VPAC Veterinary Partners - UTCVM

Saturday, July 13, 2019PROCEEDINGS BOOK

VPAC Veterinary PartnersAppreciation Conference

THE UNIVERSITY OF TENNESSEE COLLEGE OF VETERINARY MEDICINE

22019 VPAC | Veterinary Partners Appreciation Conference © University of Tennessee

BACK TO TABLE OF CONTENTS

DEA Controlled Medication Requirements for DVMs — Jeremy Long, Pharm D, FSVHP ............................................................................................. 5

Update on Treatment of MRSP Skin Infections in Dogs — Dr. Linda Frank ........................................................................................................................21

Feeding Toys and Obesity — Dr. Dan Su ...........................................................................................................................................................................................25

Pneumonia in Dogs: How to Diagnose and Treat It — Dr. Liz Guieu & Dr. Kristen Marshall ........................................................................................27

One More Shot! — Dr. Marie de Swarte .............................................................................................................................................................................................40

Nutritional Management of Early CKD — Dr. Angela Witzel Rollins .....................................................................................................................................57

Ultrasound of the Thorax – It’s Not Just for the Heart — Dr. Silke Hecht ...........................................................................................................................58

Welcome to the Stone Age: Diagnosis, Medical and Surgical Treatment Options — Dr. Cassie Lux ....................................................................70

Oral Lesions in a Horse Following Ingestion of Broomsedge Hay — Dr. Meggan Graves ..........................................................................................73

Discospondylitis in a Tennessee Walking Horse Mare — Dr. Meggan Graves ...................................................................................................................75

Sepsis in Neonatal Foals — Dr. Melissa Hines ...................................................................................................................................................................................81

Equine Hoof Sepsis — Dr. Neal Valk.....................................................................................................................................................................................................96

Equine Lameness Diagnosis — Dr. Steve Adair .............................................................................................................................................................................101

Cesarean Section in Small Ruminant Practice — Dr. David Anderson ............................................................................................................................... 123

Salt Toxicity in Pot Belly Pigs – A Review — Dr. Jennifer Sexton ......................................................................................................................................... 134

Muzzle Your Fears – Aggressive Dog Handling — Bonnylee Kennedy LVMT ................................................................................................................. 138

Finding Balance: Patient Care and Stress — Erin Morrison LVMT ......................................................................................................................................... 141

Is Age a Disease? Anesthetic Considerations for the Geriatric Patient — Jessica Birdwell, LVMT, VTS (Anesthesia) ................................... 161

Opioids? How about Nopioids! — Jessica Birdwell, LVMT, VTS (Anesthesia) ..................................................................................................................172

Putting Pep Back in Their Step! Osteoarthritis Management in Companion Animals — Dawn Hickey LVMT, VTS (physical rehab) .....177

Food Toxicitiesin Commercial Foods — Dr. Claudia Kirk .............................................................................................................................................................183

Emergency Triage: Quick Tips and Tricks — Dr. Liz Guieu ......................................................................................................................................................188

Grain-Free Diet Associated Dilated Cardiomyopathy – An Update — Jena West BA, LVMT ................................................................................205

Diabetic Ketoacidosis: More Than Just “The Sugars” — Eric Hilton BSc, RVT, LVMT, VTS (ECC)......................................................................... 232

Wellness Rocks! A Circle of Life Introduction to Wellness in Veterinary Medicine — Becky Jones-Johnson, LMSW, BCC .....................254

Is your practice supporting the UTCVM Companion Animal Fund? ...................................................................................................... 3

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TVPAC Veterinary Partners

Appreciation Conference

This is an interactive PDF! You may choose to print this document, scroll through the PDF to view each topic sequentially, or simply navigate through this PDF using the embedded links that are on every page. To jump to any of the topics listed below, just click on either the title or the page number and you will be automatically taken to that page. To return to this table of contents, click the link in the top right corner of each page that says BACK TO TABLE OF CONTENTS.



Is Your Practice Supporting the UTCVM Companion Animal Fund?Pet Memorial gifts are one of most thoughtful ways to acknowledge the loss of a pet to your clients. Your gift is recognized with a letter to your client from the Dean of the College of Veterinary Medicine.

With a minimum donation of $10 per pet, your client will know that you have contributed to the Companion Animal Fund at UTCVM. The fund provides for many things in the Small Animal Hospital, such as: • equipment and supplies, • clinical study initiatives of faculty, students, interns and residents, • travel funds to attend professional conferences and meetings, • publications of manuscripts and educational materials, • improvements in examination rooms, treatment areas, reception areas

and offices.

To better serve you and your clients, the Companion Animal Memorial Fund is now on-line. Pet memorial gifts made on-line will be able to be processed more timely and efficiently. The effectiveness of your thoughtful gift will also increase with letters being sent much faster.

If you are using the service, THANK YOU. If not, we encourage you to consider this compassionate and charitable marketing tool. We appreciate your support of UTCVM, and we hope that the letters acknowledging gifts are comforting and encouraging to your clients.

For information on how to begin using the pet memorial online service, visit together.tennessee.edu/CompanionAnimalMemorial

Kippy ToddAssistant DirectorUTCVM Advancement & Alumni Relations

(865) [email protected]

Elizabeth WeatherlyDirectorUTCVM Advancement

(865) [email protected]

https://together.tennessee.edu/CompanionAnimalMemorial

mailto:ktodd%40utfi.org?subject=UTCVM%20Companion%20Animal%20Fund%20

mailto:eweatherly%40utfi.org?subject=UTCVM%20Companion%20Animal%20Fund



SMALL ANIMALPRACTITIONERS

Saturday, July 13, 2019

PROCEEDINGS


BACK TO TABLE OF CONTENTS7/11/19

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DEA Regulation

Current Veterinary Requirements:

tightening regulationsJeremy Long, Pharm.D., FSVHP

Veterinary Medical Center Pharmacy

Drug Abuse

• According to the Centers for Disease Control and Prevention, the #1 cause of death in 17 U.S. states is prescription drug abuse, surpassing motor vehicle accidents.• Approximately 70,000 Americans died from overdose last year• Half of which were due to improper use of legally owned prescriptions• 56% of teens believe it is easier to get prescription drugs than illicit

substances• Could be twice this amount since unless drugs are suspected no autopsy

• Approximately 1 in 6 Americans have admitted to abusing prescription drugs

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Drug Abuse

The United States makes up only 4.6% of the world’s population, but it consumes 80% of its opioids – and 90% of the world’s hydrocodone supply

Hydrocodone, Oxycodone, Morphine, Fentanyl, Oxymorphone(Opana), Buprenorphine(Suboxone), Methadone, Hydromorphone (Dilaudid), Codeine

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Signs of drug abuse

• How do you know if a client may be abusing opioids• While these may all be ordinary occurrences, some warning signs that

a client is potentially abusing opioids may include:• Suspect injuries in a new patient• Asking for specific medications by name• Asking for early refills every fill (DEA counts exactly to the day!!!)• Asking for refills for lost or stolen medications• Pet owner is insistent in their request

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Signs of employee abuse of diversion

• Some warning signs that veterinary staff may be abusing opioids include:• Mood swings, anxiety, or depression• Mental confusion and an inability to concentrate• Making frequent mistakes at work• Not showing up for work• Frequent Extended bathroom breaks• Combating opioid addiction and addressing misuse of pain medication

continues to be one of FDA’s highest priorities. Veterinarians as medical professionals have an opportunity to partner with FDA and others to take on this deadly epidemic. the agency encourages them to continue to work with their clients and both local and national organizations to join in the fight.

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Abuse by humans cause restrictions on Veterinary Practice• Human abuse of controlled medications cause regulations that affects

veterinary practice.• Gabapentin now a CV.• Very closely watched as it is frequently used in combination with narcotics!

• Tramadol is now a CIV.• Both of these medications are used in veterinary practice, but

because of abuse on the human side we have to follow the same requirements.

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State regulations for controlled medications

• Each state creates its own regulations for the practice of veterinary medicine within its borders. These include regulations about secure storage of controlled substances, like opioids, and under what conditions veterinarians can prescribe them to patients.• Please always have a lockable location for any controlled medications

that are kept in clinic, on personnel, in vehicles, or in on-call bags, etc…• Think about anywhere you may put controls at any given time!• DEA WILL BE LOOKING FOR THESE MECHANISMS TO BE WORKING AND IN

PLACE IF THEY COME VISIT YOU, EVEN FOR AN INFORMAL INSPECTION!!!

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DEA RECORD KEEPING REQUIREMENTS

• According to federal regulations, all Drug Enforcement Administration (DEA) applicants and registrants shall meet the following record keeping requirements:• Your records must show the flow of controlled substance into and out of the

practice – including any time a controlled substance is acquired, dispensed, administered, distributed, stolen, lost, disposed of and inventoried;• You must keep two physically separate files – one for Schedule II substances, and

one for Schedule III-V substances (the files can be stored together);• Your controlled substance records must be readily retrievable;• You must store all copies of DEA Form 222* (the form used for ordering Schedule

I and II controlled substances) in a substantially constructed, securely locked cabinet and you must immediately report to the DEA any change in a copy (or copies) of the form’s status (used/unused, lost, stolen);



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• Each practitioner must maintain inventories and records of controlled substances listed in Schedules I and II separately from all other records maintained by the registrant. Likewise, inventories and records of controlled substances in Schedules III, IV, and V must be maintained separately or in such a form that they are readily retrievable from the ordinary business records of the practitioner. All records related to controlled substances must be maintained and be available for inspection for a minimum of two years.

Inventory• Each registrant who maintains an inventory of controlled substances must

maintain a complete and accurate record of the controlled substances on hand and the date that the inventory was conducted. This record must be in written, typewritten, or printed form and be maintained at the registered location for at least two years from the date that the inventory was conducted. After an initial inventory is taken, the registrant shall take a new inventory of all controlled substances on hand at least every 2 years.• We RECOMMEND at least yearly, or 6 month intervals!

• Each inventory must contain the following information:• Whether the inventory was taken at the beginning or close of business• Names of controlled substances• Each finished form of the substances (e.g., 100 milligram tablet)• The number of dosage units of each finished form in the commercial container (e.g., 100

tablet bottle)• The number of commercial containers of each finished form (e.g., four 100 tablet bottles)• Disposition of the controlled substances• It is important to note that inventory requirements extend to controlled substance samples

provided to practitioners by pharmaceutical companies.



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Reporting Loss

•YOU MUST REPORT ANY LOSS OF CONTROL MEDICATIONS TO THE DEA WITHIN 24HOURS OF FINDING!!!

Disposal of Controlled Substances

• A practitioner may dispose of out-of-date, damaged, or otherwise unusable or unwanted controlled substances, including samples, by transferring them to a registrant who is authorized to receive such materials. These registrants are referred to as "Reverse Distributors." The practitioner should contact the local DEA field office (See Appendix E) for a list of authorized Reverse Distributors. Schedule I and II controlled substances should be transferred via the DEA Form 222, while Schedule III–V compounds may be transferred via invoice. The practitioner should maintain copies of the records documenting the transfer and disposal of controlled substances for a period of two years.



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• You may transfer controlled substances to another DEA registrant but all transfers must be recorded and cannot comprise more than 5% of all the dosage units you distribute and dispense;• You must report thefts or significant losses within one business day to

the DEA, the state controlled substance authority, and local police. The occurrence must be recorded on DEA Form 106;


• You may issue prescriptions for controlled substances in writing, verbally, or electronically (using systems meeting DEA criteria), or by fax (note that a paper prescription is needed before any pharmacy can dispense a Schedule II substance). Prescriptions must include the following: • Date;• Signature of registrant;• DEA registration number;• Patient’s name/address;• Practitioner’s name/address;• Drug name, strength, dosage form and quantity;• Directions for use (frequency and route of administration); and• Number (if any) of refills authorized

• Note that Schedule II drugs cannot be refilled.• Note that state law may restrict the ability to refill or the number of refills.



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Your usage logs will be your biggest source of frustration. They must include:

• 1. The controlled substance type2. Bottle number3. Lot number4. Expiration date5. Beginning balance6. Balance forward on:

a. The end of every completed pageb. The beginning of every new page

7. Remaining balance after each draw

Your usage logs will be your biggest source of frustration. They must include:

8. Date bottle placed into use9. Page number10. For each draw

a. Dateb. Patientc. Person who made the draw

11. All errors/corrections requirea. A single line out (no scribbling over)b. Accompanying initials of the person recording the correction

12. Remember, these are legal documents!!



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State regulations for controlled medications

• Not only are states changing reporting requirements, some are also setting limits on the number of pills that can be prescribed at one time and some are even limiting the duration of a patient’s treatment with opioids. States such as Colorado and Maine require veterinarians to look at a pet owner’s past medication history before dispensing opioids or writing an opioid prescription.• To ensure that they are in full compliance with current state laws,

veterinarians can contact their State Board of Veterinary Medicine and their State Board of Pharmacy for updated regulations.

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Tennessee requirements for opiate prescriptions

• The biggest change has to do with how much of a drug you can get and when. Under the new law, pharmacists can only partially fill a prescription for no more than half of the number of days it’s written for. And there are limits on prescriptions, too: • General prescriptions are limited to a 3-day supply for initiation of therapy, then can be

increased to a 10-day supply (and no more than 500 cumulative morphine milligram equivalents).

• Prescriptions after surgery are limited to a 20-day supply (maximum 850 cumulative MMEs).

• “Medical necessity” prescriptions are limited to a 30-day supply (maximum 1,200 cumulative MMEs).

• DVM’s are exempt from this, but pharmacist may not fill prescriptions unless they follow these requirements.• Please EXPECT to be asked to provide a valid DEA and NPI number to pharmacies

when prescribing a controlled substance.

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MME (Morphine Equivalents)

• Link to State of Tennessee Tenncare requirements• https://tenncare.magellanhealth.com/static/docs/Program_Informati

on/TennCare_MME_Conversion_Chart.pdf

• Find your favorite and keep iton hand for reference.

***It looks good to have around!***

FDA and DEA requirements for controlled medications

• FDA approves controlled drugs and monitors reported adverse events associated with these drugs. The Drug Enforcement Administration (DEA), however, creates and enforces the regulations regarding controlled substances. Veterinarians should contact their local DEA office if they have questions about the federal regulations regarding controlled substances.• Practitioners are required to store stocks of Schedule II thru V controlled

substances in a secured locked, substantially constructed cabinet.• When controlled substances are stolen from the clinic, veterinarians must

report the theft to DEA and to their local police department as soon as possible.• Diversion is going to be an increased emphasis by the DEA.

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FDA and DEA requirements for controlled medications• Prior to March 2018, there had been two FDA-approved opioid products approved for use in animals. Wildlife

Laboratories, the sponsor of a potent analog of fentanyl called carfentanil (marketed as Wildnil), voluntarily relinquished the approval for this drug in March 2018, as it hadn’t been marketed in at least five years, and because the sponsor wanted to avoid the possibility of diversion of the drug if marketed in the future.• Carfentanil is now showing up in the heroin chain and is causing overdose deaths.

• Recuvyra (fentanyl), now the only FDA-approved opioid for use in animals, is not being marketed. Therefore, veterinarians who need to use an opioid to control pain in their patients use products approved for use in humans.

• FDA has pre-approval (abuse potential review) and post-approval safeguards in place for these drugs, and requires Risk Evaluation and Mitigation Strategies (REMS) for some products to ensure that the benefits outweigh certain risks.

• Do not expect many outpatient pharmacies to be able to understand and/or dispense CII prescriptions for Veterinary Practice. And do not blame them for not being able to fill. The pharmacy regulations for dispensing these medications is VERY difficult and may hard blocks are installed into the pharmacy software.

• While veterinarians using approved human opioids extra-label in animals do not have to follow the human drug’s risk mitigation requirements, they do have to follow the regulations for extra-label use in animals. FDA also strongly encourages veterinarians to read the label information for human opioid drugs and take any associated training. Veterinarians can find a list of FDA-approved human drugs marketed under REMS programs on FDA’s website 23

DEA, FDA and State inspections

• How to be ready for a DEA, FDA or State inspection for controlled medications?• 1. Documentation• 2. Documentation• 3. Documentation– Document every time a controlled drug is used.

***Do not write that 5 bottles of ketamine was used for a heard of 100 cows. Document how much was used on each cow. • Document how much was used on each animal. (even mice for

research)

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Owners storage of controlled medications

• Pet owners may be unaware that pet opioid prescriptions in the home pose a risk for accidental or intentional misuse by family members or guests. Whenever pets are actively receiving opioids, veterinarians should advise pet owners to secure the opioids and store them out of sight. When the pet owner has unwanted opioids, disposing of the medication should be a priority. Because of their inherent risks, FDA has specific recommendations for opioid disposal.

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Animal Anecdotes:

• A dog thinks: ‘Hey, these people I live with feed me, love me, provide me with a nice warm, dry house, pet me and take good care of me … THEY MUST BE GODS!’• A cat thinks: ‘Hey, these people I live with feed me, love me, provide

me with a nice warm, dry house, pet me and take good care of me … I MUST BE A GOD!’



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Pet overdose on opiates.

• Not only can people overdose on opioids, but so can pets. Working dogs, like narcotics detection dogs, are particularly susceptible because they may inhale the powdered drug. Because fentanyl and fentanyl-related drugs are potent, it only takes a tiny amount of drug to cause an overdose. Veterinarians can contact the The University of Tennessee College of Veterinary Medicine’s for suspected cases of canine opioid overdoses.• Narcotic detection dog handlers should have naloxone with them.

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Prevention is the most cost effective way to treat addiction

•1. Deceasing the supply of controlled medications on the street is a very effective way of decreasing drug abuse.•2. This is one of the reasons that the DEA and other enforcement agencies are looking for drug diversion.

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• Q: What are the requirements for writing veterinary prescriptions?• A: The AVMA's Principles of Veterinary Medical Ethics require a

Veterinarian-Client-Patient Relationship (VCPR) before a veterinarian can write a prescription for an animal patient. In addition, most states have laws that specifically require a VCPR for a veterinarian to be able to write a prescription.Each state's veterinary medical board regulates how prescriptions must be written – specifically, what information must be included on the prescription.Although this is not a requirement, a third resource is the FDA's "A Microgram of Prevention is Worth a Milligram of Cure: Preventing Medication Errors in Animals" document, which provides additional guidance on writing prescriptions.

Q: Do I have to give my client a written prescription?• As a veterinarian, when you determine that a medication is needed for a

patient, you can discuss with your client the benefits of having the drug dispensed directly from your clinic. If your client still wants the prescription filled elsewhere, you should comply with their wish and provide a written prescription. For more information about this, see the AVMA's Principles of Veterinary Medical Ethics. • Most pharmacist have very little if any veterinary pharmacy training. Make

sure you are aware of your state's rules and regulations regarding prescriptions. • Some states require veterinarians to write prescriptions for clients to have

filled elsewhere if requested by the client, while some are less strict about prescriptions; in addition, specific guidance on ways the prescription can legally be filed (via a written prescription, telephone or fax) might be offered by your state.



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Q: Whom should I contact to report a problem with a drug obtained from a pharmacy?• A: The state boards of pharmacy oversee the practice of pharmacy

within the state and ensure state rules are followed. Contact your state board of pharmacy if you suspect that the pharmacy's dispensing practices may be in violation of the law. Also, if the pharmacy is based out of another state, call that state's board of pharmacy.• Please try to work with and resolve problems with the pharmacy

directly first.

Q: Can I enter an agreement with a pharmacy that will give me a commission based on drug sales?• A: Gaining an undisclosed commission through an agreement with a

pharmacy could be viewed as a deceptive business practice by your state board and thus might be a violation of your state's practice act. You should check with your state veterinary medical board for rules and requirements about disclosure of business relationships and advertising guidelines.• Tennessee specifically prohibits rewarding practices with rebates and

commissions through their anti-kickback laws written into the TN pharmacy laws.

[email protected] 865-974-5670



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Update on treatment of MRSP skin infections in dogs

Linda A. Frank, MS, DVM, DACVD

INTRODUCTION The primary coagulase positive staphylococcal species that cause pyoderma in small animals include S. pseudintermedius, S. aureus, and S. schleiferi coagulans. Methicillin-resistant S. pseudintermedius (MRSP) has emerged over the past decade as a clinically important pathogen. It is usually multi-drug (MDR) or extensively drug resistant (XDR). Infection with MRSA occurs sporadically in our small animal patients. In every case where it has been investigated, at least one person in the household or clinic was colonized with the same strain. Staphylococcus schleiferi schleiferi is a coagulase negative Staphylococcus that is also a known pathogen. Methicillin resistance is identified in 40-80% of the isolates. It is frequently fluoroquinolone resistant but resistance to other classes of antibiotics is less common. Other coagulase negative Staphylococcus spp. are more likely to be opportunistic; thus, their significance from culture must be determined for each case. Methicillin resistance in Staphylococcus spp. is mediated by the mecA gene. This gene encodes penicillin binding protein 2a (PBP2a), which has a low affinity for binding all β-lactam antibiotics including cephalosporins. The presence of methicillin resistance is determined by the oxacillin disk. The terms multi-drug resistance (MDR) implies resistance to at least 3 antimicrobial classes and extensively drug resistance (XDR) implies resistance to all but 2 or fewer antimicrobial classes. It is important to remember that expression of antimicrobial resistance is NOT a virulence factor. Development of pyoderma is associated with disruption of the epidermal barrier due to underlying disease processes, such as allergies or endocrinopathies. Failure to identify the underlying cause predisposes to recurrence of the infection. THERAPEUTIC CONSIDERATIONS Management of pyoderma requires recognition of the type and depth of infection and, in many instances, identification of the pathogenic organism in order to make appropriate treatment recommendations. Treatment choices vary depending on whether the pyoderma is a first-time infection or whether it is recurrent in nature. Treatment choices also depend on whether the infection is focal or generalized, surface, superficial or deep. General principles of antibiotic usage apply in all cases of bacterial skin infection. Antibiotic dosage should be based on the body weight of the animal and the full dosage administered. Length of antibiotic administration should be 7 days past clinical remission in uncomplicated infections and 10-14 days past clinical remission in



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complicated infections such as recurrent or deep infections and those associated with immunosuppression. This usually results in 4 to 5 weeks of antibiotics for superficial infections and 6 or more weeks for deep infections. Concurrent steroid use is contraindicated when treating skin infections. Corticosteroids will mask the clinical response, making the lesions look resolved when they are not. This may result in discontinuation of the antibiotic too soon, encouraging the development of recurrent infections. It will also interfere with diagnostic procedures. Last, many cases of pyoderma have an underlying cause such as allergy or endocrinopathy. Remember to look for an underlying cause for all cases of recurrent pyoderma. TOPICAL THERAPY FOR MRSP Topical therapy is recommended for surface and superficial pyoderma involving MRS, especially for localized lesions. Topical therapy alone is about 50% effective in resolving bacterial pyoderma. Aggressive topical therapy, consisting of bathing and sprays or mousses, may yield better results. Chlorhexidine 2-4%, chlorhexidine/miconazole, benzoyl peroxide, and ethyl lactate containing shampoos all have demonstrated beneficial responses in dogs with infections. Bathing should be done two to three times per week with a 10-minute contact time. In cases of recurrent or resistant infections, a topical antimicrobial spray or mousse is very beneficial when used once to twice daily in addition to frequent bathing. Focal lesions can be treated with chlorhexidine spray, mupirocin ointment, benzoyl peroxide gel, nisin wipes, or fusidic acid (not available in the USA). Topical products containing steroids (including Gentocin spray) should be avoided. SYSTEMIC THERAPY FOR MRSP (see table for dosages) Cultures should be obtained if empiric therapy failed, there is a history of MRSP or other MRS, or the pet has had prior exposure to many classes of antibiotics. It is likely that other pets in the household will be colonized with the same resistant bacteria; therefore, pets with infections from households with known MRSP should always be cultured rather than empirically treated. Cultures should always be obtained before changing classes of antibiotics. Antibiotic choices for treating MRSP might include clindamycin, doxycycline, fluoroquinolones, chloramphenicol, rifampin, or amikacin. Remember, by definition, MRS organisms (determined by the oxacillin disk) are resistant to ALL β-lactam antibiotics including cephalosporins, carbapenems and cephems regardless of in vitro susceptibility. If clindamycin is available, I usually choose that antibiotic because it has very few side effects. Unfortunately, repeat exposure to clindamycin results in the development of resistance. Clindamycin can display inducible resistance in which the resistance is not expressed until exposure to the antibiotic. It is important that the laboratory you use performs D-testing to determine if inducible resistance exists. Beware of clindamycin



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susceptibility and erythromycin resistance. Likely, clindamycin would not work in this case. Doxycycline is another good choice to treat bacterial skin infections caused by susceptible MRSP strains. Tetracycline susceptible means that the staphylococcus is susceptible to all tetracylines. Unfortunately, if the bacteria expresses resistance to tetracyclines, we cannot be certain whether doxycycline will or will not work without further testing. In the USA, many MRSP clonal sequence types are resistant to all tetracyclines. Fluoroquinolones should never be used for empirical treatment of Staphylococcus sp.. Resistance via mutation develops rapidly. In addition, fluoroquinolone use appears to select for methicillin resistance in human medicine. Do not assume you are dealing with MRSP if pyoderma fails to respond to a fluoroquinolone! Ciprofloxacin has variable oral bioavailability and should be avoided in dogs. Chloramphenicol is a bacteriostatic, narrow spectrum antibiotic. It is reserved for treatment of methicillin resistant S. pseudintermedius which are sometimes only susceptible to this antibiotic. Chloramphenicol is administered three times daily. In addition to this inconvenient frequency of administration, it often causes gastrointestinal disturbances, may be hepatotoxic, is associated with drug interactions, may cause bone marrow suppression, and has been associated with hind-limb weakness and tremors. Rifampin is a bactericidal antibiotic with excellent tissue penetration. It has a broad spectrum of activity against many Gram-negative and most Gram-positive microorganisms and is the most active antibiotic known against staphylococci. Resistance to rifampin readily develops via mutation with monotherapy; therefore, it is recommended to use in combination with another antibiotic such as clindamycin or cephalexin. Unfortunately, this is usually not possible with MRSP. Rifampin is potentially hepatotoxic and this side effect appears to occur more commonly in dogs than in people. Mild increases in alkaline phosphatase activity occur frequently and appear to be benign; however, treatment should be discontinued if there are concurrent increases in other hepatic enzyme activities. Other rare signs associated with rifampin administration in dogs include thrombocytopenia, hemolytic anemia, anorexia, vomiting, diarrhea, and death. Amikacin is an aminoglycoside that is not typically considered for treating dogs with skin infections. It is an injectable antibiotic that is nephrotoxic and ototoxic. Therefore, use of this antibiotic is only based on culture and susceptibility results when no other antibiotic would be effective. While on this antibiotic, urinalysis and chemistry panels should be monitored. TREATMENT OUTCOME Methicillin-resistant staphylococcal infections do not have a less favorable outcome than susceptible staphylococcal infections. The outcome is influenced by the ability to restore



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the barrier and identification of an underlying cause for the infection. Methicillin-resistant infections may take longer to clear, treating 1 to 2 weeks past clinical cure. WHAT TO DO WITH THE MRS PATIENT? Should recommendations be made to restrict dogs from community spaces, such as dog parks? Dogs with active infection would be at the highest risk of spreading the organism and, perhaps, should be told to stay at home until treatment has started and clinical response is evident. We do not know the duration of shedding of the organism and it likely differs among species and hosts. Exposure alone does not mean that an animal will become colonized with a resistant organism. Risk of developing MR carriage include recent antibiotics, recent hospitalization or veterinary visit, and living with a pet with MRSP infection. Only a small percentage of animals are known to have MRS at the time of examination. Staphylococcus sp. are readily inactivated by routine disinfections; therefore, it is important to develop and implement routine consistent cleaning practices and good hand hygiene both in the veterinary clinic and home environment. TABLE: Common Antibiotics Used For Treating Canine Pyoderma

Antibiotic Dose Side effects Amikacin 15 mg/kg q 24 h SC nephrotoxic, ototoxic Chloramphenicol 50 mg/kg q 8 h PO gastrointestinal side effects common;

prolonged use may cause bone marrow suppression, hepatotoxicity; hind limb weakness, shaking

Clindamycin 11 mg/kg q 12 h; 22 mg/kg q 24 h PO

uncommon gastrointestinal side effects

Doxycycline 10 mg/kg q 12 h PO uncommon gastrointestinal side effects Enrofloxacin 5-20 mg/kg q 24 h PO avoid use in staphylococci infections Marbofloxacin 2.2-5.75 mg/kg q 24 h

PO avoid use in staphylococci infections

Minocycline 5-10 mg/kg q 12 h PO uncommon gastrointestinal side effects Rifampin 5-8 mg/kg q 24 h PO may cause hepatotoxicity; use concurrently

with additional antibiotic if possible based on culture; turns secretions orange



FeedingToysandObesityDr.DanSu–UTCVMNutritionResident• Weightlosstips

o Introduction§ Upto56%ofdogsand60%ofcatsintheUSareoverweightorobese,basedona2018surveybyAssociationforPetObesityPrevention

§ Obesityexacerbatesorincreasesrateofdiseasesincludingosteoarthritis,respiratorydisease,andneoplasia

§ Affectsqualityoflife,shortenslifespano Energybalance

§ Beingoverweightistheresultofimbalancebetweenenergyintakeandexpenditure

§ Treatmentincludesreducingcaloricintakeandincreasingcaloricexpenditure.

