tuesday
Time
11:15 AM - 12:05 PM

Abstract

Abstract Body

BUT IT HAS TO BE CUSHING’S…CHALLENGES IN DIAGNOSING CANINE HYPERADRENOCORTICISM

Jon M. Fletcher, DVM, DACVIM
Louisiana State University, Baton Rouge, LA, USA
jmfletcher@lsu.edu

DIAGNOSING HYPERADRENOCORTICISM (HAC)

Testing is divided into screening (confirming the presence of HAC) and differentiation (pituitary dependent hyperadrenocorticism or functional adrenal tumor). It may be necessary to perform multiple screening tests or repeat testing at a later date in order to confirm the diagnosis in early or more challenging cases.

SCREENING TESTS

Urine cortisol to creatinine ratio (UCCR)

-Most commonly used to rule out HAC when there is a low clinical index of suspicion
-False-positive results are common because stress/non-adrenal illness can cause an increase in the UCCR
-Recommend performing a low-dose dexamethasone suppression test or ACTH stimulation test after obtaining a positive UCCR because of the lack of specificity (high risk of false positive results)

-Protocol:

---Client/owner collects a urine sample at home. Urine should not be collected in the hospital or within 48-72 hours of a clinic/hospital visit because the stress of a clinic/hospital visit has been shown to increase the UCCR and increases the possibility of a false-positive result.
------Typically recommend first urination in the morning
------Using pooled samples (3 consecutive days) may provide a more representative result

-Interpretation:

---Normal ratio (below the laboratory cut-off)– HAC is very unlikely
---Abnormal ratio (above the laboratory cut-off)– recommend performing another screening test (low-dose dexamethasone suppression test or ACTH stimulation test) to confirm HAC prior to initiating therapy

Low-dose Dexamethasone Suppression Test (LDDS)

-Highly sensitive test
-Greater chance of false-positive result with non-adrenal illness than ACTH stimulation test (not a significant concern if screening an appropriate population)
-Can also serve as a differentiating test if positive and meet criteria for pituitary dependent HAC



-Protocol:

---Collect baseline blood sample
---Administer 0.01-0.015 mg/kg of dexamethasone or dexamethasone SP intravenously (preferred) or intramuscularly
---Collect blood samples at 4 and 8 hours after the administration of dexamethasone

-Interpretation:

---Normal dog- complete suppression at 4 and 8 hours
---Consistent with HAC- lack of suppression at 4 and/or 8 hours
------Lack of suppression does NOT confirm the presence of a functional adrenal tumor (FAT).
---Consistent with pituitary dependent hyperadrenocorticism (PDH)
------Suppression at 4 hours with an escape at 8 hours
------Suppression at 4 and/or 8 hours to less than 50% of the baseline cortisol concentration

ACTH Stimulation Test

-Less sensitive test than LDDS test
-Less chance of false-positive result than LDDS test
-Only test that can diagnose iatrogenic HAC

-Protocol:

---Obtain baseline blood sample
---Administer synthetic ACTH (cosyntropin or tetracosactrin) intravenously at a dose of 5 μg/kg (maximum dose 250 μg/dog)
---Obtain blood sample 1 hour after administering ACTH (post-ACTH). Some clinicians also collect a 2-hour post-ACTH sample in order not to miss (get a false-negative result) the small percentage of dogs that have peak cortisol secretion after 2 hours rather than 1 hour.

-Interpretation:

---Normal dog- post ACTH cortisol concentration below the laboratory cut-off
---Consistent with HAC- post ACTH cortisol concentration above the laboratory cut-off

Basal or Resting Cortisol Concentration

-No diagnostic value for HAC

Below is the author’s approach to screening for HAC. The decision to perform additional screening tests following a negative LDDS test is based on the degree of clinical suspicion. In situations of high clinical suspicion, it is important to remember that no screening test is perfect. It may be necessary to perform multiple screening tests or repeat testing at a later date in order to confirm the diagnosis in early or more challenging cases.

cushings1.png

DIFFERENTIATING TESTS

High-dose Dexamethasone Suppression Test

-Protocol (same as LDDS test but with higher dose of dexamethasone):

---Collect baseline blood sample
---Administer 0.1 mg/kg of dexamethasone or dexamethasone SP intravenously (preferred) or intramuscularly
---Collect blood samples at 4 and 8 hours after the administration of dexamethasone
-Results can support the presence of PDH
-Results CANNOT confirm the presence of a FAT

-Interpretation:

---Consistent with PDH
------Complete suppression at 4 and/or 8 hours
------Cortisol concentrations less than 50% of baseline concentration at 4 and/or 8 hours
--Lack of suppression does NOT confirm the presence of a FAT.