• Toolstohelpincreasechanceofsuccessandcompliance.

o Toolsforasuccessfulweightlossplan§ Plan

• SetgoalforidealBCS,weighto Idealweight=[weight–(estimatedweightfrombodyfat)]/80%

o Feedforidealweight§ RER=70x(idealweightkg0.75)§ Factorforweightloss:0.8-1.0,candecreaseto0.6ontherapeuticweightlossdiet

• Selectdietandprescribefeedingamount,includingtreatallowance.

o Providetreatideasforowners,andcaloricinformationfortreats(babycarrots=5calorieseach,etc.)

• Rateoflosso Dog:1-2%perweeko Cat:0.5-2%perweek

• Monthlyfollowupsuntilreachingidealweight.

§ Food• Therapeuticweightlossdiets

o Allowforcaloricrestrictionwithoutnutrientrestriction,especiallyprotein.

o Higherfeedingvolumetohelpwithsatiety



• Treatso Allocatedailydietastreatso Vegetableso Providelistforownersorrefertoresourceslikewww.skipthepie.orgforcaloricinformationoffood.

§ Feedingtoys

• Prolongsmealtimeandincreaseactivity• Providesenrichment

§ Automaticfeeders• Redirectssourceoffoodawayfromowners,decreasebeggingbehavior

• Utilizingmultiplefeederscanhelpwithmulti-pethouseholdwithIDidentification

• Worksfordryandwetfood

§ Foodscales• Utilizefoodscaleforfeedinginsteadofmeasuringcups• Allowsforconsistencyandeaseofadjustmentgoingforward



19-06-18

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Pneumoniaindogs:howtodiagnoseit,howtotreatit?

Drs.L.Guieu&K.MarshallUTCVMEmergency&CriticalCare

Outline

•  Definition&etiology•  Presentingcomplaintsandclinicalsigns•  Diagnostictests•  Treatment&monitoring

Definition&etiologies•  Definition:acquiredinflammationofthelowerairways&lungparenchymaassociatedwithaninfectiousprocess

Infectiouscauses-  bacteria-  virus-  fungi-  protozoa-  helminths

Non-infectiouscauses-  idiopathiceosinophilic

pneumonia-  inflammationassociatedwith

inhaledallergens-  endogenouslipidinfiltration



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Bacterialpneumonia•  Occurssecondaryto:–  inhalation/aspirationofinfectiousagents–  spreadofaninfectionfromthepleuralspace(ie.penetratingthoracictrauma)

–  hematogeneousspread(ie.septicpatients,phlebitis)

Primarybacterialpneumonia-  B.bronchiseptica-  Mycoplasmaspp.-  S.equizooepidemicus-  S.canis-  Yersiniapestis

Secondarytootherprimaryinflammatoryeventsorpredisposing

disturbances

-  thatleadtofailureoroverwhelmingofthehostdefensemechanisms

Predisposingdisturbances•  Aspirationpneumonitis

•  Systemicimmunosuppression(diabetismellitus,cushing,oncologypatients)

•  Damagetotherespiratoryepithelium(smokeinhalation,neoplasia,viral/parasiticinfection)

•  Bronchiectasia

•  Pleural/mediastinal/airwayinfection,primarydefectiverespiratorydefenses(primaryciliarydyskinesia)

Concurrentpredisposingdisorderinupto60%ofpatients

Aspirationpneumonia

•  Riskfactors:–  recentgeneralanesthesia–  endotrachealintubation&tracheostomy–  unconsciousnesswithattenuationofthegagreflex–  laryngealmass/paralysis/surgery–  gastro-intestinaldisturbances:esophagealforeignbody,megaesophagus,gastricobstruction

–  gastricintubation–  inducedvomiting–  forcefulfeeding–  prolongeduseofantacidmedication

Needtomonitorthesepatientsclosely



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History&physicalexamfindings•  Travelhistory,vaccination,environment(ie.crowdedhouse,

presenceofpuppies)

•  Respiratorysigns:–  nasaldischarge–  cough,hemoptysis–  tachypnea,dyspnea

Physicalexamfindings•  Thoracicauscultation:

–  crackles–  wheezes–  dulllungsounds

•  Systemicsigns:–  mentation:normal,lethargy,obtundation–  anorexia,inappetence–  fever

•  Other:–  neurologicdisorders

DiagnosticEvaluation

100x



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Thoracicradiographs

•  3-viewsrecommended:–  leftlateralviewneededtobetterevaluate

pneumoniaintherightlung!

AspirationpneumoniaX-rays

Alveolarpatterninrightcranial&middlelunglobes

ImagecourtesyofA.Hespel

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Airbronchograms:bronchifilledwithairsurroundedbycollapsedalveoli&alveolifilledbyexsudate

↑softtissueopacity

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Alveolarpatterninrightcranial&middlelunglobes

Megaesophagus


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Alveolarpatterninleftcraniallunglobes


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Thoracicradiographs

•  3-viewsrecommended:–  leftlateralviewneededtobetterseepneumoniaintherightlung!

•  Alveolar/alveolo-interstitielpatternAirbronchogram&↑softtissueopacityAssymetricdistribution

•  Megaesophagus,neoplasia,bronchiectasia…



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Transtrachealwash,broncho-alveolarlavageorfine-needleaspiration

•  Indications:–  recurrentpneumonia–  poorresponsetocurrentantibiotictherapy–  sepsis


•  Fluidcytology/in-houseGramstain

Ciliatedepithelialcells

Coccobacillilineduponcilia=B.bronchiseptica

Cytobrushlowerairways


•  Fluidcytology/inhouseGramstain:

Degeneratedneutrophils

Gram+bacilli



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•  Fluidcytology:suppurativeinflammationwithdegenerateneutrophils&intracellularbacteria

•  Aerobic(+/-anaerobic)culture

–  Gram-:E.coli,Pasteurellaspp.,Pseudomonasspp•  BordetellaBronchiseptica(puppies+++)

–  Gram+:Streptococcusspp,Enterococcus,Staphylococcusspp.–  Anaerobes:10-21%ofcases


Benefitsofperforminganinvasiveprocedureshouldoutweigh

theriskofworseninghypoxemia&shouldnotdelayantibiotictherapyinitiation

Monitorthesepatientscloselyonrecovery!

Evaluationofoxygenation

•  Pulseoximetry:– hypoxemia:SpO2<95%• SpO2<93%àO2supplementation

•  Lookatyourpatientrespiratorypattern!



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Bloodwork•  Completebloodcount:

–  unremarkable–  neutropenia/neutrophilia•  withorw/oleftshift&toxicchanges

Maturesegmentedneutrophil

Bandneutrophil:-  immatureformofneutrophil-  indicatepresenceofaleftshift

Bloodwork•  Completebloodcount:

–  unremarkable–  neutropenia/neutrophilia•  withorw/oleftshift&toxicchanges

Toxicchanges:-  cytoplasmicbasophilia-  Döhlebodies-  relatedtoeffectofinterleukinsduringneutrophilsmaturation

-  oftenpresentincasesofsepsis

Bloodwork

•  Biochemistry:– ↑liverenzymes&renalvalues–  hypoalbuminemia

•  Coagulationprofile



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TreatmentandMonitoring

Antibiotictherapy•  Empiricantibiotictherapy(pendingculture&sensitivity

results)–  basedonpreviousantibiotictherapy,BALfluidcytologyfindings

–  stablepatients:ampicillin,clindamycinIV

–  puppieswithkennelcough:doxycycline,enrofloxacin

–  patientswithsignsofsepsis:ampicillin,enrofloxacinIV•  currentveterinaryguideline:nodelaybymorethan1-2hoursifsignsofsepsis

–  2weekscourse,recheckX-rays,pursueantibioticaweekafterclearX-rays

Antibiotictherapy•  Monitortheresponsetotherapy:

–  improvedmentation–  resolutionofhyperthermia–  cardiovascularstability–  progressiveimprovementinoxygenation

•  Forpatientsonbroadspectrumantibiotics:–  de-escalateantibiotictherapywhenculture&sensitivityresultsback!

Ifnoimprovementàantibiotictherapymightneedtobereviewed



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O2therapy

•  SpO2monitoredeithercontinuouslyorintermittentlyq1-6hoursdependingonclinicalprogression

•  O2supplementationwhenSpO2<93%

•  TITRATEO2togetaSpO2of95-96%–  tolimitriskofO2toxicity–  BUTalsolookatyourpatient’sresponsetoO2therapy

O2therapy

Sedation

•  Tolimitanxiety&optimizeventilation•  Butorphanol

–  0.2-0.4mg/kgIV–  Useitcautiously:anti-coughproperties

•  Midazolam0.2-0.4mg/kgIVACE5-10µg/kgIV



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Chestphysiotherapy•  NebulizationofNaCl0.9%q4:

–  tomaintainhydrationofthemuco-ciliarysystem

–  toloosenthepurulentsecretionsinthelowerairways

–  tooptimizeproductiveclearance

–  nebulizationwithaminoglycosides(gentamicin)forpatientswithB.bronchiseptica

Nebulization&coupage•  Coupage:

–  applyhandoneachsideofthechest

–  tomobilizeairwaysecretion&promotecough

–  benefitsremaincontroversialinthehumanmedicine

Mobilization

•  Stablepatients:walks•  Inrecumbentpatients:positionchangesq2-4hours–  tolimitatelectasis&aidinmobilizationofrespiratorysecretions

Monitortherespiratorypattern&pulseoximetryfollowingpositionchange



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•  Indicatedforpatientswithcontagiouspneumonia•  Wearfull-lengthlong-sleevedgown&gloves,shoecovers&mask

•  Handhygieneofupmostimportancebefore&afterhandlingthesepatients

•  Allnecessarymaterialavailableintheisolationroom

Isolation

Fluidtherapy

•  Correctionofhypovolemia:–  tooptimizelungperfusion&ventilation/perfusionmatching–  avoidoverzealousbolusingofisotoniccrystalloids

•  Dailyfluidrequirementassessment:–  dehydrationcouldaffecttherespiratoryairwaymucuswatercontent&impairthemuco-ciliaryapparatusfunction

Preventionofaspiration•  Identificationofpatientsatriskforaspiration!!!

•  Priortoanesthesia:–  6hoursfasting+/-short-termantacidmedications–  placenasogastrictube&suctionstomachcontents–  maropitantpre-operatively

•  Intubationinseverelydepressedpatientswithlossofgagreflex–  oralcarewithdilutedchlorexhidine0.05%–  weargloves–  checkthecuffpressure



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Preventionofaspiration•  Feedingplan:

–  Oralnutrition:•  onlyifmentationappropriate•  avoidforcefeeding•  megaesophagus:standingposition,meatballs

–  Enteralfeeding:•  checkforanysignsofnauseaduringfeeding•  checkforgastricdistention(A-FASTexam)•  smaller&morefrequentmeals•  useofprokineticssuchasmetoclopramide,cisaprideorerythromycininpatientswithregurgitationorileus

Prognosis

•  Goodresponsetotherapyinmostpneumonia

•  Whenunderlyingcauses(iemegaesophagus),highriskofrecurrence

•  Inpersistingpneumonia,ruleoutabcess,bronchiectasia,neoplasia,inappropiateantibiotic/poorcomplianceoftheowners

Questions?



7/2/19

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One more shot!Marie de Swarte

DVM, DECVDI, DACVRClinical Assistant Professor of Radiology

Outline

Case-based presentation Don’t be shy, participate!

Case 1 - Cassie

u 8 yo female Golden Retriever

u Hit by car 4 days ago

u Motor present, no anal tone

https://www.thesprucepets.com/thmb/lf_bKsXU1WWVec7FkQTFI2FxBvc=/960x0/filters:no_upscale():max_bytes(150000):strip_icc()/golden-retriever-sitting-down-in-a-farm-837898820-5c7854ff46e0fb00011bf29a.jpg



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Case 1

Case 1

Case 2 – Betsy Boo

u 5 yo female spayed English Shepherd

u Patient was chasing a truck and got her left hind limb caught in the tire

https://gfp-2a3tnpzj.stackpathdns.com/wp-content/uploads/2016/07/English-Shepherd-e1533690964233.jpg



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Case 2

Case 2

Case 3 - Belle

u 9 yo female spayed Labrador Retriever

u Coughing blood for 3 weeks

https://www.animalwised.com/dog-breeds/labrador-retriever.html



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Case 3

Case 3

Less mistakes

Happier clients



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Case 4 - Grace

u 6 yo female spayed German Shepherd

u Regurgitations

https://www.fetchpetcare.com/wp-content/uploads/2017/09/img_2562.jpg

Case 4

Case 4



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Case 5 - Jonesy

u 8 yo male neutered Boxer

u Received meloxicam for 5 days (last dose 4 days ago)

u Hematemesis and melena for 3 days

http://mentalfloss.com/article/72669/10-sporty-facts-about-boxers

Case 5

Case 5



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Case 5

Case 6 - Beo

u 3 yo male neutered Bernese Mountain dog

u 6 days of anorexia and lethargy

u Febrile

https://www.akc.org/dog-breeds/bernese-mountain-dog/

Case 6

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Case 6

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view thorax and abdomen

u Lesions may only be visible on viewu Thorax:

u Atelectasis of the dependent lung .

u Most ventral aspect of lungs .

u Abdomen:

u Especially useful for GI disease

u !

u Give you more confidence in your diagnosis

u Help determine which is the best next step

u Allow for accurate monitoring

Case 7 - Beau

u 7 yo male neutered Papillon

u Probable soft tissue sarcoma removed from left medial antebrachium 10 months ago

u Recurrence 4 months ago surgical removed

u Staging

https://www.akc.org/expert-advice/lifestyle/4-papillon-characteristics/



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Case 7

Case 7

Specific views



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Case 8 - Lazarus

u 1 yo male neutered Staffordshire Terrier

u Acute left hind limb lameness 1 week ago

u Progressed to non-weight bearing lameness 2 days ago

https://dogs.lovetoknow.com/dog-breeds/american-staffordshire-terrier-breed-overview

Case 8

Case 8



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view

Case 9 - Todd

u 6 yo male neutered domestic shorthair

u Stranguria

u History of oxalate stones and cystotomy in the past

https://www.petfinder.com/cat-breeds/american-shorthair/

Case 9



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Case 9

Case 10 - Allen

u 9 yo male neutered Bichon Frisé

u Stranguria

https://www.akc.org/dog-breeds/bichon-frise/

Case 10



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Case 10

Case 11 - Holly

u 10 yo female spayed Labrador Retriever

u Straining to urinate for approximately 24 h

u History of urinary tract infections

http://www.vetstreet.com/dogs/labrador-retriever

Case 11



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Case 11

calculi

Case 12 - Molly

u 6 yo female Domestic shorthair

u Ingested ribbon 4 days ago

u Vomiting was induced using hydrogen peroxide and the patient vomited some ribbon

u Remaining ribbon removed by endoscopy

u Decreased appetite for a day, vomiting, uncomfortable on abdominal palpation

https://www.petbarn.com.au/petspot/cat/cat-breeds/domestic-shorthair-cat/



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Case 12

Case 12

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Case 13 - Rebel

u 1 yo male neutered Mixed breed dog (30 kg)

u Acute vomiting

u Vomited part of a cloth toy

https://canna-pet.com/are-mixed-breed-dogs-healthier-than-purebreads//

Case 13

Case 13



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.

u Animal positioned in right lateral recumbency (left lateral if the patient is suspected to have a portosystemic shunt)

u Red rubber catheter inserted into .

u Dose of :

u Dog 1-3 ml/kg

u Cat 20-30 ml total

u Take lateral radiograph:

u If not enough , inject some more and repeat the radiograph

u If enough , take a VD

Thank you for your attention!

Any questions?



Nutritional Management of Early CKD: IRIS Stage 1 and 2

Angela Witzel Rollins, DVM, PhD, DACVN

Nutrition is arguably the most important aspect of chronic kidney disease (CKD) management. Because CKD encompasses a wide spectrum of pathology and severity, nutritional goals will also vary by stage of disease and underlying etiology. Most therapeutic diets designed for CKD utilize a combination of moderately restricted protein, phosphorus, and sodium with moderately elevated concentrations of omega-3 fatty acids and potassium. The goals behind lowering the concentration of protein in diets fed to dogs and cats with CKD are to reduce the amount of nitrogenous waste products produced during cellular metabolism, while also minimizing the amount of protein entering the glomerular filtrate of the kidneys. In dogs and cats with naturally occurring renal disease, restriction of protein in combination with other dietary modifications appears beneficial, particularly in later stages of disease. However, more research is needed to determine if protein restriction is harmful or helpful for in early stages of CKD. While the degree of protein restriction required for CKD management is debatable, the need for phosphorus restriction is less controversial. Reducing phosphorus in the diet reduces hyperphosphatemia and the sequela of renal secondary hyperparathyroidism in later stages of kidney disease. While phosphorus restriction has not been specifically evaluated in early stages of CKD, it is generally accepted that lower dietary phosphorus is unlikely to have significant negative consequences. Sodium restriction has been recommended as a method of combatting hypertension associated with CKD. Hypokalemia is a well-recognized consequence of renal disease in dogs and cats and most prescription renal diets have moderately high levels of potassium. Diets high in omega-3 fatty acids reduce glomerular capillary pressure, proteinuria, and abate the decline of GFR in dogs with experimentally induced CKD. In addition, cats fed a therapeutic kidney diet with a higher concentration of EPA had longer survival times compared to cats eating other therapeutic kidney diets. There is still much to learn about the nutritional needs of dogs and cats with IRIS stage 1 and 2 CKD. While the combination of moderately low protein, low phosphorus, moderate sodium, and moderately high potassium and EPA/DHA is proven to reduce uremia and extend the lifespan of dogs and cats with later stages of CKD, controversy remains regarding the optimal dietary protein concentrations for early stages of this disease. Dogs and cats with early stages of CKD will likely tolerate higher concentrations of protein as compared to those with severe azotemia. With the advent of new therapeutic renal diets targeted to early stages of CKD, it is reasonable, and likely advantageous, to feed a diet incorporating the principles of traditional renal diets while also providing higher concentrations of protein.



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Silke Hecht, Dr. med. vet., DACVR, DECVDI

Professor in Radiology

University of Tennessee College of Veterinary Medicine

Resources

Normal thorax:

• Evaluation of thoracic structures hampered by interposition of aerated lung tissue

• Can see thoracic wall, lung surface, intrathoracic fat, and possibly cranial mediastinal vessels

Abnormal thorax:

• Pulmonary consolidation, thoracic masses and/or pleural effusion may provide an “acoustic window”

Introduction and Indications



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Thoracic radiography should always precede thoracic ultrasonography:

• Identify lesion

• Confirm presence of a suitable acoustic window

• Rule out entities precluding ultrasound examination (e.g., pneumothorax)

Examination Technique





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Technique

Technique

Ultrasound allows assessment of

• Lesion location (“sliding”, “extrapleural sign”)

• Lesion extent/size and margination

• Lesion echotexture and echogenicity

• Bone involvement

• Presence of foreign material, gas and fistulous tracts

Examples: Neoplasms, abscesses, traumatic lesions…

Thoracic Wall



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9‐year‐old English BulldogChest Wall Mass

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9‐year‐old English BulldogChest Wall Mass

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Thoracic Wall AbscessDraining Tract



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Pleural effusion:

• Amount

• Distribution

• Echogenicity

Pleural surface

Pleural thickening, masses and nodules

(Pneumothorax)

Pleura and Pleural Space

Pleural Effusion

Pleural Nodules and Masses



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Ultrasound most useful in evaluation of the cranial mediastinum

In some cases, evaluation of the caudal mediastinum possible (transhepatic approach)

Ultrasound facilitates differentiation between different etiologies of mediastinal widening on radiographs:

• Accumulation of fat

• Mediastinal effusion

• Cranial mediastinal mass

Helpful in evaluation of the cranial mediastinum in cases of concurrent pleural effusion

Mediastinum

3‐year‐old FS DSHCranial Mediastinal Mass – Lymphoma

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3‐year‐old FS DSHCranial Mediastinal Mass – Lymphoma

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Cranial Mediastinal Mass

Cranial Mediastinal Mass Lesion (Cyst)

Caudal Mediastinal Mass



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Pulmonary mass lesions and nodules• Solid lesions (usually hypoechoic) surrounded by normal lung• Acute angle with thoracic wall• Move with respiration

Alveolar infiltrates/consolidation• Often hypoechoic, lung lobe usually normal shape

Abnormal position (?) and echogenicity• Lung lobe torsion

Atelectasis (= Pulmonary collapse)• Best evaluated if secondary to effusion, otherwise not seen• Small, triangular portions of lung floating in effusion

Lung

Pulmonary Disease

15‐year‐old FS DachshundPulmonary Carcinoma

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15‐year‐old FS DachshundPulmonary Carcinoma

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182775 11‐year‐old DSH Diagnosis: Histoplasmosis!

Pulmonary Mass Lesions

“Hepatization” of Lung



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Abnormal Position (?) and Echogenicity

Lung lobe torsion

Atelectasis

Diaphragmatic HerniaRupture = traumatic diaphragmatic hernia

True (congenital) diaphragmatic hernia

Others



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Diaphragmatic Rupture

True Diaphragmatic Hernia

4‐year‐old FS DSH3‐day history of lethargy and anorexiaPCV 10%

12‐year‐old MC Labrador Retriever

Intermittent retching cough that has gotten worse for the past week

Clinical Case

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Clinical Case

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Clinical Case

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Ultrasound Guided Procedures



Welcome to the Stone Age: Surgical Management of Urolithiasis Cassie Lux, DVM, DACVS-SA

VPAC 2019 University of Tennessee, Knoxville, TN

Urolithiasis is the most common reason to perform a cystotomy in dogs and cats. Urinary stones are most commonly located in the lower urinary tract (LUT), primarily the urinary bladder, although they are also found within the urethra. The incidence of urinary stones within the ureters and kidneys (upper urinary tract; UUT) appears to be increasing, although the true frequency is unknown.

Preparation of a dog or cat for removal of urinary stones via surgery will depend on the location of the stones, although preparation for a full abdominal exploratory is recommended in case of unexpected findings or complications. The animal should be shaved and prepared in sterile fashion from 2cm cranial to the xyphoid to 2cm caudal to pubis and lateral to both inguinal folds allowing for a ventral midline approach. This preparation should allow for conversion to a full open surgery should a complication arise or unexpected findings during surgery require it. Access to the vulva or penis for catheterization may be necessary during surgery, so a perineal (vulva and cat prepuce) shave and prep should be performed. To prepare the preputial cavity for surgery in a dog, a 2 minute flush with 0.05% chlorhexidine diacetate is recommended to prevent contamination.

Techniques for removal of kidney and ureteral stones have shifted from invasive surgical procedures to less invasive techniques. Nephrectomy or renal stone removal via a pyelolithotomy or nephrotomy is possible, but techniques which allow placement of endoscopes within the kidneys or ureter to allow laser breakdown of the stones into smaller fragments (allowing removal without an incision) are being performed in some institutions. Devices such as ureteral stents or subcutaneous ureteral bypass (SUB) systems, with the assistance of fluoroscopy, allow surgeons to avoid incisions into the ureters yet provides drainage from the kidney to the urinary bladder. These techniques are preferred over nephrectomy, and the mortality and complication rates associated with the less invasive procedures appear to better. In dogs, it is still common to incise into ureters to remove stones or reimplant ureters into the urinary bladder if a portion of the ureter cannot be salvaged.

Techniques for removal of bladder and urethral stones are similarly shifting to less invasive procedures. The standard open cystotomy is commonly performed, however techniques that utilize smaller abdominal and bladder wall incisions, and a cystoscope for stone retrieval, are also common and less invasive. The cystotomy should be performed on the ventral wall of the bladder, from apical to mid body. The area of the trigone should be identified and avoided during surgery. It is recommended to use a monofilament absorbable suture (PDS or Maxon) for bladder wall closures, particularly if the infection status of the urine is unknown. The type of suture pattern used to close the bladder wall is generally surgeon preference, but is generally a single layer continuous or interrupted pattern. Rarely, is a two layer closure required. It is important to have the appropriate containers available to collect stones for analysis and culture, and bladder wall for biopsy and culture. It is recommended to submit a sample of urinary stone or bladder wall for culture as about 24% of dogs with a negative urine culture will have a positive culture of the bladder wall or stone. Postoperative radiographs are performed to confirm all stones have been removed prior to recovery, as residual stones are seen in as much as 14-20% of dogs and cats.



Ideally, all stones within the urethra of a dog or cat will be retropulsed into the urinary bladder. The likelihood of this being successful can be improved with general anesthesia to aid in muscle relaxation and use of an assistant to provide compression on the urethra rectally during retropulsion. When stones cannot be removed from the urethra, the location of obstruction determines any definitive urethral procedure. For male dogs with stones in the penile urethra (typically near the os penis) a scrotal urethrostomy (SU) can be performed and stones can remain in the urethra distal to the urethrostomy site. In addition, this procedure can be used in dogs with highly recurrent stones such as urate and cysteine stones, which are at high risk for obstruction. This procedure requires neuter of the dog, and if the neuter occurs at the same time as the urethrostomy procedure, bleeding complications are more likely. The SU utilizes the area of the urethra as it widens into the perineal region at the location which is most superficial to skin. The urethra should be incised on midline from the caudal aspect of the scrotum extending the length of the scrotum cranial, ideally 3-4cm in length. The urethrocutaneous anastomosis should be completed with monofilament rapidly absorbable (4-0) suture such as Monocryl with interrupted sutures the most caudal extent and continued cranially with simple continuous patterns. Hemorrhage from the anastomosis site is common for an average of about 4 days postoperative but can last even up to 2-3 weeks. In male cats, a perineal urethrostomy (PU) should be performed when stones are lodged within the distal urethra, if they cannot be retropulsed into the urinary bladder. Typically, a PU can be recommended in cats following repeated obstructive episodes or when there is a distal urethral tear or stricture. The PU performs the function of externalizing the cat’s widest urethral portion (the pelvic urethra) to the level of the skin, thereby minimizing obstruction due to small stones or urethral spasm. To assure that the dissection for the PU is completed enough to provide the widest urethra, the anatomic landmarks of the ischiocavernosus muscle and bulbourethral glands should be reached and identified, respectively. The most dorsal portion of the urethrocutaneous anastomosis is closed with simple interrupted sutures at the 10, 12, and 2 o’clock positions, and the remainder can be closed with simple continuous patterns. The suture should be monofilament, rapidly absorbable and small gauge. Typically, Monocryl from 4-0 to 5-0 in size is used, and although bleeding from the site does occur, its often mild.

Postoperatively, intravenous fluids be helpful to flush out blood clots that occur due to surgery. In general, urinary catheters are not needed postoperatively unless there is concern that the bladder has reduced blood supply or that there is previous trauma to the proximal urethra that might leak urine or potentiate an obstruction. Urethrostomy procedures shorten the overall urethral length, and therefore predispose to urinary tract infections. It is less common for this to be a major issue in scrotal urethrostomy, but it is recommended to monitor long term for infection in both PU and SU procedures.



LARGE ANIMALPRACTITIONERS


PROCEEDINGS



Oral Lesions in a Horse Following Ingestion of Broomsedge Hay Dr. Meggan Graves – University of Tennessee College of Veterinary Medicine

Summary An adult mare presented acutely down in the pasture on January 21, 2018. A pasture mate was also found dead in the field. Upon arrival at the farm, the mare was found in right lateral recumbency with a heartrate of 60bpm, evidence of struggle, and profuse watery diarrhea. An oral exam revealed a capillary refill time of 3 seconds and severe ulcers. The ulcers were filled with seed heads and hemorrhage with evidence of chronicity. The mare was humanely euthanized and submitted for necropsy. No ulcers or grass awns were found in any other area of the gastrointestinal tract. Hay samples were submitted for analysis and species identification. A gross exam was performed on the pasture mate and revealed similar oral ulcers. Nine other horses remaining in the field were seen to have excessive hemorrhagic salivation and swollen lips. The owner had been feeding this hay as the only source of forage since early fall. Background Although foxtail has been reported to cause oral irritation and ulceration in horses, to the author’s knowledge, broomsedge has not been implicated to do so. Broomsedge is routinely found in hay fields sporadically, but it is rarely the predominant forage; however, with intense drought and economic strains, many are feeding low quality local hay. This case is deemed important as an effort to educate others of the potential serious deleterious effects of feeding broomsedge hay. Case Presentation A long time horse owner and beef producer was feeding a herd of 11 horses round bale hay from a nearby field. The producer noted that when they cut the hay, a layer of white seed heads was noted to be abundant on the forage before baling. The horses reside on a 20 acre pasture with two spring-fed water sources and are not handled or halter broken. Routine preventative care was past-due for the herd. After receiving a call from a neighbor of a down horse seen the field, the producer discovered one horse dead and another down and unable to rise. The producer made multiple attempts to assist the horse to stand with a tractor without success. Upon arrival at the farm, the horse was found in right lateral recumbency. She had a rectal temperature of 99.2°F, heartrate of 60 bpm, respiratory rate of 24, and pink mucous membranes with a capillary refill time of 3 seconds. She was noted as a 3/9 body condition score. The mare passed profuse watery diarrhea while down with periodic paddling of front limbs. A foul odor was noted from the oral cavity and further examination revealed several oral ulcers with hemorrhage and “hair-like” seed packed inside. Investigations Hay samples were collected, photographed, and submitted for analysis. Differential Diagnosis The round bale of hay was identified on site as broomsedge bluestem and presumed as the causative agent of the chronic ulcerative stomatitis and glossitis. Treatment Due to financial constraints, the owner declined any further diagnostics, treatment, or hospitalization and elected humane euthanasia. Outcome & Follow-up A necropsy was performed and revealed generalized serous atrophy of fat (emaciation) and severe multifocal ulcerative glossitis and stomatitis with intralesional plant material. No embedded plant material



was found in the rest of the alimentary tract. Histological evaluation confirmed similar plant features as reported for foxtail. Additionally, this horse had abundant gravel and dry ingesta in the right dorsal colon, likely leading to the colic symptoms observed. Animal Control was involved in investigating this case and ensuring proper care for the remaining members of the herd. Discussion Grass species that have been documented to cause ulcerative stomatitis include yellow bristle grass (Setaria lutescens), varieties of triticale and prairie foxtail (Setaria geniculata) (1-3) To the author’s knowledge there are no published cases of ulceration following ingestion of broomsedge; however, foxtail has been noted to cause similar lesions to that seen in this case with widespread ulceration of the lips, tongue, oral cavity and nasopharynx in horses. Horses typically present with decreased appetite, bleeding ulcers along the margins of the lips, edema and proliferative periodontal gingivitis, and ulceration of the tongue.(4) Additionally, horses have been found to have hemorrhagic salivation, a foul odor of the mouth, and in some cases, coughing.(3) In most cases, ulcerative lesions resolve completely following removal of the offending forage.(5) It has been noted by Johnson et al. that the feeding of poor quality forage may be a direct result of recent droughts and the reduced availability of better quality forage for horses, thus leading to an increase in such cases.(4) Several differentials for ulcerative stomatitis exist. Highly contagious viral diseases like Vesicular Stomatitis cause erosions and ulcers on the horses’ lips, palate, and tongue. Horse may also have lesions on the prepuce, udder or coronary bands, as well as, exhibit fever.(6, 7) Since the primary control measure is quarantine, it is essential that a timely differential diagnosis be made. Some authors have reported that hay contaminated with Setaris spp. as less palatable to horses and rarely voluntarily eaten; however in a feeding trial, horses great desire for S. viridis.(5, 8) Broomsedge thrives on infertile soils with nitrogen levels and outcompetes other grasses.(9) Learning Points/Take Home Messages

• Broomsedge hay causes chronic, severe ulcerative stomatitis and glossitis. • Ulcers are embedded with seed heads. • Broomsedge hay is found to be poor quality feed source for the nutritional needs of a horse.

References 1. Bankowski R, Wichmann R, Stuart E. Stomatitis of cattle and horses due to yellow bristle grass (Setaria lutescens). Journal of American Veterinary Medical Association. 1956;129(4):149-52. 2. McCosker JE, Keenan DM. Ulcerative stomatitis in horses and cattle caused by triticale hay. Ulcerative stomatitis in horses and cattle caused by triticale hay. 1983(8):259. 3. Turnquist SE, Ostlund EN, Kreeger JM, Turk JR. Foxtail-Induced Ulcerative Stomatitis Outbreak in a Missouri Stable. Journal of Veterinary Diagnostic Investigation. 2001;13(3):238-40. 4. Johnson PJ, Lacarrubba AM, Messer NT, Turnquist SE. Ulcerative glossitis and gingivitis associated with foxtail grass awn irritation in two horses. Equine Veterinary Education. 2012;24(4):182-6. 5. Kutasi O, Andrasofszky E, Szenci O, Bersenyi A, Siller I, Abonyi T. Foxtail grass (Setaria viridis)-induced ulcerative stomatitis-gingivitis resembling viral vesicular stomatitis in horses. Livestock Science. 2017. 6. McCluskey BJ, Mumford EL. Vesicular Stomatitis and Other Vesicular, Erosive, and Ulcerative Diseases of Horses. Veterinary Clinics of North America: Equine Practice. 2000;16(3):457-69. 7. Green SL. Vesicular Stomatitis in the Horse. Vet Clinics of North America. 1993;9(2):349-53. 8. Linnabary RD, Henton JE, Heltf JP, Black RD. Oral ulcerations in a horse caused by grass awns. Journal of Equine Veterinary Science. 1986;6(1):20-2. 9. Rice EL. Allelopathic Effects of Andropogon virginicus and its Persistence in Old Fields. American Journal of Botany. 1972;59(7):752-5.



Discospondylitis in a Tennessee Walking Horse Mare Dr. Meggan Graves – University of Tennessee College of Veterinary Medicine

BACKGROUND Discospondylitis is rarely reported in horses, and there is limited information in the literature regarding case management for large animals. Furthermore, many of the case reports and research projects do not elaborate on effective pain management in conjunction with antimicrobial treatment. The case discussed here showed a significant improvement, in a short window of time, with the use of broad spectrum antibiotics and a variety of pain management techniques (opioids, NSAIDs, acupuncture). This case report also demonstrates that serum amyloid A may be useful in monitoring therapeutic response with discospondylitis. CASE PRESENTATION A 17 year old Tennessee Walking Horse mare presented for a 4 week history of pain and reluctance to move. Several factors in the history could have contributed to this horse’s presentation, including an incidence of pulling back on the lead rope while in a horse trailer 4 weeks prior; potential trauma from a bull that gained access to her pasture 3 weeks prior; and the possibility of a fall on rough terrain in the mare’s pasture. The owner had noted a hind limb weakness or instability and given the horse phenylbutazone (1 gram PO BID) intermittently for the previous 3 weeks. Veterinary examination on the farm found all vital signs to be within normal limits. Hoof testers were applied to both front feet with no response detected. The horse had no apparent cranial nerve deficits and displayed normal front limb proprioception. It was considered too dangerous to evaluate the flexion and proprioception of the hind limbs at initial examination due to the rearing of the patient, abnormal head and neck position, and the frequent offloading of the front limbs. During range of motion testing, the patient was very reluctant to move her neck laterally to the left side. When asked to walk, the patient would rear back slightly in a sickle hock stance and then return to a wide based stance prior to advancing. Once moving, no lameness was noted whether in a straight line or circling; however, the patient was reluctant to circle to the left. When left alone, the patient appeared to choose to stand close to a wall on her left side, which was perceived as a guarding tactic. A rectal exam was performed to attempt to rule-out a pelvic fracture. No abnormalities were noted, but the patient was not asked to walk during the rectal exam due to safety concerns. A presumptive diagnosis of cervical fracture was made at this time, and the patient was transported to the referral centre for further diagnostics and work-up. INVESTIGATIONS Upon presentation to the Large Animal Hospital at the University of Tennessee Veterinary Medical Centre, a neurologic exam was first repeated to ensure no neurologic deficits were present. The patient exhibited no cranial nerve deficits and appeared to have adequate proprioceptive reflexes; however, her reluctance to move her neck and pain response when the neck was touched, made the neurologic exam difficult to interpret. A 20cm by 20cm patch of localized sweating was noted on the right side of the neck at the level of C5-C7. A complete blood count and chemistry revealed high total protein (8.6 g/dL [reference range 6.0-7.8]) and globulins (5.6 g/dL [reference range 2.8-4.8]). The heat precipitated fibrinogen was 800mg/dL (reference range 200-400mg/dL). A serum amyloid A was run with a result of 2645 µg/mL (reference range 0.5-20µg/mL). Cervical radiographs were obtained as a next diagnostic step, to rule in/out potential vertebral fractures or subluxations, or intervertebral disc herniation. Due to the patient’s clinical condition and reluctance to move, sedation was not deemed necessary. Lateral digital radiographs were obtained, from the atlanto-occipital area to C7-T1. Ill-defined lysis of the caudal endplate of C5 and cranial endplate of C6 was identified, with mild sclerosis surrounding the lytic area in the cranial endplate of C6. There was near-complete collapse of the C5-C6 intervertebral disc space, and a small step at the level of the floor of the vertebral canal, with ventral displacement of C6 in respect to C5.(Figure 1) These findings were consistent with discospondylitis leading to secondary subluxation. Mild periarticular new bone proliferation, consistent with degenerative joint disease, was identified at the level of the cervical articular facet joints, most notably at C5-6 and C6-7, and was considered incidental to the current presentation.


BACK TO TABLE OF CONTENTS Figure 1: lateral view of the cervical spine, from the cranial aspect of C4 to the caudal aspect of C7. Notice the ill-defined, lysis with surrounding mild sclerosis of the caudal endplate of C5 and cranial endplate of C6 (solid arrows) and the presence of ventral subluxation of C6 with respect to C5 (dotted arrows). There is also incidental, smooth and chronic remodelling of the articular facet joints at C4-5, C5-6 and C6-7, indicative of degenerative joint disease.

DIFFERENTIAL DIAGNOSIS Based on the history gathered from the owner, cervical fracture or subluxation was high on the differential list. Intervertebral disc herniation was also discussed. Although rarely reported in the horse, one case report has documented the lack of clinical signs until reaching end-stage cervical vertebral static stenosis.(1)Both of these differentials were excluded with radiography. The elevated fibrinogen and serum amyloid A could point to meningomyelitis; however, this differential was eliminated due to lack of more severe neurologic deficits expected with this disease process with the 4 week history of clinical signs.(2) The localized patch of sweat on the right neck was presumed to be caused by damage to a sympathic nerve at the site of our lesion.(3) The radiographic findings of contiguous vertebral endplate lysis are typical for discospondylitis; a case of metastatic hemangiosarcoma with similar radiographic findings to discospondylitis has been reported in a miniature donkey, and therefore this neoplasm could not initially be completely ruled out, although deemed very unlikely.(4) TREATMENT The patient was started on trimethoprim sulfamethoxazole (20mg/kg) orally twice a day, to be continued for 2-3 months, along with firocoxib (0.3mg/kg) orally once daily. After two days of hospitalization, the patient still seemed very uncomfortable and reluctant to move, so pain management became top priority. In addition to concern for the well-being of the mare, without some level of improvement, the owners may have elected to discontinue therapy due to a guarded prognosis for recovery. The patient was started on gabapentin (10mg/kg) orally twice a day (to be continued for 1 month). At day 5 of hospitalization, no significant improvements in pain response were observed and a fentanyl (100mcg/hr) patch and methocarbamol (25mg/kg) twice a day were added. A total of two fentanyl patches were applied to the forelimb 36 hours apart.(5) Due to absorption rates, the second patch was placed 36 hours after the first patch was placed, however the first patch was not removed until 48 hours after application.(6) The methocarbamol was discontinued after 2 days due to a shortage in pharmacy. Two sessions of acupuncture were also performed during the patient’s stay, spaced approximately one week apart. Several needles were placed along the patient’s spine. An electric current was applied to several of these needles in order to increase stimulation and endorphin release. The following specific therapeutic acupoints were used and selected based on their indication for the treatment of cervical stiffness and/or pain: Bai-hui, dry needle stimulation; LI 4 bilaterally, dry needle stimulation; SI 7 bilaterally, dry needle stimulation; TH 5 bilaterally, dry needle stimulation; BL 60 bilaterally, dry needle stimulation; SI 14, SI 16, TH 15 and BL 10 (bilaterally) electro-acupuncture. (Key: LI- large intestine, SI-small intestine, TH- triple heater, BL- bladder. These refer to the acupuncture meridians on which each specific point is located. Hz- hertz.) Treatment duration for both sessions was 20 minutes following insertion of the needles. Electro-acupuncture utilized a frequency of 20 Hz. An interesting observation made by the acupuncturist was that the mare raised her head significantly higher during the treatments than at any other time during her hospitalization. The patient also appeared to relax during the treatments. OUTCOME AND FOLLOW-UP The patient remained at the referral centre for 2 weeks, improving substantially during hospitalization. On the day of admittance, she was unwilling/unable to walk more than a few steps; by the last day of her


BACK TO TABLE OF CONTENTSstay, she was able to walk out of her stall and move about the hospital fairly comfortably. The mare was observed voluntarily raising and lowering her head more readily, in addition to some mild improvement in lateral motion. A two week follow up call (4 weeks post admission) revealed that the owner was very happy with the patient’s progress, and that she was beginning controlled exercise. An on-site visit was made to re-evaluate the mare 2 months following admission. When asked about current therapies, the owner stated that due to the mare’s marked improvement, pain medication had been discontinued only a few days after discharge. It was at this visit that the authors also learned the owner had discontinued antibiotic therapy 4 weeks prior, meaning the mare only received 6 weeks of trimethoprim sulfamethoxazole, including her hospital stay, instead of the recommended 3 months. Despite this premature termination of antibiotics, the mare was found to have a serum amyloid A measurement of 0µg/mL, a stark contrast to the previous 2645µg/mL at admission. This change could be interpreted as resolution of inflammation, suggesting the possible lack of need for antibiotics in some cases of discospondylitis. Lateral radiographs of the caudal cervical region were taken with a portable digital radiograph unit in the field. These revealed more severe lysis of the C5-6 endplates, which had progressed to affect the body of these vertebrae (especially C6) with increased underlying sclerosis. There was unchanged subluxation at this level (Figure 2). The mare was observed to have some reluctance to lateral movement to the left, as compared to the right, but was able to bend the neck a full 90° in either direction laterally. The localized patch of sweat on the right neck was still present.

Figure 2: lateral view of the C5-6 vertebrae, obtained two months after the initial study. There has been progressive lysis of the caudal endplate of C5 and cranial endplate of C6 (solid arrows) with increased underlying sclerosis, shortening of C6, and complete collapse of the intervertebral disc space. Mild new bone proliferation is seen ventrally (arrowheads), consistent with early development of bridging. The previously identified ventral subluxation of C6 with respect to C5 is stable, as is the incidental chronic remodelling of the articular facet joints.

DISCUSSION Although uncommon, discospondylitis (the inflammation of an intervertebral disc and adjacent vertebral endplates) is a condition seen in many domestic animals. It is more commonly seen in dogs than large animal species; however, it has also been reported in bovine, porcine, caprine, and equine patients.(7-12) Thought to be most commonly due to haematogenous spread of bacteria (reported isolates include Streptococcus sp., Staphylococcus sp., Brucella abortus, and Rhodococcus equi) from distant sites (frequently the genitourinary tract) the infection can occasionally be established by means of penetrating wounds, surgery, or migrating plant material.(7, 13-15) The patient did not have any recent history of illness or cause for infection, however a previous mild infection could have gone unnoticed by the owner. Isolation of the bacterial cause of discospondylitis is typically unrewarding, and due to financial limitations of the owners, pursuit of the agent was not performed.(14) Blood or urine cultures, surgical curettage and culture were not completed. CSF analysis was not pursued, since in most cases of discospondylitis the CSF is normal as the infection is located outside the meninges. Trauma has been indicated as a possible cause of discospondylitis in the horse, and given the patient’s history and lack of elevated white blood cells on the leukogram, could have been the inciting cause.(16) Regardless of the initial cause, once the infection or sterile inflammatory process had been established in the vertebral endplates, endplate erosion occurred. This inflammatory storm, coupled with bone erosion, results in pain and reluctance to move, especially when in high motion locations like the cervical and lumbosacral areas.(3, 17-20)


BACK TO TABLE OF CONTENTS Imaging the equine spine can be difficult. In this case, the lesion was located in the cervical spine, which can be easily radiographed. In cases where radiography is not a viable option, nuclear scintigraphy can be used to help locate an area of active bone turnover; however, bone scintigraphy will not distinguish between causes of increased bone turnover, such as trauma, infection or bone neoplasia.(11, 21, 22) Trans-rectal sonography can also be used to localize discospondylitis lesions in the caudal lumbar and lumbosacral spine(11) Antibiotic therapy has been the main focus for treatment of discospondylitis since its first discovery.(13) Typically the patient is placed on a broad spectrum antibiotic for a minimum of 2-3 months until no longer symptomatic; however antibiotic therapy may not be warranted in cases of inflammation alone, as is possible in this case presented. Although this patient never had a heartrate above 44bpm, and continued eating and drinking throughout her stage, her reluctance to move and limited range of motion prompted the introduction of pain management techniques. Due to the risk of right dorsal colitis from long term usage of phenylbutazone, firocoxib should be considered when managing painful cases for prolonged periods of time. Firocoxib has previously been used successfully to manage chronic osteoarthritis symptoms. It is also fairly well absorbed orally (~70%) making it a good option for long term care by the owner.(23, 24) Gabapentin has been used in horses with mixed reviews and efficacy; however, it was added in this case due to its success with controlling neuropathic pain in other domestic species. (25-27) The exact mechanism of action for gabapentin is still unknown, but several possibilities have been described.(28, 29) Despite the lack of knowledge about its mode of action, gabapentin is structurally similar to gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter. Therefore, it has the potential to produce analgesic effects, as well as, skeletal muscle relaxation.(30) Fentanyl patches have been utilized in other reported cases of discospondylitis with questionable success.(9) Fentanyl has been shown to be more potent and to have an improved onset of action when compared to morphine, and the transdermal application allows for continuous analgesic properties. Fentanyl patches, used in combination with non-steroidal anti-inflammatories, have been shown to improve analgesia when compared to using NSAIDS alone, which was the target goal of including it with this case.(6) The authors have found no reports in the literature regarding the use of acupuncture with discospondylitis; however, as western and eastern medicines continue to merge, complementary use of acupuncture may prove beneficial. Acupuncture has been demonstrated to be advantageous in a variety of areas in equine practice, pain modulation, and advanced healing including: paralysis or nerve injury, laminitis, orthopaedic issues and lameness.(31-36) Six intervertebral acupuncture points exist between the cervical vertebrae. Electro-acupuncture involves passing an electric current through a needle located at an acupoint.(37) Electro-acupuncture has been reported as more effective than other forms of needle placement with positive documented results in cases of cervical hyperpathia.(38) Additionally, it is known for an analgesic effect.(39-41) This multimodal approach to pain management was deemed necessary due to the chronicity of the disease process and the necessity for clinical improvement in order for the owner to continue therapy. Though there are mixed reviews of the pain modulators utilized in this case in equids when used individually, the combination appeared to have a positive effect in the recovery of this patient. REFERENCES 1. Olson EJ, Hunt LM, Pool RR, Wilson JH, Speltz MC, Olson EJ, et al. Equine intervertebral disk disease: A case report. Journal of equine veterinary science. 2006;26(9):413-9. 2. Mittelman NS, Divers TJ, Engiles JB, Gerhold R, Ness S, Scrivani PV, et al. Parelaphostrongylus tenuis Cerebrospinal Nematodiasis in a Horse with Cervical Scoliosis and Meningomyelitis. Journal of Veterinary Internal Medicine. 2017;31(3):890-3. 3. Dyson SJ. Lesions of the Equine Neck Resulting in Lameness or Poor Performance. Veterinary Clinics of North America: Equine Practice. 2011;27(3):417-37.


BACK TO TABLE OF CONTENTS4. Cole Macgillivray K, Sweeney CR, McLear R, Habecker PL. Vertebral Body Hemangiosarcoma in a 16-year old Miniature Sicilian Donkey. Veterinary Radiology & Ultrasound. 2003;44(4):429-32. 5. Maxwell LK, Thomasy SM, Slovis N, Kollias-Baker C. Pharmacokinetics of fentanyl following intravenous and transdermal administration in horses. Equine Veterinary Journal. 2003;35(5):484-90. 6. Thomasy SM, Slovis N, Maxwell LK, Kollias-Baker C. Transdermal Fentanyl Combined with Nonsteroidal Anti-Inflammatory Drugs for Analgesia in Horses. Journal of Veterinary Internal Medicine. 2004;18(4):550-4. 7. Colbourne C, Raidal S, Yovich J, Howell J, Richardson J. Cervical diskospondylitis in two horses. Australian Veterinary Journal. 1997;75(7):477-9. 8. Hillyer MH, Innes JF, Patteson MW, Barr ARS. Discospondylitis in an adult horse. Veterinary Record. 1996;139(21):519. 9. Alward AL, Pease AP, Jones SL. Thoracic discospondylitis with associated epaxial muscle atrophy in a Quarter Horse gelding. Equine Veterinary Education. 2007;19(2):67-71. 10. Coleman MC, Chaffin MK, Griffin J, Corapi WV, Norman TE, Johnson AL, et al. Multicenter, retrospective study of vertebral osteomyelitis and diskospondylitis in adult horses. 2012. p. S94-S. 11. Sweers L, Carstens A. Imaging Features of Discospondylitis in Two Horses. Veterinary Radiology & Ultrasound. 2006;47(2):159-64. 12. Levine GJ, Bissett WT, Cole RC, Janke JJ, Nunes J, Porter B, et al. Imaging diagnosis - bacterial diskospondylitis in a goat. Veterinary Radiology & Ultrasound. 2006;47(6):585-8. 13. Thomas WB. Diskospondylitis and Other Vertebral Infections. 2000. p. 169-82. 14. Adams S, Steckel R, Blevins W. Diskospondylitis in five horses. Journal of the American Veterinary Medical Association. 1985;186(3):270-2. 15. Chaffin MK, Honnas CM, Crabill MR, Schneiter HL, Brumbaugh GW, Briner RP. Cauda equina syndrome, diskospondylitis, and a paravertebral abscess caused by Rhodococcus equi in a foal. Journal of the American Veterinary Medical Association. 1995;206(2):215-20. 16. Dyson SJ. The Cervical Spine and Soft Tissues of the Neck2011. 606-16 p. 17. Ross MW. Diagnosis and management of lameness in the horse. 2nd ed. / Mike W. Ross, Sue J. Dyson.. ed. Dyson SJ, editor. St. Louis, Mo: St. Louis, Mo. : Elsevier Saunders; 2011. 18. Levine JM, Levine GJ, Hoffman AG, Mez J, Bratton GR. Comparative Anatomy of the Horse, Ox, and Dog: The Vertebral Column and Peripheral Nerves. Texas A&M University: Compendium Equine; 2007. p. 279-92. 19. Clayton HM, Townsend HGG. Cervical spinal kinematics: a comparison between foals and adult horses. Equine Veterinary Journal. 1989;21(3):193-5. 20. Levine JM, Levine GJ, Hoffman AG, Mez J, Bratton GR. Comparative Anatomy of the Horse, Ox, and Dog: The Vertebral Column and Peripheral Nerves. Texas A&M University: Compendium Equine; 2007. p. 279-92. 21. Markel MD, Madigan JE, Lichtensteiger CA, Large SM, Hornof WJ. Vertebral body osteomyelitis in the horse. Journal of the American Veterinary Medical Association. 1986;188(6):632-4. 22. Winter MD, Berry CR, Reese DJ. Nuclear scintigraphy in horses. Compendium (Yardley, PA). 2010;32(12):E5. 23. Donnell, Jr., Frisbie DD. Use of firocoxib for the treatment of equine osteoarthritis. Veterinary Medicine : Research and Reports. 2014;2014:159-68. 24. Koene M, Goupil X, Kampmann C, Hanson PD, Denton D, Pollmeier MG. Field Trial Validation of the Efficacy and Acceptability of Firocoxib, a Highly Selective Cox-2 Inhibitor, in a Group of 96 Lame Horses. Journal of Equine Veterinary Science. 2010;30(5):237-43. 25. Caldwell FJ, Taintor J, Waguespack RW, Sellers G, Johnson J, Lin H-C. Effect of PO Administered Gabapentin on Chronic Lameness in Horses. Journal of Equine Veterinary Science. 2015;35(6):536-40. 26. Terry RL, McDonnell SM, Van Eps AW, Soma LR, Liu Y, Uboh CE, et al. Pharmacokinetic profile and behavioral effects of gabapentin in the horse. Journal of Veterinary Pharmacology and Therapeutics. 2010;33(5):485-94.