Endogenous ACTH Concentration

-Single blood sample
-Immediately centrifuge and separate plasma from cells and freeze until shipping. Ship overnight on ice. This will minimize the amount of degradation, which is a concern with inappropriate sample handling.
-Possible to confirm PDH or an FAT

-Interpretation:

---Consistent with PDH- ACTH concentration is normal or increased
---Consistent with presence of a FAT- ACTH is low or undetectable

Ultrasonography

-Evaluate size and appearance of adrenal glands
-Can confirm presence of an adrenal tumor
-Aid in the detection of concurrent illness

Below is the author’s approach to differentiating PDH from FAT. The author believes it is important to confirm a FAT with ultrasound and endogenous ACTH prior to surgery because asymmetric adrenal gland enlargement and nodular hyperplasia is not uncommon with PDH.

cushings2.png


OCCULT HYPERADRENOCORTICISM

-Historically known as “atypical hyperadrenocorticism”
-Clinical signs, physical examination findings, and clinicopathologic findings support a diagnosis of HAC, but the UCCR, LDDS test, and ACTH stimulation test fail to support the diagnosis.
-It has not been proven that sex hormones are responsible for this syndrome.
-Reasons to suspect Occult HAC
---Clinical signs consistent with HAC
---Cortisol concentrations on ACTH stimulation test and LDDS test are below the reference interval
-Presence of an adrenal tumor supports the diagnosis
---Lack of tumor does not rule out diagnosis
-If clinical signs are mild, retest for classical HAC when signs worsen
-If clinical signs are moderate/severe, perform an abdominal ultrasound
---Normal adrenal glands- reconsider diagnosis
---Bilateral adrenomegaly- consider confirming PDH with cross-sectional imaging
-May be mild or early HAC
-May be food-dependent HAC (considered rare)
-Specificity of sex hormone panel is low- interpret with caution


REFERENCES

Behrend E.N., Melian C. Hyperadrenocorticism in dogs. In J. Rand (Ed.), Clinical endocrinology of companion animals. Ames, Iowa: John Wiley & Sons, Inc; 2013.
Behrend E.N. Canine Hyperadrenocorticism. In EC Feldman, RW Nelson, C Reusch, JC Scott-Moncrieff (Eds). Canine and Feline Endocrinology. Elsevier Health Sciences; 2014.
Behrend E.N., Kooistra H.S., Nelson R., Reusch C.E., Scott-Moncrieff J.C. Diagnosis of spontaneous canine hyperadrenocorticism: 2012 ACVIM consensus statement (small animal). J Vet Intern Med; 2013
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Trilostane Treatment and Monitoring: Is the ACTH stimulation test gone for good?

Lecture Time
12:10 PM - 12:35 PM
Authors
Room
Hall 717
Date
07/16/19, Tuesday
Time
12:10 PM - 12:35 PM

Abstract

Abstract Body

TRILOSTANE TREATMENT AND MONITORING: IS THE ACTH STIMULATION TEST GONE FOR GOOD?

Jon M. Fletcher, DVM, DACVIM

Louisiana State University, Baton Rouge, LA, USA

jmfletcher@lsu.edu

TRILOSTANE

Trilostane (Vetoryl®, Dechra Pharmaceuticals) is licensed for use in dogs for the treatment of pituitary-dependent hyperadrenocorticism as well as for hyperadrenocorticism resulting from a functional adrenocortical tumor. It is an orally active synthetic steroid analog that inhibits 3-beta-hydroxysteroid dehydrogenase (and 11-beta hydroxylase) in the adrenal cortex leading to decreased production of cortisol and to a lesser extent aldosterone. Trilostane is not cytotoxic and does not damage the adrenal cortex so withdrawal of the drug should result in a fairly rapid increase in the cortisol concentration unless adrenal necrosis has occurred. Adrenal necrosis is an uncommon complication that can occur during treatment with trilostane and is thought to be related to an increased ACTH concentration (endogenous and potentially exogenous from repetitive ACTH stimulation testing associated with therapeutic monitoring). Numerous clinical trials have confirmed the efficacy of trilostane for the treatment of hyperadrenocorticism, and the majority of dogs have good clinical response with minimal side effects/complications.