BACK TO TABLE OF CONTENTS27. Rose MA, Kam PCA. Gabapentin: pharmacology and its use in pain management. Oxford, UK2002. p. 451-62. 28. Berry DJ, Beran RG, Plunkeft MJ, Clarke LA, Hung WT. The absorption of gabapentin following high dose escalation. Seizure: European Journal of Epilepsy. 2003;12(1):28-36. 29. Stefan H, Feuerstein TJ. Novel anticonvulsant drugs. Pharmacology and Therapeutics. 2007;113(1):165-83. 30. Dirikolu L, Dafalla A, Ely KJ, Connerly AL, Jones CN, Elkholy H, et al. Pharmacokinetics of gabapentin in horses. Journal of Veterinary Pharmacology and Therapeutics. 2008;31(2):175-7. 31. Faramarzi B, Lee D, May K, Dong F. Response to acupuncture treatment in horses with chronic laminitis. Canadian Veterinary Journal. 2017;58(8):823-7. 32. Therapieform ERUE, Herold I, Kreis T. Treatment of equine upward patellar fixation by acupuncture Behandlung der proximalen Patellafixation des Pferdes mit Akupunktur. Zeitschrift fur Ganzheitliche Tiermedizin. 2016;30(3):89-92. 33. Jeong H, Kim N, Kim M. Use of electroacupuncture treatment on traumatic facial nerve paralysis in a horse. Journal of Veterinary Clinics. 2015;32(1):105-7. 34. Sleeper MM, Fishman K, MacKay RJ, Brown M, Bauck AG, Xie H. Acupuncture and traditional Chinese veterinary medicine for treatment of a mare with rectal paralysis. Equine Veterinary Education. 2018;30(9):460-3. 35. Schweinitz DGv. Electroacupuncture for nerve injury in the horse. Equine Veterinary Education. 2014;26(1):24-6. 36. Haussler KK. Acupuncture treatment of lameness and back pain. In: Baxter GM, editor. Adams and Stashak's lameness in horses. Chichester, UK: John Wiley & Sons; 2011. 37. Xie H, Ott EA, Harkins JD, Tobin T, Colahan PT, Johnson M. Influence of electro-acupuncture on pain threshold in horses and its mode of action. Journal of Equine Veterinary Science. 2001;21(12):591-600. 38. Amezaga Urruela M, Suarez-Almazor ME. Acupuncture in the treatment of rheumatic diseases. Current rheumatology reports. 2012;14(6):589. 39. Bossut DFB, Leshin LS, Stromberg MW, Malven PV. Plasma cortisol and beta-endorphin in horses subjected to electro-acupuncture for cutaneous analgesia. Peptides. 1983;4(4):501-7. 40. Acupuncture-Chapter 93. 792-803 p. 41. Hamra JG, Kamerling SG, Wolfsheimer KJ, Bagwell CA. Diurnal variation in plasma ir-beta-endorphin levels and experimental pain thresholds in the horse. Life Sciences. 1993;53(2):121-9.



1

Sepsis in Neonatal FoalsMelissa T. Hines

University of TennesseeCollege of Veterinary Medicine



2

Remains the leading cause of morbidity

& mortality in the neonatal

period

Long term sequelae

Arthritis, osteochondrosis?



3

What is sepsis?

Sepsis clinical syndrome defined by infection + SIRS



4

SIRS

• Systemic inflammatory response regardless of etiology• Changes in 2 of the following• Body temperature• Heart rate• Respiratory function• White cell counts



5



6

Assessment of colostrum

Specific gravity > 1.060



7

Transfer of passive immunity: Absorption

• Small intestine: nonselective absorption of large molecules

• Absorptive efficiency declines to 22% at 3 hours and 1% at 20 hours

• Not significantly impacted by not suckling

Jeffcott LB. J Comp Path. 1974;84:279

Failure of transfer of passive immunity:Many tests available

Radial immunodiffusion“gold standard”

Ideally > 800 mg/dl< 400 mg/dl – FPT400-800 mg/dl – partial FPT

FPT not a disease in itselfa risk factor



8

Prevention/treatment of FPT

• Need 1-2 g/kg IgG• Colostrum ~ 5000 mg/dl

• 1-2 liters (~ 50 g/L)• Equine• Bovine

• Plasma ~ 2000 mg/dl

• Seramune – 30 g/300 ml

Components of colostrum



9

Prevention?

• Environmental management

• Transfer of passive immunity

• Provide colostrum prior to udder seeking

Diagnosis of sepsis – can be difficult

• Blood cultures

• No specific clinical signs/laboratory findings



10

Sepsis score

• ? - Not perfect but can be a useful tool

• Correlation with prognosis

Serum Amyloid A (SAA) – neonatal screening

• Clinically normal foals • 0 ug/ml – normal• 20-100 ug/ml – “gray zone” – repeat in 12-24 hrs• > 100 ug/ml – infection

• Clinical signs• > 100 ug/ml – infection• < 100 ug/ml

• consider antimicrobial treatment• Follow concentrations

• Following response to treatment Slovis N, Stablelab



11

Diagnosis

• Ideal marker yet to be identified

• Often have co-morbidities

Bacteria isolated from foals: 1979-2010 (Theelen MJ, et al, EVJ 2014)

• Gram – bacteria remain the most common• Esp. Enterobacteriaceae

• Gram + bacteria increasing• Enterococcus sp. Increasing



12

Enterococcus(Willis et al, Vet J 2019)

• Large genus of gm + cocci• Increasing in foals – esp from UG tract

• Antimicrobial susceptibility • Unpredictable• Often MDR - can act as donors of antimicrobial resistance

genes to other bacteria• Less likely to survive to discharge (49.9% vs 63.5%)

Antimicrobial susceptibility patterns: 1979-2010(Theelen MJP, et al, EVJ 2014)

• 1091 isolates from 588 foals• Decrease in susceptibility of some isolates• Gentamicin• Ceftiofur • Other

• Increase in MIC values for amikacin• Enterococcus – more resistant to imipenem, ticarcillin/clavulanic acid



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Conclusions

• Amikacin and ampicillin• Amikacin >> gentamicin• Ampicillin – 70.7% of Enterococcus spp. susceptible

• TMS – not sufficiently active in vitro against many isolates• Decrease in susceptibility to ceftiofur (esp of Enterobacteriaceae) of concern

Conclusions

• Geographic variation• Enterobacteriaceae and Enterococcus inherently unpredictable• Culture still recommended



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Initial antimicrobial treatment of foals with sepsis: do our choices make a difference?

• 213 foals < 30 days of age with sepsis, 306 isolates• All bacteria susceptible to initial antimicrobial Rx• 65.4% survival

• One or more isolates resistant• 41.7% survival

Theelen MJP et al, Vet J 2019)

Supportive care



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EQUINE HOOF SEPSIS Neal Valk, DVM, DACVS

Clinical Assistant Professor, Equine Field Services

University of Tennessee College of Veterinary Medicine

INTRODUCTION

Equine hoof sepsis, defined here as bacterial invasion and infection within the confines of the hoof capsule, is an extremely common condition affecting the hooves of all domestic equidae. In general equine practice, it is the most common cause of acute onset severe single limb lameness. Despite the high incidence of this condition, there exists many different approaches to diagnosis, treatment and clinical management. While all veterinarians who regularly treat horses are familiar with hoof sepsis, there appears to be a lack of consensus regarding proper treatment protocols. The purpose of this presentation is to discuss the etiology and pathophysiology of equine hoof sepsis and to describe my approach to the diagnosis and management thereof. I will also present and discuss specific conditions that may mimic hoof sepsis will be presented and discussed.

HOOF ABSCESSES

A hoof abscess most often develops when bacteria gain access to the inside of the hoof capsule, generally through a defect in the white line or bars, which represent the forward extension of the white line. I consider these “garden variety” abscesses, and differentiate them from those caused by puncture wounds or external trauma to the hoof (discussed later). Predisposing factors include aberrations of the white line (e.g., “stretched white line” in laminitic hooves), significant hoof overgrowth or imbalance leading to abnormal stress on the hoof capsule and separation between the sole and wall (e.g., flares), distal hoof wall cracks and the recent trim of a severely overgrown hoof. There is anecdotal evidence to suggest that a recent change in environmental moisture level may contribute to the formation of hoof abscesses, but scientific support is lacking. Once bacteria gain access to the interior of the hoof, they set up house between the hoof capsule and corresponding coria. Most often, the bacteria involved are anaerobic gas forming varieties that create an expansile lesion, which, along with the body’s inflammatory reaction leading to pus formation, slowly separates the hoof capsule from the coria. Pressure exerted on the sensitive coria by gas and fluid accumulation causes the clinical signs of inflammation and severe pain associated with the condition. In most cases, there is no clinically significant active infection of the soft tissues of the hoof.

Hoof abscesses can occur in equidae of any age, breed or discipline, shod or barefoot. They seem to be less common in foals and yearlings than in adults. Retrospective studies suggest that shod horses are at lower risk for developing hoof abscesses, but in my experience, the incidence is not significantly higher among well-maintained barefoot horses.



The history is quite variable, but most often describes an individual that was normal one day, and severely lame the next. Degree of lameness can range from mild/moderate and intermittent, to severe, non-weight bearing. Knowledge of the animal’s recent hoof care history is valuable, as this can often assist in the diagnosis. A thorough history can also help to rule out other differential diagnoses (e.g., laminitis).

The presence of a bounding digital pulse is the clinical hallmark of inflammation within the hoof capsule, though the presence of heat is variable. With time, it is common for swelling to develop at the level of the coronary band and slowly progress proximally to the pastern, fetlock or carpus/tarsus. This benign edema is differentiated from cellulitis by the absence of pain on palpation of the swollen tissue. Thorough examination of the hoof begins with cleaning, using a hoof pick and wire brush. Once the presence of an obvious foreign body is ruled out, a systematic attempt to localize the source of pain is undertaken. Any defect in the hoof capsule or visible tract should be noted. If the hoof is overgrown, trimming is recommended before proceeding. Careful palpation of the coronary band and frog should be performed, followed by application of thumb pressure to the sole and white line prior to the use of hoof testers. In young or severely painful animals, hoof testers are unnecessary and only serve to inflict additional pain. Foals are not accustomed to having pressure applied to their feet, and will often react to any amount of pressure. Draft breeds will often not respond to hoof tester application due to hoof mass, and I routinely use a farrier’s driving hammer to localize pain within the hoof capsule. Significant focal pain response to palpation of the coronary band generally suggests that an abscess is expanding proximally between the hoof wall and laminar corium, and is in the process of erupting. In these cases, the alignment of the horn tubules of the wall is used to locate the point of entry on the solar surface. In the shod hoof, careful evaluation with hoof testers in the proximity of the nails or gently tapping on each individual nail may reveal a nail-hole abscess. Removal of the offending nail often results in adequate drainage with the shoe left in place.

Radiographic evaluation of the hoof is rarely needed, but can be a useful diagnostic aid if no defect is found on the bottom of the hoof. Typically, an area of gas opacity on the radiograph between the capsule and the corium supports the diagnosis, provided there are no other significant radiographic findings. If the abscess cavity is occupied by fluid alone, radiographs will generally appear normal.

Treatment consists of opening the abscess cavity to allow drainage to occur. I prefer to use a small loop knife and bone curette to explore areas of suspicion, but I only remove horn that is abnormal. As a rule, I NEVER USE TOOLS TO INVADE A HOOF CAPSULE THAT IS NORMAL IN APPEARANCE. It is unwise to blindly hack into normal sole, hoping to stumble upon an abscess. If the abscess is encountered, the smallest opening needed to provide adequate drainage is created. Removing too much horn can predispose to prolapse and trauma of the exposed corium, leading to a prolonged recovery. Once the pressure within the abscess cavity is relieved, lameness resolves rapidly. Most horses become sound at the walk within 24 hours. Extremely large abscesses may require several days before soundness is restored, due to pain arising from the separation between the sole and solar corium.

Once the abscess has been drained, measures are taken to protect the exposed corium and prevent dirt and debris from entering and obstructing the drainage tract. Multiple techniques exist, but I prefer the placement of a cotton ball soaked in povidone iodine solution into the abscess cavity. The owner is instructed to change the packing once daily for five to seven days, then leave the packing in place. No other aftercare is needed in the majority of cases. When the packing cannot be maintained in place



alone (eg, sole defect), a hoof bandage, therapeutic boot or hospital plate shoe can be employed. Tetanus prophylaxis is ensured. The use of analgesics or antibiotics are not necessary in most cases. I prefer to have the horse turned out following drainage of the abscess, as loading the hoof will help expel the contents. Work can resume when the horse trots sound on a firm surface. Total duration from diagnosis to return to full function varies, but generally is less than 10 days with an uncomplicated abscess.

When an abscess cannot be drained through an opening in the capsule, I prefer to let it run its course and erupt spontaneously at the coronary band. Soaking the hoof in Epsom salt solution and applying a poultice to the coronary band (e.g., magnesium sulfate paste or Animalintex under a light wrap) may hasten the eruption and resolution of the abscess. If an abscess has already erupted at the coronary band, or when signs of imminent eruption are present, I prefer not to attempt to open the abscess through the hoof capsule, as it does not improve the outcome.

Prognosis for an uncomplicated hoof abscess is excellent, and recurrence is rare. Recurrence in the same location multiple times (more than twice) should be investigated by thorough clinical and radiographic examination.

PUNCTURE WOUNDS AND STONE LACERATIONS

Puncture wounds and stone lacerations of the equine hoof differ from common abscesses by virtue of their etiology. Primary abscesses develop as the result of bacteria tracking up a preexisting defect in the hoof capsule, while puncture wounds and stone lacerations cause acute bacterial inoculation by directly penetrating the capsule. The result is similar, but complications due to trauma are more likely in the latter group. I must emphasize that I will NOT be covering synovial sepsis caused by penetrating wounds in this presentation.

Puncture wounds from penetrating objects can occur anywhere in the hoof. For our purposes, I will discuss only those that do not involve synovial sepsis and are amendable to treatment in the field. If the penetrating object is present on initial evaluation, the diagnosis is straightforward and a judgement can be made regarding the need for radiographic evaluation. If the penetrating object is near the periphery of the solar aspect of the hoof, it likely has not punctured the navicular bursa or coffin joint. If the object is found soon after penetration, and abscess will not yet have developed. In this case, local wound care, tetanus prophylaxis and antibiotic therapy are warranted, but do not preclude the development of an abscess in the near future. When recognition of the cause is delayed, or in instances when a simple puncture wound is discovered (no foreign object), the wound will have likely progressed to an abscess. Treatment at this stage is identical to that of a primary abscess. Puncture wounds are more likely to cause direct infection of the soft tissue structures of the hoof (e.g., the coria) in addition to an abscess, and thus often warrant antibiotic therapy. Radiographs are indicated to rule out bone involvement if lameness persists following standard treatment. Puncture wounds near the margin of the third phalanx (P3) can cause fracture fragments that become bone sequestra, leading to chronic infection and persistent lameness. I recommend radiographs on those cases were lameness does not significantly improve within five to seven days following treatment.



Stone lacerations occur when the hoof is placed on a firm object under a load, as when a galloping horse steps on a sharp rock or metal stake. The sole fractures, allowing bacteria to enter, but the fracture closes when the hoof is unloaded. Immediate lameness may be recognized, but generally resolves rapidly. However, an abscess will often develop two to three days later. Most owners are unaware of the initial insult, and have the horse examined when an abscess has formed and lameness is severe. Treatment is the same as for a primary abscess. In my experience, stone lacerations rarely cause soft tissue infection, but can occasionally cause P3 margin fractures and bone sequestrum formation. Radiographs are warranted if lameness does not resolve in a timely manner.

Small solar lesions caused by punctures or stone lacerations can be difficult to visualize. I have found that thorough cleaning of the foot, judicious sole paring and topical application of alcohol can dramatically improve the visibility of these lesions. One must be extremely careful when using hoof testers on lacerated soles, as it is easy to inadvertently penetrate the lesion, causing impressive blood loss.

Prognosis is excellent in most cases. When a bone sequestrum is present, surgery is performed to remove the fragment and any remaining necrotic bone, but prognosis for these cases is very good as well. Complications are rare, and include osteomyelitis and extension of infection to synovial structures.

KERATOMA

Keratomas are benign, space occupying tumors that occur mainly within the epidermal lamellae on the inner aspect of the hoof wall. They are not common.

Progressive expansion of a keratoma between the hoof capsule and P3 leads to resorption of bone and the characteristic radiographic appearance of these lesions. Lameness may or may not be present. Disruption of normal hoof architecture by a keratoma can lead to secondary abscess formation. Abscess recurrence in the same location is common, and should lead one to suspect a keratoma. If the lesion extends to the white line at the bearing surface of the hoof, it will sometimes cause a deviation of the white line towards the center of the foot.

Surgical removal is the treatment of choice for keratomas, but will not be discussed. I emphasize them only to illustrate their importance as a differential diagnosis for recurrent hoof abscesses. Prognosis is not well established.

CORONARY BAND FOREIGN BODIES

Penetration of the coronary band by a foreign body, usually a sliver of wood, is not common, but does occur frequently enough that the average equine practitioner will encounter the condition sometime during his or her career. It is more common in horses that have access to wooded areas. The lesion develops when the animal’s coronet band is penetrated by a small stick, which subsequently breaks off flush with or slightly below skin level. These cases are most often misdiagnosed as hoof abscesses that have ruptured at the coronary band.



On examination, marked (grade 4/5 or 5/5) lameness is apparent. A bounding digital pulse is present, and focal swelling may have developed, depending on the duration of the condition. Often a small horizontal opening is visible at the level of the coronary band. Palpation of this opening elicits a pain response, suggestive of a recently erupted abscess. However, the horse usually does not respond to hoof testers as would be expected with an abscess. Occasionally the offending object can be seen or recognized on palpation, but more often, it is too deep to identify.

Treatment consists of exploration and retrieval of the foreign body after performing local anesthesia to desensitize the foot. Lavage is performed, and the wound left open to heal by second intention. In chronic cases, antibiotic therapy may be warranted. Prognosis is excellent if synovial sepsis is not present.

SUMMARY

Sepsis of the equine hoof is a very common cause of severe lameness. Fortunately, treatment is relatively straightforward and effective. It is important for the practitioner to understand that if it looks like an abscess, smells like an abscess and feels like an abscess, it is probably an abscess. Radiographs are typically only indicated when the diagnosis is in question, or when the patient fails to respond to routine therapy.

References available upon request



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THE UNIVERSITY OF TENNESSEE COLLEGE OF VETERINARY MEDICINEDEPARTMENT OF LARGE ANIMAL CLINICAL SCIENCE

Equine Lameness DiagnosisSteve Adair MS, DVM, DACVS, DACVSMRUniversity of Tennessee Veterinary Medical Center

What is lameness?• Lameness is an abnormality of the normal gait• A manifestation of signs of inflammation, including

pain, or a neurological disease, or a mechanical defect, that results in a gait abnormality characterized by abnormal motion

• Lameness is usually evident as asymmetry of movement

Lameness• Diagnosing lameness entails:

– recognizing lameness– determining which limb (or limbs) is involved– localizing lameness to a particular structure

• Most common reason for poor performance• Dx of lameness remains much an art



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Lameness• Causes of lameness:

– Pain - most common by far– Neurological disease (e.g., wobbler)– Mechanical (e.g., ossifying or fibrotic myopathy)

Goals of the Lameness Exam

• Make a diagnosis…

• Identify and localize lameness

• Provide treatment options and prognosis

Steps• History• Visual examination at rest• In motion examination• Manipulation• Localization• Diagnostics



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Conditions for Exam• Adequate time• Good weather• Quiet area• Horse off medications• Owner/Agent available• Horse must be lame

Equipment• Hoof testers• Hoof knife• Longe line• Other

Steps• History

– Signalment and use of the horse – What has the owner or trainer noticed?– Duration/severity of signs

• Are the signs getting worse/staying the same/getting better?– Any treatments? Response?

• Is the horse currently on any medication?– When was the horse last shod?



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Steps• History• Visual examination at rest

– Conformation– Stance– Swelling– Palpation

• Check digital pulses• Run your hands over tendons, joints, etc.

Conformation

Certain conformationalfaults predispose to lameness

Steps• History• Visual examination at rest• In motion examination

– Hard, flat surface– Evaluate all gaits– Is the horse lame? (yes / no / can’t tell)



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In Motion Examination• Gaits

– Walk– Trot, pace– Canter

• Sound horses have equal anterior and posterior phases

• Sound horses will have “normal” foot flight arc

In Motion Examination• Walk

– Watch foot fall pattern• Normal: heel to toe, balanced medial/lateral• Swinging phase: no interference• Listen to hoof strike

• Trot– Lameness is most obvious at the trot

• Always one pair of limbs on the ground– Use loose lead, slow trot

• Observe from front/hind and side

• Which limb is lame???– Determine which limb the horse is

landing on hardest– Forelimb:

• head bob (grade 2 and >>)• Shifting of the shoulders (grade 2

and <<)• Shortened posterior phase

suggestive of soft tissue problem

In Motion Examination



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• Rear limb– Asymmetrical Pelvic

Movement• Gluteal rise (“hip hike”, grade 3

and >>)• Gluteal drop (“dropped hip”,

grade 3 and >>)– Head bob on contralateral

forelimb (grade 3 and >>)– Shortened posterior phase

suggestive of soft tissue problem

– Determine which limb is hitting hardest

In Motion Examination

Head Nod• DOWN ON SOUND• If an animal is lame in front, the head will go down

when the sound limb comes in contact with the ground.

• If the animal is lame behind, the head will go downwhen the lame limb contacts the ground.

• Assess the total vertical displacement of the tuber coxae during trotting

• The side which shows the greatest displacement is the lame limb

Asymmetrical Pelvic Movements



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Rule of Sides• If the head goes down when the left fore hits the

ground the lameness is on the right side (front or back)

• If the head goes down when the right fore hits the ground the lameness is on the left side (front or back)

AAEP Lameness Grading Scale• Grade 0: Lameness not perceptible under any circumstances.• Grade 1: Lameness is difficult to observe and is not consistently

apparent, regardless of circumstances (e.g. under saddle, circling, inclines, hard surface, etc.).

• Grade 2: Lameness is difficult to observe at a walk or when trotting in a straight line but consistently apparent under certain circumstances (e.g. weight-carrying, circling, inclines, hard surface, etc.).

• Grade 3: Lameness is consistently observable at a trot under all circumstances.

• Grade 4: Lameness is obvious at a walk.• Grade 5: Lameness produces minimal weight bearing in motion and/or at

rest or a complete inability to move.

Classification of Lameness• Supporting limb lameness• Swinging leg lameness• Mixed lameness



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Steps• History• Visual examination at rest• In motion examination• Manipulation

– Hoof testers– Longe line – Flexion tests– Riding

• Hoof testers– Repeat on sensitive

spots, trot after applying pressure for 30 – 60 seconds

– Also a good time to evaluate consistency of sole, shoe/hoof wear, hoof conformation

Manipulation

• Lunge line– Work in 10 to 20 meter

circle at all gaits– Usually exaggerates

lameness on limb to the inside of the circle

• Opposite for conditions affecting only the medial side of the limb

– Lameness only observed on the lunge are grade ≤2

Manipulation



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Flexion tests• Goal: isolate lameness by manipulation • Try to “standardize” flexion's• Record results as:

– No change– Slight positive: somewhat exacerbated lameness– Moderate positive: exacerbated lameness down , but

only part of the way back– Severe: marked exacerbation of lameness down, back

and for a period of time following

Flexion Tests - Sequence• Distal forelimb (30 sec)• Proximal forelimb (60 sec)• Distal rear limb (30 sec)• Full rear limb (60 sec)• Stifle & Hip (60 sec)

• Hold 30 seconds

Forelimb fetlock flexion



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• Hold 60 seconds

Proximal Limb Flexion

• Hold 30 secs

Rear Fetlock Flexion

- Hold 60 seconds- Flex as much as horse

permits

Proximal Rear Limb Flexion



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Stifle & Hip- Stresses medial stifle & hip

Hold for 60 sec

Stresses cruciate

Other Manipulations• Tendons/ligaments

– Suspensory ligament and branches– SDFT/DDFT

• Sesamoid bones• Effusions

– Joints, tendon sheaths• Riding/driving

Steps• History• Visual examination at rest• In motion examination• Manipulation• Localization

– Manipulations may help– Regional and articular anesthesia



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Steps• History• Visual examination at rest• In motion examination• Manipulation• Localization• Diagnostics

Diagnostics• Radiography• Ultrasound• Nuclear scintigraphy• Computed tomography• Magnetic resonance imaging• Thermography

• Diagnostic technique

• Diagnostic views

• Adequate interpretation

Radiography



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• Useful for variety of lesions• Useful for serial monitoring• Underestimates degree of

damage

Ultrasound

• Detects bone metabolism• Technetium 99 phosphate

• Three phases:• Circulatory• Soft tissue • Bone

Nuclear Scintigraphy

• Excellent for bone lesions• Can do 3D reconstructs

Computed tomography

Cyst



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MRIGold standard for soft tissue injury

Thermography

• Visualization of skin surface temperatures

• Sensitive to ±0.2°C• Useful adjunct for

evaluation of back pain, saddle fit, hoof balance

Lameness Evaluation

• Be methodical

• Be aware of subtle changes

• Be patient…..



15

EQUINOSIS Q

• Generally highly subjective evaluation based on evaluator’s experience

• Greatly varies between evaluators

• Human eye has limited ability to detect subtle changes in movement

• AAEP lameness grading scale attempts to standardize but still allows for variations between evaluators

LAMENESS EVALUATION

INDICATORS OF LAMENESS• Vertical motion of the head and pelvis are the best

indicators of lameness• Limb movement and pelvic rotation allow for false

positives and false negatives• Limb movement and pelvic rotation are highly

dependent on body conformation and surface during the evaluation



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• Trot is a symmetric gait• Center of mass of the body

has the greatest vertical excursion at the trot

• Therefore, evaluation of lameness is best done at the trot

LAMENESS EVALUATION

LAMENESS EVALUATION: FORELIMBS• In a sound horse in motion, the head normally falls

when landing on a limb and then rises when the horse is pushing off that same limb

• This results in the head moving up and down twice in one complete stride

• Classic “down on sound” only describes really lame

• In actuality:– torso will fall less on the painful

limb during the stance phase (weight bearing) of the stride

– torso will also rise less during the 2nd ½ of the stance phase of the stride

– Eventually, as the lameness increases, the movement of the head due to lameness overtakes the normal pattern of head motion

LAMENESS EVALUATION: FORELIMBS



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LAMENESS EVALUATION: HINDLIMBS• Vertical pelvic motion is more sensitive to change

associated with lameness than pelvic rotation (“hip hike” and “hip dip”)

• When a sound horse is in motion, the pelvis moves down during the 1st ½ of the stance, and up during the 2nd ½ of the stance (push-off)

• When a horse is lame, the pelvis will not rise as high pushing off of the lame limb, or fall as far landing on the lame limb

• When horses are lunging, their torso is tilted toward the center of the circle (up to 18o). This creates a potential natural asymmetry in both vertical head and vertical pelvic movement. This asymmetry can be quite dramatic in some horses, even when lameness is not present.

• Lunging typically exacerbates forelimb lameness and masks hindlimb lameness

• Horses do not lunge right vs. left symmetrically

LAMENESS EVALUATION: LUNGING

LAMENESS EVALUATION: Equinosis Q• With very mild lameness, it is difficult to detect the

asymmetry of the vertical motion of the head and/or pelvis

• As the degree of lameness is increased, the asymmetry also increases

• Using the Equinosis Q, one can easily determine the horse is lame if unable to observe with the naked eye

• The Equinosis Q quantifies the degree of lameness for accurate and objective evaluations

• Equinosis Q allows for specification of impact vs. push-off lameness



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• Ability to objectively track improvement of lameness and success of therapy via serial evaluations and dual reporting

LAMENESS EVALUATION: Equinosis Q

• Research utilized treadmills and high-speed cameras to mathematically characterize normal and impaired gait

• Measured vertical acceleration of the torso to determine asymmetries in head and pelvic position between left and right halves of stride

• Translated research and adapted the analysis to be used in the field

Equinosis Q - DEVELOPMENT

• Horses need to have a minimum of 25 strides at a trot in a straight line for evaluation

• The system can determine trot vs. slow down and turning, and those steps not at a trot are eliminated from the analysis

Equinosis Q



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• 3 Body mounted inertial sensors– Poll- Neoprene head

bumper and double sided velcro strips

– Right front pastern-Neoprene pastern wrap and double sided velcro strips

– Between tuber sacrale on dorsal midline of pelvis-double sided velcro strips and duct tape

Equinosis Q

• Head and Pelvis-accelerometers

• Right forelimb- gyroscope• Each sensor samples 200

times per second• 150 yard transmission

range• Real time data collection

sent to tablet

INERTIAL SENSORS

• Allows for objectivity of localizing lameness by having a capability for dual reporting

• Can be used with diagnostic analgesia giving quantitative analysis of improvement after a block

• Can be used to objectively quantify the results of flexion by comparing post-flexion to pre-flexion

Equinosis Q



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• Useful with multiple limb lameness to determine the primary cause of lameness and the compensatory lameness

Equinosis Q

• Ray diagrams allow for quick qualitative analysis

• x-axis: Max Diff Head (difference in the maximum position of the head after stance phase of right front limb compared to left front limb)

• y-axis: Min Diff Head (difference in the minimum position of the head during stance phase of right forelimb compared to left forelimb)

Equinosis Q: FORELIMB

• Ray diagrams allow for quick qualitative analysis

• x-axis of both plots is the number of strides in the entire data set; each red plus green ray is a stride

• The length of each red plus green ray is a measure of the amplitude of asymmetry of pelvic motion for that stride.

• y-axis in each plot shows Max Diff Pelvis (difference in the maximum position of the pelvis after the stance phase of right hind limb compared to left hind limb) and Min Diff Pelvis (difference in the minimum position of the pelvis during the stance phase of right hind limb compared to left hind limb).

Equinosis Q: HINDLIMB



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• Max Diff Head, Min Diff Head, Max Diff Pelvis and Min Diff Pelvis are reported as a mean value, followed by its standard deviation over all analyzed strides.

• These are specific measures of head and pelvis vertical height asymmetry between the right and left halves of the stride.

Equinosis Q

Max Diff Head• A Max Diff Head greater than +6.0

mm or less than -6.0 mm is consistent with forelimb lameness.

• A Max Diff Head greater than +6.0 mm may indicate either a right forelimb impact lameness or a left forelimb pushoff lameness.

• A Max Diff Head less (more negative) than -6.0 mm may indicate either a right forelimb pushoff lameness or a left forelimb impact lameness.

Min Diff Head• A Min Diff Head greater than +6.0 mm

or less than -6.0 mm is consistent with forelimb lameness.

• A Min Diff Head greater than +6.0 mm may indicate a right forelimb impact, midstance, or pushoff lameness.

• A Min Diff Head less (more negative) than -6.0 mm may indicate a left forelimb impact, midstance or pushofflameness.

Equinosis Q: FORELIMB

Max Diff Pelvis• A Max Diff Pelvis greater

than +3.0 mm or less than -3.0 mm is consistent with hind limb lameness.

• A Max Diff Pelvis greater than +3.0 mm is consistent with a right hind limb push off lameness.

• A Max Diff Pelvis less (more negative) than -3.0 mm is consistent with a left hind limb push off lameness.

Min Diff Pelvis• A Min Diff Pelvis greater

than +3.0 mm or less than -3.0 mm is consistent with hind limb lameness.

• A Min Diff Pelvis greater than +3.0 mm is consistent with a right hind limb impact lameness.

• A Min Diff Pelvis less (more negative) than -3.0 mm is consistent with a left hind limb impact lameness.

Equinosis Q: HINDLIMB



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• Collect a baseline trial, without flexion, of the horse trotting off in one direction only for 8-12 strides

• Select flexion performed and repeat trial of the horse trotting

Equinosis Q: FLEXION TEST

• Quantitates lameness during evaluations that can be placed in records

• Removes ambiguity between evaluators

• Allows for serial examination comparisons

• Does not replace the veterinarian or complete lameness exam

• Does not “pinpoint” location of lameness

Equinosis Q

• http://equinosis.com/• “The Biomechanics of Vertical

Torso Motion In Equine Lameness: Head Nods and Hip Hikes.” Keegan, Kevin G. Hagyard Bluegrass Symposium, October 2014.

• “Recognition of lameness: Man versus machine.” Dyson, Sue. The Veterinary Journal. Vol 201, Issue 3; Sept 2014. Pgs 245-248.

• Kinematics/kinetics. Keegan, K. G.; Baxter, GE. M.; John Wiley & Sons, Chichester, UK, Adams and Stashak’s lameness in horses, 2011, Ed.6, pp 165-172, 15 ref.

RESOURCES



Cesarean Section in Small Ruminant Practice: How to make the best out of a bad situation

David E Anderson, DVM, MS, Diplomate ACVS

Professor and Head, Large Animal Clinical Sciences College of Veterinary Medicine

University of Tennessee

Birthing in llamas and alpacas is a rapid process. Studies in South America documented that > 80 % of crias (neonatal llama or alpaca) are born between 6 am and 1 pm.1 Stage II labor (expulsion of the cria) occurs over a period of 10 to 15 minutes (range, 6 to 47 minutes). 1 Dystocia is an uncommon event in llamas and alpacas. Studies in South America found that dystocia in alpacas (1660 birthings observed) occurred in 1.6% of birthings and that 25 % of these occurred in primiparous females. Data in a smaller number of llamas (234 birthings observed) demonstrated dystocia in only 1 female (0.4 %).1 Interestingly, causes of dystocia differ in South America and North America. Uterine torsion is rarely found in descriptions of dystocia in South America. Causes of dystocia in these populations include fetal malpositioning with 30% of those occurring with the fetus in a posterior presentation and 70% in anterior presentation. 1 Markedly less information is available documenting causes of dystocia in North American herds.2,3 What data is available seems to indicate that uterine torsion is a common cause for veterinary intervention of dystocia.2,4 The author’s opinion is that fetal malpositioning is associated with the majority of dystocia in llamas and alpacas and that uterine torsion is over represented in the literature because these cases are more likely to be presented to teaching hospitals for treatment.3 Uterine Torsion

The term uterine torsion refers to a condition where the pregnant uterine horn rotates along the long axis of the uterus from the normal position and does not return to a normal position. Uterine torsions are most often diagnosed because of abnormal clinical signs in either the dam or gestating fetus. In nearly all cases of diagnosed uterine torsion, the veterinary examination of the female is performed because of abnormal dam behavior noted by the owner. Uterine torsion was reported to account for 60% of dystocia cases presented to a veterinary teaching hospital2 and has been reported to cause 30% of dystocias in Dromedary camels in another institution5. Discussions have occurred among veterinarians regarding the possibility that uterine torsion may occur and resolve without clinical signs being noted. The author has diagnosed uterine torsion in a llama as an incidental finding during routine pregnancy examination. The diagnosis was made during rectal palpation of the uterus in a 5 year old llama which had a fetus consistent with a 6 to 7 month gestation. A right horn pregnancy was present with a > 270 counter-clockwise rotation. In this case, no clinical signs of distress were noted in either the dam or fetus and the torsion was not addressed. On re-evaluation 24 hours later, the torsion was no longer present and the female carried the pregnancy to term and gave birth to a healthy cria. This observation is offered only as an illustration that uterine torsions likely occur at some stages of pregnancy without our knowledge and without causing harm. The author does not advocate delays in treatment of uterine torsion, especially when clinical signs are present. The author feels that uterine torsion should be addressed as an emergency in



order to save the viability of the fetus and the life of the dam. Fatalities of the fetus and dam have been observed because of delays in treatment and deaths have been caused by ischemia to the uterus, rupture of the uterus, and fatal hemorrhage into the abdomen.

Uterine torsion most commonly occurs in late gestation in llamas and alpacas with most cases occurring after the 9th month of gestation. In a report of 20 uterine torsions in llamas and alpacas, 90% of the effected females were > 335 days gestation.2 Unlike horses and cattle in which uterine torsion most often occurs at term, uterine torsion in alpacas and lamas frequently occurs 2 to 6 weeks before the due date for parturition. When possible, the author leaves the gestating cria in utero to continue to a natural birthing process (e.g. in females having a uterine torsion > 2 weeks pre-partum and closed cervix). Poor survival of crias born after having induction of parturition or born pre-maturely has been reported. 7 In that study, induction of parturition was attempted with fluprostenol, oxytocin, or 3 different dosages of dexamethasone. Alpacas having been given fluprostenol delivered a live cria a mean of 21.5 hours after treatment. Oxytocin and dexamethasone at < 0.05 mg/kg failed to induce parturition. Dexamethasone at 0.5 mg/kg resulted in stillborn fetuses. Thus, neither oxytocin nor dexamethasone should be used for induction of parturition in alpacas. The author routinely monitors fetal heart rate, placental thickness, and placental fluid echogenicity to assess fetal well being. C-section is performed if the cria is determined to be at risk. Ultrasonographic monitoring of the cria can include echotexture of the fluids within the heart and body cavities of the cria. Evidence of impending fetal distress include decreasing heart rate, placental fluids developing a turbid appearance on ultrasonography, rapid changes in placental thickness, and apparent separation of the placenta from the endometrium.

The ability to diagnose the direction of uterine torsion is critical to non-surgical correction. Failure to correctly diagnose the direction of torsion before attempting correction by rolling can cause exacerbation of the torsion, loss of blood flow to the fetus, or ischemia to the uterus. The direction of the rotation of the uterine horns can be described as either clockwise (torsion of the left horn to the right side) or counter-clockwise (torsion of the right horn to the left side). This refers to the direction of rotation of the gravid uterine horn about the long axis of the uterus and the non-gravid horn similar to the direction of the rotation of the hands of a clock. This terminology assumes that the observer is standing behind the animal and looking at the rear end of the llama or alpaca. The rear quarters are used to visualize a clock face with the vulva at the center. In a normal, non-gravid uterus, the uterine horns are positioned at 3 O’clock (right horn) and 9 O’clock (left horn) on the clock face. During pregnancy, the gravid horn of the uterus (long or minute arm of the clock) rotates ventrally and toward midline because of gravity. This shifting of the gravid horn creates a 90 degree rotation ipsilateral to the gravid horn. Although the uterus is rotated, the broad ligaments of the uterus are parallel and course from the caudo-dorsal attachments in a cranio-ventral position. The broad ligaments remain relatively parallel to each other and become more obvious as the pregnancy advances and the uterus becomes laiden with fluid.

Uterine torsions are based (maximum point of gravity) in the gravid horn. Thus, clockwise torsions occur when a left horn pregnancy is present and counter-clockwise torsions occur when a right horn pregnancy is present. In the situation when the left horn (minute hand) rotates dorsal and lateral to the right horn (hour hand), then the horn is



described as having moved clockwise similar to the hands of the clock. In the situation of a counter-clockwise uterine torsion, a right horn pregnancy is present and the gravid right horn (minute hand) rotates dorsal and lateral to the left horn (hour hand) of the uterus. The torsion can be anywhere from 90 degrees to 360 degrees and beyond. The caudal extent of the torsion is normally near the cervix, but may be based in the uterine body cranial to the cervix or in the vagina caudal to the cervix. In term pregnancies, the torsion often prevents the cervix from dilating fully and will prevent birth if it is not corrected. In a report of 20 occurrences of uterine torsions diagnosed in 11 llamas and 3 alpacas, 95% were in a clockwise direction. 2 Interestingly, the author found that of 13 uterine torsions diagnosed in 10 alpacas and 3 llamas, 60% were in a counter-clockwise direction (Anderson, unpublished data). These differences exemplify the need for accurate diagnosis of the direction of uterine torsion before attempting non-surgical correction.

The cause of uterine torsion is unknown. Studies in other species have documented risk factors including large fetal size, having a male fetus, breed predispositions, and maternal illness.8 In the author’s opinion, dam behaviors such as rolling excessively, right horn pregnancies, and prolonged gestation are associated with increased risk of uterine torsions. Excessive rolling is often seen when females are moved to a new area during late gestation. This situation occurs when females are moved to a new pasture or to maternity pens or barns.

Clinical Signs of uterine torsion are variable. Clinical signs range from mild including depression, lethargy, reluctance to rise, and anorexia, to more severe signs of colic including increased heart rate and respiratory rate, rolling, thrashing, vocalizing, and straining without effect. Uterine torsion should be suspected when a dam is in late gestation and shows signs of abnormal behavior, distress, abnormal labor, or labor without progression.

Vaginal speculum examination or transvaginal palpation can be used to diagnose the presence of a uterine torsion in many cases. A vaginal speculum is placed into the vagina and the vestibule is inspected for deviations, compression, or twisting of the walls of the vagina or vestibule. The author prefers to use a human rigid sigmoidoscope for vaginoscopic examinations, but any suitably sized and cleansed tube and light source may be used. Diagnosis of uterine torsion is made when the vaginal vault is twisted and narrowed and the direction of the torsion is inferred by the direction of the twisting or distortion of the vaginal vault. However, the examiner must understand that distortion of the vagina is consistently observed only with post-cervical uterine torsion. The author has diagnosed many cases of uterine torsion where the vaginal examination has been non-diagnostic. In the author’s opinion, rectal examination or exploratory laparotomy are the prefered methods for definitive diagnosis of uterine torsion.

Careful rectal plapation can be used to identify the uterus and broad ligaments. In the author’s experience, the broad ligaments are thinner, more pliable, and less easily defined compared with that of cattle and horses. Thus, some experience is required to accurately identify the uterus and broad ligaments. Rectal examination must be performed carefully so as not to perforate the rectum. Techniques used to increased the safety of rectal palpation include restraint in a camelid stocks, sedation with drugs having analgesic properties (e.g. narcotics, alpha-2 agonists), use of large quantities of obstetrical lubricant, epidural anesthesia (e.g. 2% lidocaine HCl), and application of lidocaine jelly directly on the anal sphincter and in the rectal lumen. Diagnosis of uterine



torsion is based on palpation of deviation of the broad ligaments. Normally, both broad ligaments course from caudal and dorsal in the pelvic canal to cranial and ventral in the abdomen. In the presence of a uterine torsion, the broad ligament associated with the gravid uterine horn courses from caudal and dorsal to the horn, across the pelvic canal dorsal to the cervix and uterine body, and cranial and ventral to the contralateral side of the abdomen. The broad ligament associated with the non-gravid horn courses from caudal and dorsal in the pelvic canal, can be felt continuing ventral to the cervix and uterine body, but can not be palpated as it continues cranial and ventral in the abdomen.

Rectal palpation is often difficult in alpacas because of their small size, but most mature llamas can be palpated if proper pre-cautions are observed. A solid sided llama or alpaca restraint chute is important to allow easy and efficient reproductive examinations. Performing these diagnostic tools on free standing females or females pressed against a wall are stressful for the patient, veterinarian, and owner. Sedation should be used sparingly. When needed, butorphenol tartrate (0.1 mg/kg IV) provides excellent sedation with minimal to no untoward effects on the fetus. Before rectal palpation, I prefer to place 60 to 100 ml of lubricant into the lumen of the rectum. In small females, 5 ml of lidocaine can be added to help relax the anal sphincter. If the female is fractious, epidural anesthesia (lidocaine HCl 2%, 1 ml/45 kg maximum dose) may be used. Rectal palpation should be performed with caution because rectal tears have occurred in llamas and alpacas. The examiner should make the owner aware that bleeding from the anal sphincter is common when rectal palpation is performed. This is caused by over-stretching of the mucous membrane and sphincter muscle. This unlikely to pose a risk to the animal but does cause swelling and discomfort. Rectal examination should be used to assess fetal movement, uterine tone, position of the broad ligaments, and the presence of adhesions or other periuterine masses. An interesting observation is that we have found the head and front limbs of the fetus within the pelvic canal up to 3 months before parturition. Also, we have failed to find the head and feet of the fetus within the pelvic canal as early as 3 days before parturition in llamas and alpacas that ultimately delivered in cria in a anterior, longitudinal, dorsosacral position.

Uterine torsion can be corrected either with medical or surgical intervention. Medical intervention generally entails rolling the female while stabilizing the uterus to “untwist” the torsion. Transvaginal correction can be done if cervical dilation is sufficient for entry of a hand into the uterus alongside of the fetus. In a report of 20 uterine torsions diagnosed in 14 llamas and alpacas, 5 were corrected by transvaginal manipulation and 8 were corrected by rolling of the dam combined with application of external compression on the abdomen. 2 If sedation is needed to roll the dam, the author prefers to use a mixed agonist-antagonist narcotic (e.g. butorphenol, 0.05 to 0.1 mg/kg, IV) to minimize cardiopulmonary effects on the dam and fetus. The rolling procedure is done by placing the dam on the same side as the direction of the torsion. For example, if a llama has a clockwise uterine torsion (twist to the right, left horn over top of right horn), then the llama would be placed on her right side to begin the procedure. Then, transabdominal palpation is used to identify and stabilize the gravid horn of the uterus by feeling the fetus. Most often, the backbone of the fetus is present along the abdominal wall. While maintaining pressure on the gravid horn, the female is rolled over her back to her other side. Alternatively, a plank has been used on the outside of the abdomen to help keep the uterus in place while the dam is rolled. This procedure may need to be repeated multiple



times. The author’s rule of thumb is “three times and you’re cut” - meaning that if the torsion can not be corrected within three attempts, then surgical correction is done. A rectal examination is done after each attempt to determine the extent of correction. Correction of the torsion is confirmed by palpating the broad ligaments, uterine body, and fetus. If rolling is successful the dam should be walked but not allowed to roll for 30 minutes to 1 hour and then re-examined. In the author’s experience, uterine torsion often reoccurs within a short period of time in up to 20 % of females. This may be associated with incomplete correction during the rolling procedure. If rolling is not successful, a decision should be made quickly regarding surgical correction.

Surgical correction of uterine torsion can be done under clean field conditions. In a case report of 20 uterine torsions, 7 required celiotomy to correct the torsion. 2 For flank procedures, the hair overlying the left paralumbar region of the llama or alpaca is clipped using a number 40 clipper blade. Then, the skin is aseptically prepared for surgery. The proposed site of the incision is anesthetized using 2% lidocaine HCl. Care must be taken to minimize the total dose of lidocaine used because llamas and alpacas are more susceptible to lidocaine toxicity than cattle. The author uses a dose of 4 mg/kg body weight as the maximum tolerable dose of lidocaine. The author prefers to approach the abdomen from a left sided laparotomy.6 Care must be taken in this approach because, unlike cattle, sheep, and goats, the spleen of llamas and alpacas is positioned in the mid-portion of the flank region. The spleen can be easily injured during opening of the transversus abdominus muscle and peritoneum. The site for paralumbar incision is made starting at a point 6 to 8 cm cranial and ventral to the tuber coxae and extending 8 to 10 cm carnially and ventrally toward the costochondral junction. The incision is made only large enough for the surgeon to introduce a hand and arm so that the uterus can be corrected in position blindly. If the cria is known to be compromised, a 15 cm incision will accommodate exteriorization of the uterus for C-section. If a left flank laparotomy is being done for correction of a clockwise uterine torsion, then the left uterine horn (gravid horn) must be grasped using the hand to cup the bock bone of the fetus, pushed to the right side, then elevated dorsally and then to the left side. If a left laparotomy is being done for a counterclockwise torsion, then the right horn of the uterus is located and a cupped hand used to pull the fetus toward the left side and then moved dorsally and toward the right side. Correction of the torsion is confirmed by palpating the broad ligaments, uterine body, and fetus. After the torsion has been corrected and the viability of the fetus confirmed, the laparotomy incision is closed in 2 layers. The abdominal muscles and fascia of llamas and alpacas is thin and has poor holding power for sutures. Careful reconstruction of the abdominal wall with size No. 1 synthetic, absorbable suture material having good retention of tensile strength (e.g. PG-910; PDS) is done. Then, the skin is closed using No 1 nylon or polycaprolactam with a continuous interlocking suture pattern. If the fetus is at term (partially open cervix), compromised, or determined to be dead, a c-section can be performed at the same time. In rare cases, the uterus cannot be corrected without removal of the fetus. This is a judgment call that the surgeon makes during procedure. The author prefers to leave the fetus in situ when the uterine torsion has occurred sufficiently pre-term so as to pose high risk for survival outside of the uterine environment. In a report of 7 celiotomies done to correct uterine torsion, 6 were done in term females. In tehse 6 females, the crias were removed by hysterotomy and 4



(66%) of the crias survived. In the remaining female, the fetus was left in situ and was delivered stillborn at a later date.

Uterine torsion presents a significant risk to the live of the dam and cria. Death has been seen in dams because of hemorrhagic shock, toxemia associated with uterine ischemia, septic peritonitis, and acute catastrophic events (e.g. cerebellar herniation 10 days post-non-surgical correction of a uterine torsion in a 3 year old alpaca). Possible complications of uterine torsion can include fetal death or compromise, premature birth, death of the dam, uterine compromise by ischemia, rupture of the uterine or ovarian artery with hemorrhage, uterine rupture and subsequent peritonitis, and, if surgical correction is necessary, all of the complications associated with laparotomy and c-section such as retained placenta, metritis, and adhesions.

Return to breeding soundness is of concern to breeders. Of 14 llamas and alpacas having uterine torsion on 20 occassions, non-surgical correction was successful in 13 and celiotomy was required in 7. 2 Of 20 occassions of uterine torsion, 14 crias were born or delivered alive and 6 crias were stillborn. All camelids having non-surgical correction of uterine torsion successfully return to breeding; 5 out of 7 camelids having celiotomy returned to breeding soundness.

Fetal death or disability has been seen because of diminished fetal blood flow, placental edema, placental separation, and trauma. Of 20 occassions of uterine torsion in 14 llamas and alpacas, 14 crias were born or delivered alive and 6 crias were stillborn. 2 Based on the author’s experience, we expect a > 80% maternal survival rate and a > 70% fetal survival rate. Frequent evaluation of the dam and fetus if transvaginal delivery or C-Section is not done are useful in determining if the fetus is at risk. Careful and detailed evaluation on a regular basis (e.g. q8 hours or q12hours) can allow intervention and emergency delivery of the fetus if needed. The authors uses a combination of dam behavior, ultrasonography, fetal heart rate, and fetal cardiotocography to monitor the condition of the placenta and fetus.1,9-11

CESAREAN SECTION Dystocia is relatively uncommon in llamas and alpacas. In South America fewer

than 2% and in North America fewer than 5 % of birthings are expected to require assistance.1,14,15 Problem birthings may be defined as failure of transition from stage I to stage II labor or when little to no progress is made for 20 minutes or more after the start of stage II labor. The most common causes of dystocia in llamas and alpacas are fetal malpositioning, uterine torsion, and poor cervical dilation. 2

Patient assessment is critical to successful alleviation of dystocia.3,6 Cardiovascular shock must be treated prior to correction of dystocia. Females having clinical signs of dehydration, hypotension, and shock should have an IV catheter placed and crystalloid fluids administered as needed (e.g. 0.9% saline, 45 ml/kg body weight over 1 hour; hetastarch, 10 ml/kg body weight over 30 minutes). Non-steroidal anti-inflammatory drugs (e.g. flunixin meglumine, 1 mg/kg, IV) and/or antibiotics (e.g. ceftiofur, 2 mg/kg body weight, IV) may be used when appropriate. If the dam is stable or after supportive therapy has been initiated in the dam, the presentation, position, and posture of the fetus and presence and extent of vaginal and uterine injury should be determined. If the size of the dam precludes evaluation of the uterus or fetus, then ultrasonography may be done to assess the fetus. Immediate exploratory surgery and C-section may be the most prudent action if labor has been prolonged, fetal heart rate can



not be assessed, or the condition of the fetus or birth canal precludes transvaginal delivery.

Dystocia may be relieved without surgery if the following criterion can be achieved: 1) the cervix is adequately dilated and the pelvis is of adequate size to extract the fetus, 2) the pelvic dimension allows introduction of a hand into the uterus for fetal manipulation, and 3) the uterus has sufficient room to grasp and manipulate the fetus. If these criteria cannot be met, the decision to perform a C-section should be made without delay. In my experience, uterine laceration is more likely to occur in llamas and alpacas compared with sheep or cattle. Thus, caution, liberal lubrication, and restraint or sedation of the dam are useful to successful resolution of dystocia.