DOSING RECOMMENDATIONS

The manufacturer recommends starting trilostane therapy at a dose of 2.2 – 6.7 mg/kg (1 – 3 mg/lb) once daily with food (Vetoryl® package insert).

The most common starting dose in our hospital is 1 – 2 mg/kg (0.5 – 1 mg/lb) every 12 hours with food. Some authors have recommended administering this dose once daily, but in our experience once daily administration in this dosage range (1 – 2 mg/kg) does not provide adequate cortisol suppression and clinical control in most cases.

Dosing frequency continues to be a topic of debate. While once daily administration may improve compliance and reduce the cost of treatment, it is our experience that twice daily administration of a lower dose results in superior clinical control and reduces the risk of complications associated with excessive cortisol suppression.

The commercially available capsule sizes (5 mg, 10 mg, 30 mg, 60 mg, 120 mg) allow the targeted dose to be administered to most dogs without the need for compounding. If an additional size is needed, the commercially available product (Vetoryl®) can be reformulated into the appropriate capsule size by a compounding pharmacy.

MONITORING AND DOSAGE ADJUSTMENT

Dechra’s European division has recently changed the monitoring recommendations for Vetoryl® because of a shortage of synthetic ACTH in Europe. Research performed at the University of Glasgow and surrounding veterinary practices in the United Kingdom found that the pre-trilostane (before the next dose) resting cortisol concentration correlated better with clinical control than did the post-pill resting (baseline) and/or post-ACTH cortisol concentrations. It is important to recognize that the pre-trilostane resting cortisol is not the same as the post-trilostane resting cortisol (baseline sample of the ACTH stimulation test performed after trilostane administration), which is not a useful monitoring tool. Although multiple research groups have shown that the post-trilostane ACTH stimulation test (historical monitoring approach) is not a very useful monitoring tool, they have been unable to identify an alternative and superior monitoring option. The pre-trilostane (before the next dose) resting cortisol concentration may be a better alternative to the post-trilostane ACTH stimulation test. In Europe, the manufacturer recommends combining clinical assessment with the pre-trilostane resting cortisol concentration (ideal range: 1.5 – 5 mg/dL [40 nmol/L – 140 nmol/L]) to determine if a dosage change is necessary. It is important to note that clinical assessment and the presence of clinical signs should always be considered when determining if an increase in the trilostane dosage is warranted regardless of the monitoring protocol utilized. It should also be noted that using the pre-trilostane resting cortisol concentration for monitoring should be reserved for dogs that are clinically well. Dogs that are exhibiting signs of cortisol deficiency should have a complete evaluation including an ACTH stimulation test performed.

Although the monitoring recommendations have not “officially” changed in the United States, a number of institutions in the US are evaluating the use of the pre-trilostane resting cortisol concentration for monitoring trilostane therapy. Similar to what has been reported by researchers in the UK, we have found the pre-trilostane cortisol concentration and clinical assessment/response to be an effective and safe way to monitor most dogs that are clinically well. If a single cortisol measurement is to be used for monitoring purposes (synthetic ACTH is not available or an ACTH stimulation test cannot be performed because of financial limitations), the pre-trilostane cortisol concentration will likely provide the most clinically useful information.

Current Monitoring Options

Pre-trilostane resting cortisol concentration (attractive because inexpensive and convenient)

Post-trilostane ACTH stimulation test (remains most common monitoring protocol in US)

Pre-trilostane cortisol + post-trilostane ACTH stimulation test (recommended for any dog exhibiting signs of cortisol deficiency)

It is very important that clinical control and/or persistence of clinical signs associated with hypercortisolemia be considered when interpreting the results of any monitoring test/protocol and determining if a trilostane dosage increase is necessary.

Author’s Recommendations Based on the Post-ACTH Cortisol Concentration 2-4 hours after trilostane administration.