In dystocia, if the uterus or fetus is not accessible or the cervix is closed immediate C-section is indicated. Damage to the cervix or uterus is more likely when trying to force manipulation of the fetus despite inadequate space or cervical dilation. If the size of the dam precludes transvaginal palpation, immediate C-section should be chosen. Delay in the decision to perform surgery may result in fetal and/or maternal death. Unlike cattle, fetal maturity is highly variable in llamas and alpacas. Although induction of parturition and elective C-section are commonly and successfully performed in cattle with expectation for both maternal and calf viability, this has not been found in llamas and alpacas. In a study of induction of parturition in term alpacas, fetal mortality rates varied from 40 to 90 %.7 Thus, the author does not recommend elective C-section in llamas or alpacas. If maternal conditions (e.g. pelvic fracture or neoplasia) require C-section, the author prefers to allow the female to enter into Stage I labor before scheduling surgery.

Cesarean section is most easily performed via paralumbar fossa or ventral midline laparotomy. Ventral midline laparotomy for C-section has been recommended but is best performed with the dam under general anesthesia.16 The author prefers to perform C-section via a left paralumbar approach. This allows C-section to be performed with the dam sedated and restrained in right lateral recumbency but not anesthestized (Table 1).17-

21 In my experience, crias are more vital and maternal-neonate bonding occurs more readily. Also, milk let-down and early lactation are expected to be more rapid. General anesthesia is discussed elsewhere in this text. A useful sedative for left laparotomy is butorphenol (Table 1). If necessary based on maternal activity, xylazine may be used (Table 1). Clinical depression of the fetus is minimal and xylazine may be reversed using yohimbine or tolazoline (Table 1) if needed. The female is haltered, laid down in right lateral recumbency, and the head and limbs are tied to prevent excessive movement. Then, lidocaine HCL 2% is used to establish a line block at the site of the incision. Caution should be used not to exceed 4 mg/kg body weight total dose of lidocaine (1 ml per 5 kg body weight) so as not to induce lidocaine toxicity. Lidocaine toxicity is recognized by lethargy, ataxia, slow and labored breathing, weakness, hypotension, and diminished response to stimuli.

The skin incision is begun approximately 8 to 10 cm cranial and ventral to the tuber coxae and is extended cranially and ventrally approximately 15-cm in length toward the costochondral junction. Care must be taken when incising the external abdominal oblique muscle, internal abdominal oblique muscle, and the transverses abdominus muscle so as not to invade the peritoneal cavity prematurely. With the left side approach, the C1, spleen, and left kidney lay positioned against the abdominal wall and can be



inadvertently lacerated during entry. On the right side of the abdomen, the C3, duodenum, right kidney, and small intestine lay positioned close to the abdominal wall. The uterus should be exteriorized from the abdomen if possible to prevent leakage of uterine fluids into the abdomen. This is critical if extensive attempts at manual correction of dystocia have been tried or if the fetus is dead or emphysematous. The uterus is remarkably thin and care should be exercised when opening the uterus so as not to cause injury to the fetus. In most cases, the placenta is left in situ after extraction of the fetus. If the placenta can be easily separated from the endometrial wall, it may be removed at the time of hysterotomy. In the author’s experience, the placenta is not easily removed and should be left in place so as not to cause excessive endometrial hemorrhage.

In most llamas and alpacas, the healthy uterus can be closed in a single layer with No 0 polydioxanone or polyglecaprone. When uterine laceration or compromise to the uterine wall is present (e.g. edema, mural hematoma), a double layer closure should be done to ensure that an adequate serosal seal is achieved. The uterus should be thoroughly lavaged clean of all blood clots prior to being replaced into the abdomen. However, the surgeon should not use gauze pads or other abrasive materials to remove blood or fibrin because this will increase the likelihood of post-operative adhesions. In cases where pre-operative uterine rupture occurred or the uterus is traumatized during surgery, carboxymethyl cellulose has been evaluated and advocated for prophylaxis against post-operative uterine adhesions.22,23

Ventral midline celiotomy incisions can be closed in interrupted or simple continuous suture patterns. The author uses No 1 polydioxanone or PG-910 suture material in the linea alba. Contrary to expectations in many species, paralumbar incisions have a greater risk of post-operative incisional hernia as compared with ventral midline incisions. The muscle layers should be precisely reconstructed in simple continuous suture patterns. The author prefers No 1 PG-910 or PGA because of the supple nature of the suture and tissue holding characteristics in muscle. The skin can be apposed using No 1 nylon or polypropylene suture in an interrupted or Ford interlocking suture pattern. After surgery and when the dam is standing, an abdominal support bandage can be used to minimize incision strain for 10 to 14 days. This may minimize the risk of incisional hernia.

Antibiotics and non-steroidal anti-inflammatory drugs are administered routinely before surgery and continuing for 3 days after surgery. Therapy may be prolonged if uterine laceration, abdominal contamination, or emphysematous fetus were present. Close attention should be paid to the cardiovascular stability of the dam and respiratory rate, heart rate, and rectal temperature should be determined twice daily for 5 days to monitor for the onset of peritonitis. Antimicrobial therapy should be directed against the most common bacteria resident in the normal post-partum uterus. In a review of 576 uterine microbial cultures from llamas and alpacas, Actinomyces, alpha-Streptococcus, and E coli were the most commonly isolated bacteria. Thus, antimicrobial selection should include both gram-positive and gram-negative spectrum.

Complicatiosn of laparotomy include peritonitis, hemorrhage, incisional seroma or hematoma, incisional infection, incisional dehiscence, and incisional hernia. These complications are infrequent when aseptic technique, careful tissue handleing, and accurate reconstruiction of tissues using appropriate materials and techniques are used. Interestingly, incisional hernias appear to be more common in llamas and alpacas with



paralumbar incisions as compared with other ruminant species. The author uses an abdominal support bandage for 10 to 14 days after surgery to support the incision in an attempt to minimize this risk.

Complications of C-section include peritonitis, uterine adhesions, para-ovarian adhesions, retained placenta, metritis, endometritis, and infertility. Early decision for C-section will optimize the condition of the dam, fetus and tissues and therefore minimize the risk of complications. Retention of the placenta is expected but the placenta is expected to pass within 48 to 72 hours after surgery with minimal to no treatment. The author routinely administers closprostenol (250 ug total dose, IM) on the day of surgery to ensure lysis of the CL and continuation of placental separation from the endometrium. Caution should be observed with the use of oxytocin. Oxytocin should only be used in the presence of an open cervix (5 units, IM, every 2 hours for 2 to 4 treatments). Oxytocin has been associated with abdominal pain in llamas and alpacas and the dosage and response to therapy should be closely monitored.

Cesarean section is one of the most common surgical procedures requested for large animal veterinarians to perform. There are three main goals of the Cesarean section: 1) survival of the dam, 2) survival of the fetus, and 3) maintenance of fertility. Success rates and complications associated with C-section in llamas and alpacas is limited. When C-section is performed early in dystocia and sterile technique is used, the re-breeding success rate is expected to be good. Complications reported to occur in llamas and alpacas include retained placenta, uterine prolapse, and infertility. 2 Out of 7 llamas and alpacas having C-section for correction of uterine torsion, 5 animals successfully conceived a pregnancy after uterine torsion correction. Overall, we expect 75% of females that have had a C-section to return to normal breeding soundness. REFERENCES 1. Bravo PW. Female Reproduction. In Bravo PW, The Reproductive Process of South American Camelids, Seagull Printing, Salt Lake City, 2002, pp 1-31. 2. Cebra CK, Cebra ML, Garry FB, Johnson LW. Surgical and nonsurgical correction of uterine torsion in New World camelids: 20 cases (1990-1996). J Amer Vet Med Assoc 1997;211:600-602. 3. Anderson DE, Cotton TA, Whitehead CE. Female Reproduction. In Anderson DE, Cotton T, Whitehead CE eds. Neonatology of Llamas and Alpacas, Kansas State University Continuing Education publication, 2008, pp 51-197. 4. Hopkins SM, Althouse GC, Jackson LL, Evans LE. Surgical treatment of uterine torsion in a llama (Lama glama). Cornell Vet 1991;81:425-428. 5. Tibary A, Anouassi A. Genital diseases in the pregnant female. Theriogenology in Camelidae. Abu Dhabi Printing and Publishing Company, UAE 1997, pp 353-363. 6. Anderson DE. Common surgical procedures in camelids. Journal of Camel Practice and Research 1999;6(2):191-201. 7. Bravo PW, Bazan PJ, Troedsson MH, Villalta PR, Garnica JP. Induction of parturition in alpacas and subsequent survival of neonates. J Am Vet Med Assoc 1996;209:1760-1762. 8. Frazer GS, Perkins NR, Constable PD. Bovien uterine torsions: 164 hospital referral cases. Theriogenology 1996;46:739-758.



9. Jonker FH. Cardiotocographic monitoring of the bovine fetus. University of Utrecht (ISBN 90-393-0425-4) 1993 (171 pages). 10. Jonker FH, van Oord HA, van Geijn HP, et al. Feasibility of continuous recording of fetal heart rate in the near term bovine fetus by means of transabdominal Doppler. Vet Quarterly 1994;16:165-168. 11. Jonker FH, van Geijn HP, Chan WW, et al. Characteristics of fetal heart rate changes during the expulsive stage of bovine parturition in relation to fetal outcome. Am J Vet Res 1996;57:1373-1381. 12. Rabello YA, Lapidus MR. Fundamentals of electronic fetal monitoring. Corometrics Medical Systems, Inc, Wallingford, Conn. 1988 (162 pages). 13. Deans AC, Steer PJ. The use of the fetal electrocardiogram in labor. Br J Obstetrics and Gynecology. 1994;101:9-17. 14. Johnson LW. Parturition in the llama. In: Youngquist, ed. Current Therapy in Large Animal Theriogenology. WB Saunders 1997:813-817. 15. Sharpe M, Wittum T, Lord L, Anderson DE. Epidemiologic survey of morbidity and mortality among crias. Australian Veterinary Journal, 2009, In Press. 16. Fowler M. Cesarean Section. In Fowler ME ed. Medicine and Surgery of South American Camelids 2nd ed. Iowa State University Press, Ames, 1998, pp130-132. 17. Elias E. (1991) Left ventrolateral Cesarean section in three Dromedary camels (Camelus dromedarius). Vet Surg 20:323-325. 18. Reibold TW. Engel HN, Grubb TL, Adams JG, Huber MJ, Schmotzer WB. (1994) Orotracheal and nasotracheal intubation in llamas. J Am Vet Med Assoc 204(5):779-783. 19. Sarno RJ, Hunter RL, Franklin WL. (1996) Immobilization of guanacos by use of tiletamine/zolazepam. J Am Vet Med Assoc 208:408-409. 20. Waldridge BM, Hui-Chu L, DeGraves FJ, et al. (1997) Sedaticve effects of metdetomidine and its reversal in llamas. J Am Vet Med Assoc 211:1562-1565. 21. Wilson DG. Surgery of the genitalia of llamas. In: Youngquist, ed. Current Therapy in Large Animal Theriogenology. WB Saunders 1997:840-843. 22. Moll HD, Wolfe DF, Schumacher J, et al. (1992) Evaluation of sodium carboxymethylcellulose for prevention of adhesions after uterine trauma in ewes. AJVR 53:1454-1456. 23. Ewoldt JM, Anderson DE, Hardy J, Weisbrode SE. Evaluation of a sheep laparoscopic uterine trauma model and repeat laparoscopy for evaluation of adhesion formation and prevention with sodium carboxymethylcellulose. Vet Surg 2004;33:668-672.



Table 1. Drugs used to provide anesthesia or analgesia in camelids.

Use Drug Dose Route Sedation Xylazine HCl 0.1 to 0.3 mg/kg IV, IM, S.C. Butorphenol tartrate 0.03 to 0.1 mg/kg IV, IM, S.C. Metdetomidine 10 to 30 ug/kg IM General Anesthesia Butorphenol +

Xylazine + Ketamine

0.03 mg/kg 0.3 mg/kg 3 mg/kg

IM IM IM

Tiletamine/zolazepam Halothane Isofluorane

4.7 to 6.0 mg/kg 1 to 5 % 1 to 5 %

IM OTT or NTT

Reversal Agents Yohimbine 0.125 mg/kg IV, IM Tolazoline† 1 to 2 mg/kg IV, IM Atipamasole 0.125 mg/kg IV

IV = intravenous; IM = intramuscular; OTT = orotracheal tube; NTT =

nasotracheal tube. † Caution: Acute death has been observed after rapid IV administration of tolazoline at high dosages. Adapted from Sarno19 and Waldridge20


BACK TO TABLE OF CONTENTSSalt Toxicity in Pot Belly Pigs

Jennifer Sexton, DVM 3rd Year ACVIM Candidate University of Tennessee, Knoxville Salt toxicity, or hypernatremia is a top differential for a neurologic pig. Understanding of the physiologic process and necessity of rapid treatment can lead to successful treatment. Other differentials include meningitis, toxicosis or edema disease. Sodium homeostasis relies on tight regulation between the intracellular and extracellular space, amidst cellular membranes being highly permeable to water. Sodium is the most influential and abundant cation, and has the greatest influence on the osmolality of the extracellular fluid (ECF), and subsequently, the volume of the ECF. Thus, serum sodium concentration accurately measures total body sodium concentration and the volume of the ECF. The extracellular fluid osmolality is the measure of dissolved particles in water, and the body adjusts the quantity of water that the solutes are dissolved in. Osmoreceptors within the hypothalamus sense changes in osmolality as small as 1-2%. When the osmolality becomes too high, the thirst center is stimulated. Drinking water adds fluid to the ECF and reduces the osmolality. Simultaneously, vasopressin (AVP, aka antidiuretic hormone) is released from the posterior pituitary, to bind to vasopressin receptors in the medullary collecting ducts. This increases transcription for and insertion of aquaporins into the apical membrane and allows pure water to move down the osmotic gradient and into the blood stream. ECF fluid volume also needs regulated, and this is considered to be the “sodium driven” portion, due to sodium’s electrochemical influence. Sodium retention or excretion drives a parallel movement of water and these changes are sensed by baroreceptors in various locations throughout the circulatory system. Low pressure baroreceptors are found in the atria of the heart and intrathoracic large veins. High pressure baroreceptors are found in the carotid sinuses, aortic arch and afferent arteriole of the nephron. With low ECF, the sympathetic branch of the autonomic nervous system is triggered. The cardiovascular changes are seen by an increased heart rate. The baroreceptors and decreased blood flow to the kidney will stimulate the renin-angiotensin-aldosterone system. This ultimately leads to constriction of vascular beds and attempts to maintain normal blood pressure. There is also an increase in efficiency of Na and Cl reabsorption within the nephrons. In addition, vasopressin is secreted and aids in increasing the ECF by increasing water reabsorption. An increase in ECF will cause a reduction in sympathetic tone, subsequently increasing GFR and the kidneys will undergo pressure diuresis. The atrial cardiac muscles release atrial natriuretic peptide, which is responsible for this process by dilating the afferent and efferent glomerular blood vessels. Hypernatremia comes in many forms, and occurs when an animal does not have access to water or has a neurologic disorder that prevents them from accessing water or recognizing thirst. Isovolemic hypernatremia can be caused by diabetes insipidus, insensible water loss, inadequate water intake or persistent hyperglycemia. Hypervolemic hypernatremia can be caused by iatrogenic administration of intravenous crystalloid solutions or excessive intake of sodium without adequate volume of free water.

Species

Sodium Range (mEq/L)

Canine 139-154

Equine 132-141

Feline 145-158

Human 135-145

Ruminants 135-155

VPBP 139-148



Hypovolemic hypernatremia is seen in cases of renal failure or in extra-renal causes such as gastrointestinal or third space loss. Ultimately, intracellular fluid flows into the extracellular fluid compartment until osmolality equalizes.(1-4) Pot belly pigs are seen to have hypernatremia due to either inadequate water intake or excessive sodium intake. Pigs that have acquired an unknown amount of dog or cat food can develop sodium toxicity quite acutely. The clinical presentation is caused by brain parenchymal cell dehydration and a decrease in brain volume. If this continues for too long, eventually cerebral veins will rupture and lead to subarachnoid and intracerebral hemorrhaging. Clinical signs can be as generic as depression and lethargy and as the disease progresses, be primarily neurologic. Patients may have ataxia, behavior changes, blindness, and/or muscle tremors, all of which may progress to seizures, coma and death. (1, 3-5) Diagnosing sodium toxicity depends largely on the history of the animal and a minimal database of electrolytes. Knowing serum concentrations of both sodium and glucose are the most beneficial. A CSF tap can be performed and the sodium concentration measured, but typically not performed or easily feasible. Based on history and serum concentration of sodium, the hypernatremia can be characterized as acute or chronic. Acute hypernatremia is that which occurs in a 24-48-hour period, and the sodium levels are often greater than 160 mEq/L. Chronic hypernatremia occurs over a 4-7 day period, and idiogenic osmoles are starting to contribute to the ICF osmolality. (1, 3)

Intravenous fluids are used to correct hypernatremia and replace lost water, especially from the extracellular space. It is important to know the concentrations of the IV fluids being used, to correct the hypernatremia at an appropriate rate. When treating acute hypernatremia, rapid correction can be accomplished successfully, but gradual change is more ideal. The risk for osmotic demyelination is less in this case, as idiogenic osmoles have not yet accrued in the ICF. It is recommended to reduce the sodium levels no more than 1-2 mEq/L/hr. Loop diuretics may be needed to facilitate the renal excretion of sodium at the same time. A water deficit can be calculated and some patients can be given oral fluids to replenish this, as can be calculated above. It can be distributed over frequent feedings and consist of water or milk, given over 24 hours. When continuous IV fluid therapy is available, 5% dextrose or 0.45% NaCl/2.5% dextrose can be

Byers et. al 2014

Byers et. al 2014



used to lower the ECF osmolarity. Dextrose should not be given at a rate over 8-12 mEq/L/24 hr. A more conservative route would start with sodium-rich IV fluid and then after 6-12 hours, lower IV sodium fluid concentration. (1, 3-5) When treating chronic hypernatremia, brain edema can occur quickly, due to the idiogenic osmoles that are present in the ICF. Use sodium-rich fluids, for longer periods of time by starting with a 0.9% NaCl or a hypertonic saline, for 24 hours, before stepping down the concentration. Ideally, the sodium concentration should only be 10-15 mEq/L less than the patient's serum sodium concentration. The water deficit can be calculated the same as in acute hypernatremia, but replenished over a 48-72 hour period, or longer. Observing the patient's neurologic status and serum sodium concentrations often, during treatment, will be vital. Deterioration in the neurologic status may indicate brain edema and warrants cessation of current therapy. A decline in serum sodium concentration of 0.5 mEq/L/h is a reasonable goal. It is possible to predict how 1 L of a particular IV fluid will affect a patient's serum sodium concentration. This can be used to revise the fluid therapy according to need. (1, 3-5) The severity and onset of the hypernatremia affects prognosis, with more advanced clinical signs occurring with animals that have had a rapid onset, versus those with a slow developing hypernatremia. These neurologic changes can be potentially irreversible. While this disorder can be medical managed and survival can occur, owner non-compliance with treatment and expenses can also be limiting factors. 1. Goldkamp C, Schaer M. Hypernatremia in dogs. Compendium (Yardley, PA). 2007;29(3):148, 50, 52. 2. Sam R, Feizi I. Understanding Hypernatremia. American Journal of Nephrology. 2012;36(1):97-104. 3. Byers SR, Lear AS, Van Metre DC. Sodium Balance and the Dysnatremias. Veterinary Clinics of North America: Food Animal Practice. 2014;30(2). 4. Guillaumin J, Dibartola SP. Disorders of Sodium and Water Homeostasis. Veterinary Clinics of North America: Small Animal Practice. 2017;47(2):293-312. 5. DiBartola SP. Disorders of Sodium and Water: Hypernatremia and Hyponatremia-Chapter 3. 47-79 p.

Byers et. al 2014



VETERINARY TECHNICIANS


PROCEEDINGS



"Muzzle Your Fears!" Aggressive Dog Handling

In moments of fear and anxiety, a dog’s defense mechanism can manifest into aggression in an

attempt to promote distance between them and their perceived threat. Hospitals can be an

automatic trigger for some patients, therefore, it is vital to create a less “threatening”

atmosphere for them. This can reduce current anxieties, hopefully future anxieties as well as

promoting a safe working environment for hospital staff.

Overview Benefits of reducing stress for the patient and owner

Types of aggression

Methods for handling aggressive patients

Drug protocols

Recovery with minimal handling

Benefits of reducing stress

For the patient: ________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

For the owner: ________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

Types of aggression

Fear aggression: _______________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________


In moments of fear and anxiety, a dog’s defense mechanism can manifest into aggression in an

attempt to promote distance between them and their perceived threat. Hospitals can be an

automatic trigger for some patients, therefore, it is vital to create a less “threatening”

atmosphere for them. This can reduce current anxieties, hopefully future anxieties as well as

promoting a safe working environment for hospital staff.

Overview Benefits of reducing stress for the patient and owner

Types of aggression


Drug protocols

Recovery with minimal handling

Benefits of reducing stress

For the patient: ________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

For the owner: ________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

Types of aggression

Fear aggression: _______________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

Bonnylee Kennedy, LVMT - University of Tenneessee College of Veterinary Medicine - Anesthesia




Cage aggression: _______________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

Owner aggression: ______________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

Unknown aggression: ___________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

Working dogs: _________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________


Know your triggers and what alternative methods you can use:

_____________________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

Items to have ready prior to premedication

O2 ________________________________________________________________________

IV catheter supplies __________________________________________________________

Intubation materials __________________________________________________________


BACK TO TABLE OF CONTENTS"Muzzle Your Fears!" Aggressive Dog Handling

Ambu-bag __________________________________________________________________

Monitoring equipment: _______________________________________________________

___________________________________________________________________________

___________________________________________________________________________

Drug options

_____________________________________________________________________________

_____________________________________________________________________________

_____________________________________________________________________________

Recovery

Location: ___________________________________________________________________

___________________________________________________________________________

Items to have ready:

o Owner/Handler ____________________________________________________________

o Sedation drugs _____________________________________________________________

o Muzzle ___________________________________________________________________

Prepare for IVC removal: ______________________________________________________

___________________________________________________________________________

___________________________________________________________________________

___________________________________________________________________________



1

FINDING BALANCE:PATIENT CARE AND STRESS

Erin M. Morrison, LVMT (Anesthesia)University of Tennessee, CVM [email protected]

A LITTLE INFORMATION ABOUT ME:

I enjoy:

Hiking

Knitting and crochet

All animals (especially cats)

Reading

Doctor Who

Experience in:

General practice (mixed) Shelter medicine

Emergency medicine

ICU Care

Anesthesia

OVERVIEW

Why is balance important

Recognizing Fear/Anxiety

Wants vs. Needs

Keys to Successful visits



2

WHY BALANCE IS IMPORTANT



Petunia 5y FS Chihuahua

• Vaccines• Nail trim• Pre dental exam• Blood work



3

Petunia 5y FS Chihuahua

CAUTION!!

WILL BITE

OWNER PROTECTIVE


• Vaccines• Nail trim• Pre dental exam• Blood work

• Healthy Pet• Happy Pet• Happy Owner• RETURN VISITS

GOAL:


HOW TO RECOGNIZE FEAR AND ANXIETY IN DOGS



4

FEAR AND ANXIETY

HOW TO RECOGNIZE FEAR AND ANXIETY IN CATS

FEAR AND ANXIETY



5

FEAR AND ANXIETY

FEAR AND ANXIETY

FEAR AND ANXIETY



6

WANTS VS. NEEDS

NEEDS Immediate life saving treatment

WANTS

Everything else



7

KEYS TO SUCCESSFUL VISITS

Where does it start?

Building trust

Treats

Comfort

Drugs (sometimes)

WHERE DOES IT START?




8


TRUST



9

TRUST

Teach owners condition pets

Treats and praise

TRUST

TRUST



10

TREATS

TREATS

Peanut Butter

TREATS

Peanut Butter

Easy Cheese



11

TREATS

Peanut Butter

Easy Cheese

Lickety-stick

TREATS

Peanut Butter

Easy Cheese

Lickety-stick

Mini Marshmallows (hypoallergenic)

TREATS

Peanut Butter

Easy Cheese

Lickety-stick


Baby food



12

TREATS

Peanut Butter

Easy Cheese

Lickety-stick


Baby food

Any treat they love!

COMFORT

COMFORT



13

COMFORT

COMFORT

COMFORT



14

COMFORT

COMFORT



15

COMFORT

COMFORT

COMFORT



16

COMFORT

COMFORT

COMFORT



17

COMFORT

DRUGS (SOMETIMES)

DRUGS (SOMETIMES)

Trazodone



18

DRUGS (SOMETIMES)

Trazodone

Gabapentin

DRUGS (SOMETIMES)

Trazodone

Gabapentin

Sileo

WEAR GLOVES

DRUGS (SOMETIMES)

Trazodone

Gabapentin

Sileo

Acepromazine (controversial)



19

VETERINARY BEHAVIORISTS

https://www.dacvb.org/



20

REFERENCES

Cooperative Veterinary Care, Alicea Howell, Monique Feyrecilde

Low Stress Handling, Restraint and Behavior Modification of Dogs and Cats, Sophia Yin

Photos from Google, myself, and Alyssa Stair



1

Is Age A Disease? Anesthetic Considerations For The Geriatric PatientsUniversity of Tennessee VPAC 2019Jessica Konzer Birdwell BA, LVMT, VTS (Anesthesia and Analgesia)

Objectives

• What is geriatric?• Breaking down the

systems• Learning points



2

Geriatric

• 75% of life expectancy• 30 % of animal population• Physiologic and pathologic changes• Increase mortality by a factor of 7 • Related primarily to decreased

physiologic reserve

Recommended Perioperative Items

• Thorough history• Understand medication• Body condition: wt, change, T, P, R, auscultations• CBC, Chemistry and electrolytes, T4• Urinalysis• Blood pressure• Chest radiographs• Echocardiogram• ECG



3

Critical Organ Functions: Respiratory

• Weakened respiratory muscles• Loss of elastic tissues• Decreased chest wall compliance and

recoil• Predispose to atelectasis and

hypoxemia• Increased airway resistance,

decreased pulmonary diffusion capacity and decreased capillary blood volume leading to reduced efficacy for gas exchange

• Increased susceptibility to infection

Critical Organ Functions: Respiratory Recommendations• Oxygen supplementation, pre, intra

and post• 3-5 minutes prior to anesthesia • MAC reduction in inhalants• IPPV – manual or mechanical• Oxygenation/ventilation monitoring

• SPO2, ETCO2 with capnogram, ABG



4

Critical Organ Functions: Cardiovascular• Multifactoral intrinsic physiologic changes• Myocardial fibrosis, valvular fibrocalcification, ventricular thickening• Decreased baroreceptor activity, circulation time, blood volume, blood pressure, and CO• Decreased cardiac reserve = hypotension• Compromised conduction system = arrhythmias

Critical Organ Functions: Cardiovascular Recommendations

• Preanesthetic cardiac evaluation

• ECG and pulse palpation for arrhythmias

• Negative inotropes and arrhythmogenics avoided

• Ensure adequate venous return and fluid balance to reduce hypotension caution for overload

• IBP, ETCO2, SPO2



5

Critical Organ Functions: Hepatic

• Deteriorated function

• ↓ mass and hepatic blood flow

• ↓ microsomal enzyme activity

• Generalized reduction in metabolic activity

Critical Organ Functions: Hepatic Recommendations• Liver function analysis• Coagulation profile• Monitor blood glucose levels• Monitor and maintain normotension to optimize

hepatic blood flow• Caution with anesthetics primarily metabolized

by the liver and/or protein bound• Prolonged recovery and/or reduced doses



6

Critical Organ Functions: Central Nervous System (CNS)

• Compromised motor, sensory, cognitive, and autonomic functions

• Decreased brain size, loss of neurons

• Increase CSF• Depleted neurotransmitters• Decreased cerebral oxygen

consumption• Myelin degeneration• Thermoregulatory center

weakened

Critical Organ Functions: Central Nervous System (CNS)• Compromised motor, sensory,

cognitive, and autonomic functions• Decreased drug requirements• Supplement neurotransmitters

(dopamine, norepinephrine, etc)• Provide thermoregulatory support

pre, intra, post• Oxygen supplementation



7

Critical Organ Functions: Renal

• 0.5% -1.5% renal disease increasing w/age

• CKD, urinary incontinence, bladder tumors, prostate problems

• Decreased renal mass –decreased tubular size, wt, and glomerular availability, filtration and fnc.