Post-ACTH Cortisol Concentration

Recommendation

< 1 mg/dL (< 28 nmol/L)

Stop treatment. Evaluate electrolytes; ACTH stimulation test (off of trilostane) in 2 weeks and/or re-start trilostane at a lower dose if/when clinical signs reoccur.

< 1.8 mg/dL (< 50 nmol/L)

Temporarily stop treatment. Re-start at a lower dose

1.8 – 9.1 mg/dL (50 – 250 nmol/L)

Either: Continue current dose if clinical signs are well controlled

Or: Dosage increase based on clinical assessment and persistence of clinical signs

> 9.1 – 16.3 mg/dL (> 250 – 450 nmol/L)

Either: Continue current dose if clinical signs are well controlled

Or: Dosage increase based on clinical assessment and persistence of clinical signs

> 16.3 mg/dL (> 450 nmol/L)

Dosage increase based on clinical assessment and persistence of clinical signs

Author’s Recommendations Based on the Pre-trilostane Cortisol Concentration (modified from the Pre-VetorylÒ Cortisol monitoring guidelines; Dechra Europe)

Pre-trilostane Cortisol Concentration

Recommendation

< 1 – 1.5 mg/dL (< 28 – 40 nmol/L)

Consider a lower dose

1.5 – 5 mg/dL (40 – 140 nmol/L)

No clinical signs of HAC- continue current dose

Or: Increase dosage or dosing frequency (once to twice daily) if inadequate clinical control/persistent clinical signs

3 – 5 mg/dL (80 – 140 nmol/L)

No clinical signs of HAC- continue current dose

Or: Increase dosage or dosing frequency (once to twice daily) if inadequate clinical control/persistent clinical signs

> 5 mg/dL (> 140 nmol/L)

No clinical signs of HAC- continue current dose

Or: Increase dosage or dosing frequency (once to twice daily) if inadequate clinical control/persistent clinical signs

Monitoring Frequency and Recommended Testing

10 – 14 days after initiating therapy or a dosage change: confirm that the dog is clinically well; no hormone testing necessary if no signs of cortisol deficiency

4 – 6 weeks: cortisol monitoring (see Current Monitoring Options)

2 – 3 months: cortisol monitoring (see Current Monitoring Options)

4 – 6 months: cortisol monitoring (see Current Monitoring Options), electrolytes

Recommend re-evaluation 2 – 3 times per year as long as the dose is stable, clinical signs are well-controlled, and the dog is doing well.

Dosage Adjustment

Dosage adjustments should be based on a combination of clinical assessment (persistence of clinical signs) and serum cortisol concentrations.

The trilostane dose should be increased by 5 – 10 mg/dose depending on the cortisol concentrations, severity of clinical signs, size of the dog, current dose, and frequency of administration.

If the dog is receiving once daily trilostane and the cortisol concentrations are within the recommended/acceptable ranges but clinical signs are not well-controlled (persistent polyuria, polydipsia, polyphagia, and/or other signs), divide the dose and administer twice daily. If the cortisol concentration(s) are above the recommended range(s), divide the dose for twice daily administration and increase by 10-25%.

REFERENCES

References available upon request.

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Monitoring canine and feline diabetics: beyond the glucose curve

Lecture Time
12:35 PM - 01:00 PM
Authors
Room
Hall 717
Date
07/16/19, Tuesday
Time
12:35 PM - 01:00 PM

Abstract

Abstract Body

MONITORING CANINE AND FELINE DIABETICS: BEYOND THE GLUCOSE CURVE

Jon M. Fletcher, DVM, DACVIM
Louisiana State University, Baton Rouge, LA, USA
jmfletcher@lsu.edu



MONITORING AND INSULIN DOSAGE ADJUSTMENT

Increases in the insulin dose should be based on the presence of clinical signs (polyuria and polydipsia, changes in body weight) combined with proof of hyperglycemia and/or unacceptable glycemic control (continuous glucose monitoring, blood glucose [BG] curves, glycated proteins [fructosamine, HbA1c]). Prior to recommending an insulin dosage increase, one should consider the severity of clinical signs, degree of hyperglycemia, size of the animal (typically increase by 1 unit/dose in cats/small dogs and 2-3 units/dose in larger dogs), and the current insulin dose (consider causes of insulin resistance or need to change formulations when dose is >1.5-2 U/kg). In order to avoid overdosing and hypoglycemia, it is recommended to wait at least 7-10 days following an increase in the insulin dose before considering another dosage increase.

Urine Glucose Quantification
Semi-quantitative urine glucose measurement is a crude assessment of glycemic control that confirms hyperglycemia in excess of the renal threshold (180-220 mg/dL in the dog and 200-280 mg/dL in the cat). The detection of glucosuria is of limited utility in dogs because given the current approach to managing canine diabetes, even well-regulated dogs would be expected to exceed the renal threshold for glucose at some point during the day. In most cases, it is possible to obtain similar clinical information by questioning the owner about observed polyuria and polydipsia. If urine glucose is used for monitoring in dogs, the author recommends only using it to assess for over supplementation/persistent hypoglycemia (i.e., recommend decreasing the insulin dose after documenting the absence of glucosuria) and not as a guide for increasing the insulin dose. Urine glucose measurement is no longer recommended as the only assessment of glycemic control in dogs and better monitoring techniques are available.
Urine glucose quantification can be used to assess glycemic control in cats because it is possible to safely maintain their blood glucose below the renal threshold (~250 mg/dL) for most/all of the day with long-acting insulin formulations. As a result, the presence of glucosuria suggests inadequate glycemic control and the need for more insulin. Urine glucose monitoring cannot be used to detect/confirm persistent hypoglycemia in cats that are in a diabetic remission (non-insulin dependent state) receiving insulin so blood or interstitial glucose monitoring must be used to confirm remission.

Blood Glucose Curves
Despite substantial day-to-day variability in BG curve results, a complete 12-hour BG curve can provide useful information when evaluating a poorly regulated diabetic, especially if continuous glucose monitoring is not an option. Blood glucose data collected in the home environment is likely more representative of the actual glycemic control than monitoring in the clinic or hospital. This is especially true in cats because of stress hyperglycemia. The author does not recommend in clinic/hospital monitoring for cats even if it appears they are tolerant/”not stressed”. It is recommended that BG curve data from multiple days during a 2-3 week period be evaluated prior to recommending significant changes such as a change in the insulin formulation. This will allow the clinician to evaluate trends rather than a single BG curve which may not be an accurate representation of the glycemic control. Routine blood glucose monitoring also plays an important role in detecting subclinical hypoglycemia, the occurrence of diabetic remission, and/or the return to an insulin-dependent state in cats.


Home Blood Glucose Curve Protocol

- Use a hand-held glucometer that has been validated for use in dogs and cats
- Blood glucose before food and insulin administration
- Feed and administer insulin
- Blood glucose 1 hour after food and insulin, then every 2 hours (every 4 hours in cats receiving long-acting preparations) until the next dose of insulin

Continuous Glucose Monitoring

The FreeStyle Libre continuous glucose monitoring system provides a readily available, cost-effective way to continuously assess glycemic control over a 14-day period. The system measures the interstitial glucose, stores up to 8 hours of data, and does not require blood sampling for calibration. Continuous glucose monitoring is the recommended assessment method for any challenging diabetic and has replaced blood glucose curves for monitoring in most diabetics in the author’s practice.

Glycated Proteins
The fructosamine concentration provides an estimate of glycemic control/average blood glucose concentration during the preceding 1-3 weeks. Factors or conditions known to affect the fructosamine concentration include hypoproteinemia, hyperlipidemia, azotemia, and hyperthyroidism. The fructosamine concentration is infrequently measured in our practice and may provide additional information about glycemic control in fractious diabetic cats that will not tolerate home blood glucose curves or continuous glucose monitoring or to establish a diagnosis of diabetes mellitus.
Glycated hemoglobin or HbA1c plays an important role in the detection of pre-diabetes and assessment of long-term glycemic control in people. Although previously studied in dogs and cats, species differences affected the performance of human assays and greatly limited the utility of this monitoring technique. A canine and feline specific HbA1c (A1CARETM, http://baycomdiagnostics.com) test has been developed and is now commercially available. Glycated hemoglobin provides information about the average blood glucose during the preceding ~110 days in the dog and ~70 days in the cat (lifespan of the red blood cell). This test is expected to prove useful in screening and early detection of diabetes/pre-diabetes and will likely provide a better assessment of long-term glycemic control than fructosamine.

REFERENCES

References available upon request.

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