• Reabsorption, formation, elimination and metabolism compromised

Critical Organ Functions: Renal Recommendations • Renal function analysis (UA, BUN, CRE)• IBP, NIBP, ins/outs, and hydration status• Avoid hypoxemia, hypervolemia, hypotension, and

hypercarbia to minimize post anesthesia complications

• Minimize time under anesthesia• Ensure proper fluid rates and preoperative loading

recommended• Caution with protein bound drugs



8

Critical Organ Functions: Endocrine

• Hyperadrenocorticism – decreased adrenal responsive

• Diabetes Mellitus• Hypothyroidism

Critical Organ Functions: Endocrine Recommendations• Corticosteroid supplementation pre

anesthetically• Hyperadrenocorticism – decreased adrenal

responsive• Diabetes Mellitus – BG monitoring, alpha2s?,

return to feeding• Hypothyroidism – likely to be cold



9

Critical Organ Functions: Gastrointestinal

• Increased risk of esophageal reflux• Possible compromised laryngeal and pharyngeal• Aspiration pneumonia risk• Visceral sensitivity• Motility• Immunity

Critical Organ Functions: Gastrointestinal• Maintain and recover in

sternal• Suction prior to extubation• Antiemetics, antacids• Prokinetics• Monitor for aspiration

pneumonia post• Caution with NSAIDs



10

Learning Points

• Critical organ functions reduced• Less functional reserve• Relatively poor response to stress• Less able to maintain adequate hydration• Affected by degenerative disorders• Absorption, distribution and elimination

compromised

Learning Points

• Response to drugs lower – slower recovery, slower renal and hepatic function

• Reduced thermoregulation = hypothermic

• Less tolerance to hypotension but more likely overhydration



11

References• Bryant, S. Anesthesia for Veterinary Technicians.

2010. Wiley-Blackwell Publishing.• Lumb and Jones. 2015. Veterinary Anesthesia and

Analgesia 5th ed. Wiley Blackwell.• Seymour, C and Duke-Novarkovski, T. 2007. BSAVA

Manual of Canine and Feline Anaesthesia and Analgesia. 2nd ed. British Small Animal Veterinary Association.

• Synder, L.B.C and Johnson, R. A. 2015. Canine and Feline Anesthesia and Co-Existing Disease. Oxford, UK. Wiley Blackwell.

• Thomas, J and Lerche, P. 2017. 5th ed In Anesthesia and Analgesia for Veterinary Technicians. Elsevier.



Opioids? How About Nopioids! Alternative Agents for Pain Management Jessica Konzer Birdwell BA, LVMT, VTS (Anesthesia and Analgesia)

A landmark case in 1985 embarked a movement toward improved analgesia/anesthetic

care. The mother’s account noted her son being operated on to correct a PDA and received nothing but a paralytic. She states “both sides of his neck cut, incisions on both his left and right chest, and another from his breastbone to his backbone. His ribs were then pried apart and finally the artery tied off.” Imagine, no anesthesia or analgesia for hours of operation. You the patient know what is happening but can’t move. In questioning the anesthesiologist, the mother heard claims of obstacles for proper agents for this critically ill patient. One of our biggest obstacles in veterinary medicine today is the opioid shortage. Opioids traditionally were the primary agents of analgesic support in our patients. While this is account is probably difficult to hear, it illustrates the importance for us to fulfill our veterinary oath to do no harm, regardless of the obstacles. The veterinary technician/nurse can aid in breaking down the barriers in effective pain management as client educator and patient advocate through furthering their knowledge and competence. Hopefully this lecture will provide a glimpse of opportunity for just that. This session will review what pain is, the pathway it takes through the body, then looks at utilizing a multimodal analgesic protocol with alternative agents available to tailor on a patient to patient basis. Additional guidelines for pain management are available through the ACVAA, AAHA/AAFP, and IVAPM websites or in the references listed at the end of this document. What is pain?

Pain is the recognition of noxious stimuli that signals the brain of an actual or potential injury to the tissue. It utilizes specialized nerve endings, called nociceptors, to detect the location, intensity and nature. These signals are then communicated to the brain to differentiate between noxious stimuli from innocuous: IE allowing detection for temperature extremes, excessive pressures, tissue damage, or chemical exposures vs general touch or vibrations that are nonthreatening (1). Pain can be the result of an injury or illness that leads to physical, physiological and/or emotional stress. When left untreated pain can lead to vasoconstriction, increased myocardial workload, increased oxygen demands, alterations in endocrine functions toward a catabolic state ending in wasting and death, suppressions in the immune response creating an increased risk for infection, promotions in inflammatory response that decreases overall healing, increases in drug requirements with more likelihood for or worsening of adverse effects, and overall suffering due to increased stress for patient, staff and the client, etc. Although, this lecture will not focus on the types and classifications of pain, veterinary personnel should be aware that there are differences which can affect the side effects of pain their needed analgesic treatments and responses to these treatments. Below are some brief bullet points for the recognized types and classifications. Acute Pain Chronic Pain Is a symptom of a disease Trauma, surgery, or infection related Abrupt onset with short duration Warning = biological function

IS A TYPE OF DISEASE Long onset with long duration: months → years Is not a biological function and increases stress Seldom is permanently alleviated Tranquilizers and psychotropic may be needed



Generally, is alleviated by analgesics such as opioids, NSAIDS, etc.

Physiology Pain: recognition to protect the host Pathologic Pain: results from either ailment below Fast Well localized

Stops after removal of stimuli “ouch phase” A-δ fibers

Inflammatory Tissue damage Primary hyperalgesia: inflammatory mediators at the site of injury leading to peripheral sensitization Secondary hyperalgesia: alterations in sensory processing IE central sensitization

Slow Poorly localized Continues after the stimuli has stopped Throbbing, burning, and aching Unmyelinated C fibers

Neuropathic Injury to the nervous system Can be peripheral or central sensitization. Due to trauma, vascular, endocrinopathy, or infection Commonly leads to hyperalgesia and allodynia

Combination Multitude of both fast and slow

Pain Pathway Regardless of origin, each noxious stimulus travels through the same pathway in the body. This pathway consists of four main parts: transduction, transmission, modulation and perception.

Transduction – noxious stimulus turns into electrical signals. Specialized chemical, thermal, and mechanical receptors detect the type of injury The sensory (afferent) nerve endings then translate this into electrical signals to share the message for the remainder of the pain pathway to understand. Peripheral nociceptors.

Transmission – once translated the signals travel thru the peripheral nervous system to the central nervous system or dorsal horn. The body utilizes excitatory neurotransmitters like norepinephrine and serotonin to continue the signal from the synaptic cleft to the brain. Afferent nerve (sensory) fibers = myelinated A-δ conduct fast “ouch” type pain. Efferent

(motor) fibers = nonmyelinated C fibers conduct slow, dull pain (throbbing, burning, heat) or in chronic pain

Modulation – signal passes through synapses into the CNS. There are various regions of the spinal cord and

brain involved here (dorsal horn, ventral horn, and intermediate zone, plus white matter). This is where the signals are modified by either being enhanced or inhibited. The endogenous systems process the

http://www.icagen.com/randd/paindisorders.html



information. Typical receptors here involved are NK-1, NMDA and prostaglandins for modification while GABA, opioids, and adenosine receptors inhibit the signals.

Perception- Here the brain organizes the information by interpreting the information and experiencing the stimuli. Meaning, the conscious experience with recognition of the pain signal. There somatosensory cortex within the cerebrum is responsible for this higher processing and awareness.

Multimodal Analgesia is a balanced analgesia plan that combines drug groups with varying modes of action to target the entire pain pathway. An ideal multimodal analgesia protocol provides effective analgesia by reducing the intensity of the noxious stimuli by either obtunding or interrupting nociception without depressing the natural behaviors of the host. IE making the pain more tolerable to continue functioning as close to normal as possible without harm. Advantages on this technique include an alleviation of pain, reduction in stress (patient, client, and veterinary personnel), decreased drug requirements reducing likelihood or severity of adverse side effects, improved safety, and optimal patient healing.

The following drugs groups are involved in the pharmaceutical intervention when dealing with multimodal analgesia techniques: opioids, local anesthetics, alpha2 agonists, dissociatives, non-steroidal anti-inflammatories, muscle relaxants, tranquilizers, etc. Some information of each group is provided below, but veterinary personnel should seek alternative resources and education for a complete understanding of each agent and other adjuncts. In addition, there are many non-pharmaceutical interventions that assist in the alleviation of pain that should be considered.

Opioids: Mu/Kappa receptors in the brain, cord, and peripheral tissues. Obtund transduction, modulation, perception. Inhibits perception and ↓ central sensitization. There are varied uses based on drug properties with IV, IM, SQ, PO, CRIs, transdermal, creams, locoregional, etc. routes available. Examples include but are not limited to morphine, fentanyl, butorphanol, buprenorphine, methadone, meperidine, etc.

Local Anesthetics: Sodium channel blockers. Bind to sodium channels to prevent, slow or stop nerve conduction in all neurons IE pain, sensory, motor, proprioceptive, sympathetic nerve conduction. These agents abolish both transduction and transmission signals and minimize modulation when combined w/ other analgesics. Desensitize tissues and reduce the potential for central sensitization development. They are cheap with a relatively wide margin of safety for many species, however cardiovascular and CNS toxicities are possible. Their potency is correlated to their lipid solubility, in turn their recovery is based on dissipation of the drug. Some negative side effects associated with these agents include the lack of sensory (IE protective mechanisms for heat or urination), motor (inability to move has adverse effects associated pending patient size, comorbidities, or healing), and sympathetic (can alter physiologic normal IE hypotension if given too fast, etc.). They have varied absorption rates and modalities with antimicrobial properties as well. Topical, intermittent or continuous infiltrative, regional or nerve blockades applications are possible. Examples include but are not limited to bupivacaine, lidocaine, septicaine, marcaine

Alpha2 Agonist: Obtund transmission, modulation, and perception by acting on the alpha2 adrenergic receptors. They are beneficial as an anxiolytic to reduce the stress response being experienced by the patient. It targets peripheral antinociception, prolongs the duration of adjuncts or local blockades, and synergistically acts with drugs and blocks increasing their efficacy. Adverse side effects include cardiovascular changes, vomiting, hypoinsulinoma, hyperglycemia, hypercarbia from depressed



respiratory center, and noise hypersensitivity. The following are common examples in veterinary medicine: dexmedetomidine, xylazine, clonidine, detomidine, dormosedan gel, etc.

Dissociatives: Act on the NMDA receptors to obtund perception and modulation; hence disassociate the pain. This aids in the prevention of dulling of central sensitization and wind up proving effective for both neuropathic pain or chronic pain. These agents have varied duration and modulations (IV, IM, PO, CRIs) pending dosage with lower doses typically effective for providing analgesia and higher establishing more anesthesia states. Examples include ketamine, tiletamine, amantadine, and dextromethorphan.

NSAIDS: Inactivates enzyme cyclooxygenase (COX) which helps with the inhibition of prostaglandin synthesis making them a potent anti-inflammatory aid. They obtund transduction & modulate spinal processing during modulation. They have a range of cases they are effective for from acute injuries like OHE to fracture (not primary analgesic) or chronic pain such as arthritis but are most effective with somatic analgesia. They have varied modalities and durations including but not limited to PO, IV, IM SQ, varied species efficacy with narrow safety margin and some are antipyretic (fever reducer). Commons examples in this group are aspirin, carprofen, meloxicam, deracoxib, robenacoxib, etc.

Muscle Relaxers and Tranquilizers: These agents change mentation primarily involved when dealing with chronic pain or hyperalgesic/allodynia type pains. They are effective in obtunding modulation and perception and typically are orally or intravenously administered. Their actions all vary depending on their targeted receptor IE benzodiazepines act on GABA receptors. Examples of these include benzodiazepines, tricyclic antidepressants, corticosteroids, and herbal supplements.

Other Pharmaceuticals:

Gabapentin: Anticonvulsant with analgesic properties thought to be derived by down-regulating calcium channels. It is widely used in human medicine for neuropathic and maladaptive pain conditions, but has proven efficacious in DJD, chronic musculoskeletal, and post-surgical pain in animals. The primary adverse side effect in animals is somnolence.

Maropitant: is a central antiemetic that blocks substance P from binding to NK-1 receptor during pain processing. Studies indicate it may have anesthetic-sparing effects during visceral stimulation, however, the mechanism is unknown. Many believe the effects often could originate from its action on minimizing acute vomiting perioperatively with return to feeding assisting in improved outcome postoperatively.

Tramadol: is not a true opioid but a weak mu opioid analog beneficial for mild to moderate pain primarily used to treat canine osteoarthritis, diabetic neuropathies, and other neuropathic pain. It inhibits reuptake of norepinephrine and serotonin in the pain pathway. Caution with other SSRIs leading to serotonin syndrome.

Bisphosphonates: administered intravenously exerts antiosteoclast activity relieving some discomfort with bone cancers.

Non-Pharmacologic Treatments: are available but are not discussed at length in this lecture include but are not limited to the following: Cold compression Warming – “Hot pad” Weight optimization Therapeutic exercise Acupuncture

Physical rehabilitation Myofascial trigger therapy Chiropractic therapy Therapeutic laser Nursing care

Gentle handling Caregiver involvement Improved environment Hospice



Conclusion: The purpose of this lecture was strictly an introduction for veterinary technicians on the pain pathway and the agents available to veterinary personnel outside of the typically opioids. Regardless of obstacles, the attendees should have a better realization that opioids alone are no longer the recommended main stream for analgesic treatment. Further comprehension, education, and training is needed to completely understand all the agents or modalities mentioned briefly in this discussion.

References:

DeGouff, L. 2010. Basic Physiology of Pain. Anesthesia for Veterinary Technicians, edited by Susan Bryant. Iowa: Wiley-Blackwell Publishing.

Epstein, M; Rodan, I; et al. 2015 AAHA/AAFP Pain Management Guidelines for Dogs and Cats. https://www.aaha.org/aaha-guidelines/pain-management-config/

Greene, S. 2010. Chronic Pain: Pathophysiology and Treatment Implications. From the College of Veterinary Medicine, Veterinary Clinical Sciences, Pullman, WA, USA.

Goldberg, ME and Shaffran N. 2015. Pain Management for Veterinary Technicians and Nurses. Wiley-Blackwell Publishing.

Grubb, T. 2010. Chronic Neuropathic Pain in Veterinary Patients. From the College of Veterinary Medicine, Veterinary Clinical Sciences, Pullman, WA, USA.

Lumb and Jones’ Veterinary Anesthesia, 5thed, 2015. edited by Thurmon, JC. Philadelphia: Lippincott Williams and Wilkins.

Mathews, K. 2008. Neuropathic Pain in Dogs and Cats: If Only They Could Tell Us If They Hurt. Vet Clin Small Anim 38: 1365–1414

Mathews, KA and Sinclair M. 2018. Analgesia and Anesthesia for the Injured Dog and Cat. Wiley –Blackwell Publishing.

Seymour, C and Duke-Novakovski. BSAVA Manual of Canine and Feline Anaesthesia and Analgesia 2nd ed, British Small Animal Veterinary Association. Saskatoon Canada.

Thomas, J and Lerche, P. 2017. 5th ed In Anesthesia and Analgesia for Veterinary Technicians. Elsevier.

Thurmon, J; Tranquilli, W; and Benson, G. 2011 Perioperative pain and its management. In Essentials of Small Animal Anesthesia and Analgesia. Philadelphia: Lippincott Williams and Wilkins.



PUTTING PEP BACK IN THEIR STEP: OSTEOARTHRITIS MANAGEMENT IN COMPANION ANIMALS

Dawn Hickey, LVT, VTS (Physical Rehab), CCRP, CVPP, CCFT

INTRODUCTION

Osteoarthritis (OA) is one of the most common diseases seen in companion animals, affecting up to 20% of dogs. Accurate data is lacking as to the true percentage. Based on some studies, the figure may be much higher. Incidental findings in a study of 30 dogs presenting for dental procedures were that 60% of the dogs had radiographic OA in one or more joints. Most owners of arthritic dogs do not recognize mobility issues in their dogs. Patients with OA have pain and discomfort, muscle atrophy due to inactivity, decreased range of motion (ROM) and decreased quality of life. Decreased flexibility, joint stiffness, and loss of strength progresses in a vicious cycle due to the pain associated with OA. Traditional management of dogs with OA has included anti-inflammatory and analgesic drugs, changes in lifestyle, and surgical management. The management of human OA has changed over the years and given us more options to consider with animals. We now include weight loss, exercise programs, and physical modalities to reduce the severity of symptoms and decrease reliance on medications to control pain and discomfort.

MANAGEMENT OF OSTEOARTHRITIS

Management of OA requires recognition of the problem. Owners must be educated about the prevalence of OA in their pets or they may contribute a pet’s inactivity to aging. It is also very common for owners to discount the pain the pets encounter due to the different way animals exhibit pain. The most common signs of OA in the home environment are difficulty climbing or descending stairs, difficulty laying down or getting up, difficulty moving after rest or after major activity and an inability to perform previously normal activities such as jumping in the car or on the bed. Veterinary offices should routinely perform lameness evaluations, functional evaluations and orthopedic examinations, especially in senior pets. Early recognition can make a difference in the quantity and quality of life of the animal due to the fact that the available supplements and treatments are more efficacious before the joint has fully degenerated. The most effective medical treatment of OA is multi-modal and includes weight reduction, physical modalities, controlled exercise, anti-inflammatory medications, symptom and structure modifying osteoarthritic agents and alteration of the home environment. This management continues throughout the lifetime of the animal. Owners must be made aware that there is no ‘cure’, and consistency in treatment is critical to quality of life.

Signs of pain in dogs

v sleeping more v slower on walks or not wanting to walk as far v resent being touched or brushed in certain areas v accidents in the house or walking while urinating or defecating



v taking more time standing up from a lying down position v difficulty getting into the car v carrying their heads or tails lower than normal v reluctance to go up stairs, jump on the bed; or furniture, v sitting with their hind legs stretched out (lazy sit)

Signs of pain in cats

v Withdrawal, hiding, increased ‘clinginess’ v irritability when touched, aggression toward other cats or humans v Decreased appetite v Hunched, head lowered, sitting or lying abnormally, squinting v Lack of grooming, over-grooming of painful area v Decline in bowel movements, house soiling, inability to get into litter box v Not jumping as often or as high, hesitant to jump, difficulty going up or down stairs,

stiffness, less active

RECOGNIZING OSTEOARTHRITIS

A comprehensive orthopedic exam should be performed. Be sure to examine the entire patient because most have more than one joint affected. The hips, elbows, tarsi and stifles are the most common, but don't overlook the spine, especially the T/L junction and lumbar spine. Passive range of motion (PROM) can inform you of problems within a joint such as decreased ROM, crepitus and/or pain. When performing an orthopedic exam, it is important to try and keep the dog as calm and comfortable as possible and be able to recognize vocalization for pain instead of anxiety or fear. It is crucial for the technician/nurse to pay attention to the animal’s body language and notice what happens when the veterinarian is manipulating the animal.

TREATMENT OF OSTEOARTHRITIS

The goal for management of osteoarthritis is to provide maximum benefit to patients to help restore function to the fullest extent possible and to reduce the pain and discomfort of this chronic disease condition. Successful management is always multi-modal.

Ø WEIGHT REDUCTION

Weight reduction is the single most important treatment in the management of OA. Optimal body weight helps to reduce the progression of arthritis and reduces the symptoms. In the Purina life study in Labrador Retrievers, littermates were randomly selected to be fed a calorie limited or calorie rich diet. In the calorie rich group (control), the age at which 50% of the dogs had clinical signs of OA was 7 years. In the calorie limited group, the age at which 50% of the dogs had clinical signs of OA was 12 years. Additionally, the lifespan of the control group (fed ad lib for 15 minutes twice daily) was 15% less that the lean fed dogs (75% less food than control group). In addition to restricting intake of the normal diet and eliminating treats, prescription diets are available that can dramatically assist in achieving and maintaining ideal body weight. In general,



the goal is to reduce fat composition to 20-25% of an animal's total body weight. Clinically, the ribs should be easily palpable and there should be a "waist" when the animal is viewed from above. It has also been proven that an 8-10% weight loss causes a significant decrease in lameness.

Ø PHYSICAL REHABILITATION

Recently, the use of physical modalities has received a great deal of attention in both human and veterinary medicine as another way to manage the symptoms of osteoarthritis, and to improve function, particularly muscle strengthening, flexibility and range of motion, and endurance. Some of the modalities that may be helpful include:

§ Heat - heat applied to arthritic joints may be soothing, relieve muscle

tension, and increase flexibility of joint capsules and tendons to help improve range of motion. It may not be advisable, however, to apply heat to arthritic joints that are experiencing an acute flare-up with inflammation.

§ Cryotherapy - cryotherapy, or the application of cold, may be soothing to

joints, provide analgesia, reduce inflammation, and may decrease some of the destructive enzymatic processes occurring in osteoarthritis.

§ Range of Motion and Stretching - chronic osteoarthritis often results in

diminished joint range of motion and stiffness. Proper range of motion and stretching exercises, often as part of a home exercise program, can help improve flexibility and joint function.

§ Therapeutic exercises - as a result of the pain of arthritis, many patients

limit their activity level, resulting in weight gain, decreased cardiovascular performance, muscle weakness, increased stiffness, and decreased joint range of motion. A well-designed therapeutic exercise program helps to restore or improve function in arthritic patients.

§ Aquatic exercise - aquatic exercise is another form of therapeutic exercise

and takes advantage of the buoyant properties of water to reduce weightbearing on painful, arthritic joints. In addition, the resistance that water provides encourages muscle coordination and strengthening. Arthritic patients, in particular, greatly benefit from this form of exercise.

§ TENS - transcutaneous electrical nerve stimulation is a form of electrical

stimulation that may be applied around arthritic joints to reduce pain. This form of therapy is used in people with back pain and arthritic knees to help improve comfort by flooding the spinal cord with many low intensity signals that help prevent the transmission of large pain signals. People report feeling a “pins and needles” sensation, and dogs generally tolerate the treatment quite well.



§ Extracorporeal Shock Wave Treatment - this is a relatively new form of

treatment that may have benefit for patients with osteoarthritis. A clinical study indicated that patients with severe osteoarthritis of the hip or elbow may receive a benefit equivalent to that of most NSAIDs.

§ Acupuncture - acupuncture has been used for centuries for the treatment of

many conditions, including osteoarthritis. Although there is a relative lack of research information regarding osteoarthritis treatment in dogs, anecdotal information and recent research performed on people indicates that acupuncture may benefit some arthritic patients.

§ Laser - laser energy applied in the form of “cold” (nonsurgical) laser has

been used in some arthritic patients with benefit. Although research data regarding osteoarthritis treatment is lacking in animals, anecdotal reports suggest that some patients may benefit.

§ Therapeutic ultrasound – therapeutic ultrasound has biological and heating

effects. Recent research in humans suggests that arthritic patients receiving this treatment have less pain and improved function.

§ Platelet-rich plasma – this form of therapy involves harvesting a small

amount of blood from the patient and generating plasma with platelets. Platelets are rich in growth factors and injection into joints helps to improve the anabolic-catabolic balance.

§ Autogenous stem cell therapy – this is a new concept in veterinary

medicine that uses stem cells harvested from the bone marrow or subcutaneous fat of the patient that is then processed by a laboratory. The stem cells are injected into arthritic joints under aseptic conditions. Stem cell therapy seems to “reset” the inflammatory pathways to a more favorable environment.

Ø SYMPTOM MODIFYING OSTEOARTHRITIC AGENTS.

These treatments have been the mainstay of treatment for patients with osteoarthritis and are aimed at the alleviation of inflammation and pain. Typically, nonsteroidal anti-inflammatory drugs (NSAIDs) are included in this category. A variety of NSAIDs are approved for use in dogs, including deracoxib (Deramaxx), carprofen (Rimadyl), meloxicam (Medicam), etodolac (Etogesic), and tepoxalin (Zubrin). Because dogs respond differently to various medications, several trial courses of medications may be instituted to determine which medication works best in your pet. Never combine NSAIDs with each other or administer aspirin or steroids with NSAIDs. These increase the potential for developing a gastric ulcer. Also, never administer a human anti-inflammatory medication to your pet. The metabolism of these drugs differ between dogs and humans, and may result in serious illness or death to animals. Although NSAIDs



designed for use in dogs are generally safe, all NSAIDs (as well as all medications) have the potential for adverse reactions. Common adverse reactions include vomiting, diarrhea, loss of appetite, liver disease, kidney disease, and platelet dysfunction. Therefore, the pet should be assessed for any underlying disease conditions that may affect the use of a particular medication. These tests include a physical examination, complete blood count, serum biochemistry profile, and urinalysis. Depending on the situation, other tests or re-evaluation may be recommended at regular intervals to be certain that the pet is not experiencing any reactions to medications. Recently, a variety of other medications have been used in animals with osteoarthritis to block pain by mechanisms that differ from the pain control achieved by NSAIDs. These medications include acetaminophen (Tylenol-type drugs – CAUTION - these should never be used in cats), acetaminophen with codeine, gabapentin, tramadol, and amantadine. Generally, these medications are reserved for those patients who have end-stage osteoarthritis or who have acute flare-ups of arthritis symptoms.

Ø STRUCTURE MODIFYING OSTEOARTHRITIC AGENTS

These compounds have been used in clinical patients to help modify the destructive

processes of osteoarthritis. These agents have been studied in cell culture under various conditions and may demonstrated a positive benefit to cartilage cells. Many have also undergone clinical testing in human patients and have benefitted some patients, and some have been evaluated in animals. In general, these agents have a slower onset of activity and may not relieve pain or symptoms of osteoarthritis, but it is hoped that they will slow the process of cartilage destruction and modify the biology of the condition. These agents are likely to be most beneficial in early OA than in end-stage OA. In general, these agents have few adverse reactions.

o Adequan - this drug is an injectable form of polysulfated glycosaminoglycan that

has been used to help improve the health of articular cartilage, reduce the destructive enzymes, and improve function in dogs. It is approved by the FDA for the management of osteoarthritis. However, it should not be used prior to surgery or in animals with bleeding disorders.

o Glucosamine and Chondroitin Sulfate - these substances act synergistically to

improve the environment in joints and may modify the course of osteoarthritis. A number of studies performed in humans have demonstrated that they may result in improvement in some patients.

o Hyaluronic Acid - HA is a substance found in synovial fluid and in the cartilage

matrix. Levels are often reduced in arthritic patients. Injection of HA into arthritic joints may help to improve the cartilage environment and provide some pain relief. It is used in humans with knee arthritis. An injection into the affected joint under aseptic conditions and with the patient heavily sedated are necessary for safety and comfort.



o Doxycycline - although this is an antibiotic that is often used to treat tick-borne diseases, such as Lyme disease and Rocky Mountain Spotted Fever, doxycycline also has disease modifying properties in arthritic patients by reducing the activity of destructive enzymes.

o Methylsulfanylmethane - MSM is a derivative of DMSO, which has anti-inflammatory properties. While DMSO is frequently applied topically to horses with musculoskeletal conditions, MSM is given orally and may have some benefit to arthritic patients.

o Polyunsaturated Fatty Acids - Certain forms of polyunsaturated fatty acids

(PUFA), especially omega-3 fatty acids, may reduce the production of certain eicosanoids, especially the more potent inflammatory leukotrienes and help reduce the degree of inflammation.

Ø CORTICOSTEROIDS

These medications may be administered by a pill or injection in the joint. Again, these medications, although very potent anti-inflammatory drugs, are reserved for those with severe osteoarthritis because long-term use may result in permanent damage to the cartilage, and other side effects may occur with chronic steroid use, such as increased thirst and urination, increased appetite and weight gain, and changes in the liver.

Ø ENVIRONMENTAL MODIFICATIONS

Altering the environment may be helpful for dogs with moderate to severe arthritis. The principles for dogs are similar to those for arthritic humans. Whenever possible, animals should be moved from a cold, damp outdoor environment to a warm, dry inside environment. A soft, well-padded bed should be provided. Provide good footing to avoid slipping and falling. Minimize stair climbing through the use of handicapped ramps and keeping pets on ground floors. Portable ramps are available to assist patients getting in and out of vehicles. Avoid overdoing activities on the weekends and prevent excessive play with other pets because arthritic animals may attempt to keep up, and in the process, become more lame and painful. In some instances, however, play with other animals stimulates activity and provides a welcome break in the exercise routine. Assistive devices such as slings and wheelchairs can significantly help mobility and improve quality of life for some animals.

CONCLUSION

Osteoarthritis is a common problem in companion animals. Successful management of the arthritic patient is multi-modal and must be tailored to each patient and their owner. Weight control, physical rehabilitation, and medication are the main components for OA management. Cooperation and communication among the veterinarian, therapist, veterinary technician and owner are vital to maintain quality of life in these animals.



FOOD TOXICITIES IN COMMERCIAL FOODS Claudia A. Kirk, DVM, PhD, DACVN, DACVIM College of Veterinary Medicine University of Tennessee, Knoxville, TN Background Over the past 15 years, there have been 4 major food toxicities contributing to morbidity and mortality in the pet population (Go Natural, Diamond Foods, Menu Foods, Sunshine Mills). Countless other recalls have occurred, and while reports of serious health impact were few, taken together, these minor recalls have resulted in harm to pets and sometimes people. The widespread nature of the Melamine-cyanuric acid contamination raised the level of awareness and helped include animal foods in the 2011 Food Safety Modernization Act. Frustrated with limited oversight, lack of clear regulatory authority, and lack of reporting structure, this legislation was designed to improve the safety and quality of pet foods. Nevertheless, the food supply for people and pets are constantly at risk, and it is imperative that the veterinarian team understand how to recognize and report suspected toxicity, how to preserve information to aid in discovery unsafe foods, and how to protect owner’s legal rights through documentation. Common food toxicities While the most notable pet food toxicity has been the Melamine adulteration of vegetable proteins used in pet foods, aflatoxin, bacterial contamination, and Vitamin D excess are ongoing and result in both animal and human disease. Currently, the relationship between Grain-free dog foods or BEG diets (Boutique, Exotic proteins, & grain free), initially thought to be taurine-deficiency, is a complex issue that appears related to unknown dietary factors, including a potential food toxin. In past reports, a toxin has not been identified despite substantial numbers of pet deaths and aggressive investigation by the FDA (i.e., Go Natural). Regardless, awareness of current recalls and common signs of toxicities can assist veterinary staff in recognizing a potential food toxicity, provide timely diagnostic and treatment to affected patients, and notify the appropriate authority. Aflatoxin –Aflatoxin is a naturally occurring toxic chemical by-product from the growth of the fungus Aspergillus and Penicillium on corn and other crops. The fungus develops on crops during years with severe high-temperature stress and drought. In pet foods, corn and wheat products are most at risk. Regulations require testing of grain crops by suppliers before shipment and at manufacturing facilities. Contaminated pet foods have typically occurred because of poor quality control and skipped testing; however it is possible to miss small pockets of contamination within large shipments. There are 4 natural Aflatoxins (B1, B2, G1, and G2) with B1 being the most common and highly hepatotoxic. Aflatoxins are most known for hepatotoxicity. However, they can be immunosuppressive, nephrotoxic, carcinogenic, and can cause hemolytic anemia or coagulopathies. Dogs and cats are particularly susceptible to the B1 toxin. Clinical signs are most typical of hepatic necrosis. Initially, animals often refuse contaminated food, followed by loss of appetite, vomiting, diarrhea, jaundice, bilirubinuria. A fever may sometimes be present. Bacterial contamination: Salmonella contamination is common and has resulted in many ongoing pet food recalls. Recent recalls have been associated with human illness with the same sub-type of Salmonella found in pet food products in the home. Thirty-four people, across 13 states have been infected with a drug-resistant Salmonella after exposure to pig ears leading to a current recall. This bacterial contamination has the potential to cause significant harm to the pet as well as family members. Clinical signs typically start as diarrhea (often bloody), fever, abdominal pain, and vomiting. While most pets and people will improve in 4-7 days, infections can lead to septicemia, organ failure, and death in susceptible individuals. Botulism is reported sporadically both in pet and human canned foods. A recall of Natural Balance canned varieties due to botulism occurred in 2007 due to concerns over food processing. Recently, OC Raw Dried Sardines were recalled due to excessive “sardine size” in their freeze-dried product and association of such fish with botulism. Botulism typically occurs from consumption of botulinum toxin



produced by Clostridium botulinum following inadequate canning procedures. Following ingestion the incubation period can be from 2 hours to 2 weeks; in most cases, the symptoms appear after 12 to 24 hours. Botulism is characterized by progressive motor paralysis. Typical clinical signs may include muscle paralysis, difficulty breathing, chewing and swallowing, visual disturbances, and generalized weakness may also occur. Death usually results from paralysis of the respiratory or cardiac muscles. Other bacteria or bacterial spores may contaminate pet foods. Most cause mild gastrointestinal signs, but others like E.coli 0157: H7 more commonly implicated in human food toxicities, can be fatal. Listeria has been associated with several pet food recalls and poses a particular risk to pregnant women handling the foods. Raw food diet, whether commercial or home prepared, can have high levels of bacterial contamination and should be used with caution, if at all. Melamine-Cyanuric Acid – The Menu Food recall resulted from purposeful contamination of vegetable proteins by Chinese manufacturers. The numbers of affected animals are unknown but estimated to be hundreds to thousands. Melamine is a byproduct of plastic manufacturing that is generally harmless. Chinese suppliers had been adulterating vegetable proteins so that they would appear to be of higher protein content and higher quality. Cyanuric acid is a similar by-product from melamine and alone of limited toxicity. In combination and in an acidic environment like urine, agglomeration, and crystallization of the material resulted in the obstruction of renal tubules and acute renal failure. Clinical signs are typical of acute renal failure. Small dogs and cats appear most susceptible. Vitamin D Toxicity – Vitamin D is an essential nutrient in dogs and at excessive levels can be toxic. Reports to the FDA of dry dog food from brands using contract manufacturers were reported in the fall of 2018. In 2019, Hill’s Pet Nutrition filed a voluntary recall on individual lots of canned dog foods. Vitamin mix misformulation from a major nutrient supplier appears to be the cause. Levels from 3 to 70 times the target levels have been identified. Clinical signs are not be expected at lower levels of excess, but 5-10 fold levels and higher may lead to hypercalcemia with related vomiting, loss of appetite, polydipsia, polyuria, hypersalivation, weight loss, renal failure, and death. Because symptoms are similar to vitamin D-based rodenticides, providing a comprehensive diet history, product identification, and ruling out rodenticide exposure is essential for a diagnosis. Grain-free (Deficiency or Toxicity?) - The FDA is investigating reports of diet associated DCM (dilated cardiomyopathy) following an uptick in cases since 2018. While many of the reported foods were grain-free, a broader description has emerged and coined as BEG Diets (boutique, exotic, or grain free). For many affected dogs, there has been a noted improvement in cardiac function following taurine supplementation or a diet change. Despite clinical improvements with taurine supplementation, nearly 90% of dogs have had normal blood taurine levels upon presentation, making taurine deficiency unlikely as a primary cause. Because DCM improves with diets change, despite normal taurine levels, it suggests that more complex nutrient interactions or toxicity may be responsible for these diet-associated DCM cases. Of the diets associated with DCM occurrence, many have replaced grains with ingredients such as pulses (i.e., legumes, peas, lentils,) exotic meats, exotic vegetables and/or exotic fruits. More than 90 % of the products were “grain-free,” and 93% of products included peas and lentils. Although exotic meats were initially cited as a dietary factor, the top 3 proteins were chicken, lamb, and fish. Diets were typically manufactured by smaller companies that market to a more narrowly defined audience (boutique products). These boutique products have been associated with the majority of reported DCM cases. Nonetheless, major manufacturers such as Nutro and Blue Buffalo were included in multiple reports. A variety of nutrient deficiencies, imbalances, heavy metal exposure, and nutrient excesses may impact cardiac function. Examples in people include arsenic and cobalt toxicity or selenium deficiency. Because a diagnosis of Canine DCM may be caused by genetic predisposition, taurine deficiency, or BEG diets, it is critical for the veterinary team perform a complete diet history, assess taurine status, and report potentials cases of dogs presenting with diet-associated DCM. Other toxins –Ingredients are typically screened for mycotoxins, drugs (e.g., pentobarbital), pesticides, heavy metals (e.g., arsenic in rice, lead, cadmium) and solvents which have previously been detected



in ingredients and less commonly whole foods. But it remains important to consider these compounds as well as more common contaminants. Recognition Most episodes of contaminated pet foods present as geographic or temporal clusters of cases within the same household, kennel, or area. Unusual increases in the number of animals diagnosed with liver, renal, gastrointestinal or neurologic disorders, especially when across age ranges and species should elevate the level of suspicion. While having a similar diet history is helpful, a variety of products can be affected if produced by co-manufacturers. This was a scenario for a recent vitamin D recall and the melamine recall. A complete medical history, dietary history, travel history is also important. Owners indicating the use of a new brand or bag of food, recent change in diet, altered food palatability, or decreased appetite raise the index of suspicion for contaminated food. It is critical to determine the brand, date code, and date of purchase of a suspected product. Most importantly, report suspected toxicities. When reports are combined, it can be easier to detect a toxicity when seeing patterns in a temporal cluster. Be aware of current recalls. It is crucial that the entire team is informed and can alert clients to possible risks. The AVMA posts recalls from pet food to fish food https://www.avma.org/News/Issues/recalls-alerts/Pages/pet-food-safety-365-day.aspx Reporting As soon as food contamination is suspected, the owner or veterinarian should contact the pet food manufacturer to report concerns and determine if other reports have been filed. When calling provide a clear history, signalment, clinical disease course, and comprehensive diet history. Also, report to the FDA. They can help identify reports from other manufacturers and provide advice for further testing and documentation. When reporting the diet brand, be prepared to provide complete details of the product, form, size package, flavor, date code (or best by date), where purchased, how fed, time of onset of signs in relation to consumption, clinical signs, and any diagnostic results. It is important to have a good health record of the pet to help determine if clinical signs are a natural disease process or the result of food toxicity. Not to be overlooked, general veterinary web sites (e.g., VIN) have heightened awareness and facilitated rapid and widespread communication. These sights can help determine if observations are unique to a practitioner or more extensive. Diagnosis and documentation A complete medical workup or necropsy should be provided to establish a diagnosis. Save appropriate biologic samples (i.e., serum, urine, GI contents, etc.) and food samples. Opened food samples should typically be frozen. Check with a laboratory regarding biological fluid sample preservation. During a recall, the manufacturer will often advise returning all or discarding all of a product. At least 1 kg of dry food and 4 cans of the canned product should be saved by the owner or veterinarian for subsequent confirmatory testing. Freeze opened product or store dry food in an airtight container in a cool, dry location. Have owners save all packaging, date codes, and purchase receipts. Copies should be obtained for the medical record. Manufacturers keep samples for testing, and the product date code provides critical information for their initial screening and review. Often the suspect product will be requested and a sample should be sent. Manufacturers have resources to test product for common contaminants. Independent testing may also be advised if a legal case should ensue. Documentation of communication with the manufacturer and FDA should also be included in the medical record along with the report case number. Clearly record the clinical course, diagnostic tests, treatments, and outcome. The medical record has now become a legal document for which you are responsible. As such, obtain written client authorization before the release of information, or as otherwise required by your state laws. Remember, you are helping to preserve the legal right of your client and providing essential information to identify a potential toxin impacting a broader population of pets.



Recommended Reading Stenske KA, Smith JR, Newman SJ, Newman LB, Kirk CA. (2006) Aflatoxicosis in dogs and dealing with suspected contaminated commercial foods. JAVMA, 228:1686-1691. Burns K. (2007) Events leading to the major recall of pet foods. J Am Vet Med Assoc. 230(11):1600-20. Smith, AJ, Stenske, KA; Bartges, JW; Kirk, CA. (2006) Diet-associated hepatic failure and immune-mediated hemolytic anemia in a Weimaraner. Journal of Veterinary Emergency and Critical Care, 16: S42-S47(1). FDA Investigation into potential links between certain diets and canine dilated cardiomyopathy (2019) https://www.fda.gov/animal-veterinary/news-events/fda-investigation-potential-link-between-certain-diets-and-canine-dilated-cardiomyopathy Freeman, L, Sterns, J, Fries, R, Adin D., Rush, J. (2018) Diet-associated dilated cardiomyopathy in dogs: what do we know? JAVMA, 253:1390-1394. Appendix A: FOOD TOXICITIES IN COMMERCIAL FOODS Checklist for Reporting With the recent number of pet food recalls, issues of food safety are at the forefront of veterinary medicine. Prevention of food toxicity is always the primary goal. Unfortunately, contamination with toxins, foreign materials, bacteria, or the addition of nutrient excesses does occur. Knowing the steps to take can aid in making a timely diagnosis, support product recalls, and public notifications to limit further exposure. Suspecting a food toxicity/contamination is the first step. Understanding how pet foods are made, knowing common food toxins and clinical signs, recognizing clusters of disease, or atypical presentations of disease are critical to recognizing food toxicity. Once a presumptive diagnosis is made, the following checklist is suggested or review the FDA information sheet on reporting: https://www.fda.gov/animal-veterinary/report-problem/how-report-pet-food-complaint Checklist for managing a suspected pet food contamination case.

- Retain food samples for analysis § -store 4 large cans or 1 kg of dry food when possible § -freeze and/or store at room temperature in airtight bags

- Document product name, type, and manufacturing information

§ -retain all packaging (box, bag, can, pouch, etc.) § -identify date codes, production lot numbers,

best by dates, UPC code, weight § -retain purchase receipts § -where purchased (exact location) § -date purchased

- Document product consumption history

§ -dates foods were fed, amounts, to whom, etc. § - how food was stored, prepared, handled § -consumption or palatability history



§ -onset time of clinical signs § -detailed diet history (i.e., all items fed and feeding methods) § -describe the problem (foul odor, color, swollen can, foreign objects found)

- Contact manufacturer § You should notify the manufacturer, they may have additional information. § You should wait for instructions from the FDA before returning all food to the

manufacturer or distributor.

- Notify the FDA

§ FDA Safety Reporting Portal https://www.safetyreporting.hhs.gov/SRP2/en/Home.aspx?sid=6e8b76ff-90c6-45ac-aadc-5ff41828e4e9

§ TN FDA Consumer Complaint Coordinator : ( 866-289-3399) https://www.fda.gov/safety/report-problem/consumer-complaint-coordinators

- Document communication with FDA, manufacturers, and clients

§ -record date, time, and contact person § -maintain case I.D. for each patient contact

- Submit samples to a diagnostic lab, the FDA, or manufacturer for analysis

- Submit all deceased animals for necropsy and sample collection

§ -retain tissue samples in formalin and frozen (500-1000 grams) § -consult with a diagnostic laboratory for required tissue quantity, § preparation, storage, and submission

- Maintain detailed medical records of affected animals

§ -clearly document clinical course, diagnostics, treatment, and outcome § -retain serum and tissue samples when possible for further testing

- Notify client-consumers of potential exposure or product recalls

- Examine all pets with known or suspected food exposure

§ -submit diagnostic testing as indicated § -initiate prophylactic care as indicated

- Obtain a signed client authorization prior to the release of medical information



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EmergencyTriage:QuickTips&Tricks

L.GuieuDVM,DVSc,MSc

Dipl.ACVECC,Dipl.ECVECC

•  Triage:trier.Processbywhichthestabilityofpatientsis

determined,allowingthosethatarethemostunstabletoreceiveanexamination,theimplementationofessentialtreatmentandfurtherinvestigationsassoonaspossible

•  ↓mortality•  Streamlined,efficient,clinicalexamination

PHONECALL



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2

Phonecall

•  1stlinetriage

•  Identifytrue&falseemergenciesoverthephone–  provideappropriateadvisestotheowners–  timeframetobeseenbyavet

Retchinglargebreeddog Dysuriccat

↑respiratoryeffort

Chokingdog

Panting,tachypneic

cat

Protractedvomiting&diarrhea

Laterallyrecumbent

pet

Recenttoxicingestion

Phonecall

•  Identifytrue&falseemergenciesoverthephonetoprovideappropriateadvisestotheowners+timeframetobeseenbyavet

•  Safestthingtoinstructclientistocomein-warningthemthatthetriageonadmissionwilldeterminehowquicklytheirpetwillbeseen!

•  Whencriticalpatientsareexpected:warnthefrontdeskand

theERteamsothateverybodygetready(ie.intubationkitout)



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3

INITIALPATIENTTRIAGE

Initialtriage•  Tobeperformedbyatriage/ERtrainednurseinthelobby

•  Briefmedicalhistory

•  Briefvisualinspection•  Focusphysicalexamination

signalmentreasonforseekingmedicalcareconcurrent medical conditions,medication

respiratorycardiovascularneurologic(urinary)systems

AirwayBreathingCirculationDisabilities Respiration

AlertnessPerfusion



19-06-18

4

Initialtriage•  Tobeperformedbyatriage/ERtrainednurseinthetriagearea

•  Briefmedicalhistory

•  Briefvisualinspection•  Focusphysicalexamination

signalmentreasonforseekingmedicalcareconcurrent medical conditions,medication

respiratorycardiovascularneurologicurinarysystems

Shouldtake<2min Stabletowait?

PRIMARYSURVEY



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5

History/presentingcomplaints•  ALWAYSINTRODUCEYOURSELF,MAKEEYECONTACTWITH

THEOWNERS!!!

•  Keyfactstobedetermined:–  trauma:natureofit&deteriorationsinceevent–  intoxication:type,timing&doseoftoxiningested–  seizures:howmany/howoften–  anydiarrhea/vomiting-howfrequently?–  anychangesinthebreathing?–  anychangesintheattitude?–  concurrentdiseases&currentmedications

RESPIRATORYSYSTEMEVALUATION

Goal:identifyapnea,hypoxemia,hypoventilation,respiratoryfatigue

•  A:Airwaypatency–  airwayblockedornot?–  upperairwaynoises:stertor/stridor–  ↑inspiratoryeffort(inspiratorydyspnea)



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StertorStridor

•  B:Breathing–  ishebreathing?–  respiratorypattern

Expiratorydyspnea


Restrictivedyspnea



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•  B:Breathing–  ishebreathing?–  respiratorypattern–  Videoorthopnea


•  inspiratorydyspneaàextra-thoracicdiseases•  expiratorydyspneaàlowerairwaysdiseases•  restrictivedyspneaàpleuralspacediseases•  mixeddyspneaàlungparenchymadiseases•  posturing:orthopnea,neckextended,nasalflairing


•  inspiratorydyspneaàextra-thoracicdiseases•  expiratorydyspneaàlowerairwaysdiseases•  restrictivedyspneaàpleuralspacediseases•  mixeddyspneaàlungparenchymadiseases•  posturing:orthopnea,neckextended,nasalflairing

–  respiratoryrate>40bpm–  (thoracicauscultation)

•  wheezesàasthma•  muffledlungsoundsàpleuraleffusion,diaphragmatichernia•  heartmurmuràcongestiveheartfailure

–  isitofrespiratoryorigin(neurologic,pain,shockrelated…)?



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Pain&shockrelated

Diagnostictests•  Mucousmembranecolor

–  poorlyreliable!–  cyanosisoccurswhen5g/dLofHbisnotoxygenatedóSpO2=67%,PaO2=37mmHg

•  Pulseoxymetry–  SpO2>95%–  tointerpretinlightofrespiratorypattern&effort

•  FAST-examtoidentifypleuraleffusion,enlargedleftatrium,pneumothorax,B-lines

Emergencymanagement

•  O2supplementation

•  Sedation–  Butorphanol0.2-0.4mg/kgIV/IM– Midazolam0.2-0.4mg/kgIV/IM

•  Intubation&manualventilation



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CARDIO-VASCULARSYSTEMEVALUATION

Goal:identifysignsofshock

Shock

=inadequateO2supplytothetissue

Physicalexamfindingscompatiblewithshock/poorperfusion

•  Heartrate–  cats:HR<160bpm&HR>220bpm–  dogs:HR>160bpmforsmallbreed&>100bpmforlargebreed•  muffledheartsounds:tamponnade,diaphragmatichernia,pleuraleffusion

•  Pulsequality

–  pulsedeficit–  boundingpulse:severeanemia,sepsis–  weak/absentfemoral/metatarsalpulse:hypotension–  asymetricalpulse:saddlethrombusincats



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•  CRT–  >2s(vasoconstriction)–  <1s(vasodilation=sepsis)

•  Mucousmembranecolor•  Mentation


•  CRT–  >2s(vasoconstriction)–  <1s(vasodilation=sepsis)

•  Mucousmembranecolor–  palepink:vasoconstriction,moderateanemia–  white:anemia,decompensatedshock–  injected:sepsis,fever,pain,anxiety–  brown:acetaminophentoxicity–  yellow

•  Mentation:dull,depressed

Diagnostictests•  Lactate–  normal:<2.5mmol/L–  >2.5mmol/L

•  Systolicbloodpressure–  normal:>90mmHg–  hypotension:<90mmHg–  cats:Dopplertendstounderevaluatesystolic,readingclosertothemeanarterialpressure

•  ECG:lookforarrhythmias



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Emergencytreatment•  Willreallymuchdependonunderlyingcauseidentified!

Shock•  Oxygentravel:

Respiratorysystem Heart Vessels Organs

inRBCs

Hypoxemic Cardiogenic HypoxemicHypovolemicDistributive

Metabolic

Emergencytreatment•  Willreallymuchdependonunderlyingcauseidentified!

•  Hypovolemic/distributiveshock:fluidsbolus

•  Cardiogenicshock:furosemide

…



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NEUROLOGICSYSTEMEVALUATION

Goal:identifybrain&spinalcordinjury

Worrisomeneurologicsigns•  Statusepileticus,seizure,post-ictal

•  Markedlydepressedmentation,stuporous,coma

•  Signsofintracranialhypertension–  hypertension,bradycardia,unresponsive

•  Severeacuteparalysiswithlossofnociception

Emergencytreatments

•  Seizure:Midazolam0.3mg/kgIV/IN

•  Intracranialhypertension:– Mannitol0.5-1.5g/kgIVover20min–  Hypertonicsaline3ml/kgIVover5min



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URINARYSYSTEMEVALUATION

Goal:identifyblockedcat,uroabdomen,anuria,hyperkaliemia

Worrisomefindings

•  Reporteddysuria/anuria

•  Largebladdernoteasilyexpressed

•  Absentbladderwithanuriareported(uroabdomen)

•  Bradycardia

Diagnostictests

•  Electrolytes:K+>6.5mmol/L

•  ECG



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Emergencytreatments

•  Ifcardiacarrhythmiaàcalciumgluconate-  0.5-1.5ml/kg-  IVsur10min-  souscontrôleECG-  effeten3-5min•  IfseverehyperkaliemiaàActrapid0.1-0.5UI/kgIV+

Glucose30%4-5ml/UId’ActrapidIVsur5min

Insummary…

+largebladder

Identificationofunstablepatients

•  Verbalpermission/signedmedicalconsent–  authorizesinitiationofmedicaltreatmentordiagnostics–  outlinesthecostofthiscare($500)

•  BringthepatienttotheICU

•  Haveaveterinarianlookathim/her



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UNSTABLEPATIENTS

Triagearea/ICU•  Shouldbeequippedwithsuppliestotreatacriticallyill

animal!

•  O2supplySuppliesforIV/IOcatheterization+IVfluidsECG&bloodpressuremeasuringequipmentCrashcart(fullystocked)

•  In-houselaboratoryequipment:minimumdatabase:PCV/TS,glucose,BUN,bloodgas&lactate

Unstablepatients•  IVaccessincephalicorsaphenousveins–  intra-osseouscatheter

•  Minimumdatabasepulled–  PCV/TS,glucose,lactate,BUN–  bloodgas

•  ECG

•  Bloodpressure

•  (T-FAST/A-FAST)

AnemiaHypoglycemia

Hyperlactatemia

SBP<90mmHg



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CallclinicianASAPif…

+BG<65mg/dL

Otherconditionsthatrequireimmediateattention

•  Severepain•  Trauma,activebleeding•  Openwounds,fractures•  Recentingestionoftoxin/signsofintoxication•  Recentsnakebites•  Recentseizures•  Dystocia•  Prolapsedorgans•  Hyper/hypothermia•  Burns•  Death

EXCEPTION:STATCALL



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Statcall•  Absentbreathing/cardiacarrest?LaterallyrecumbentpatientsSeverlydyspneicpatients•  BroughtbackASAPtotheICUforimmediateevaluationbya

clinician

SECONDARYSURVEY

Thankyouforyourattention!



1

Grain Free Diet Associated Dilated Cardiomyopathy

(DCM)-An UpdateJENA WEST, BA, LVMT (VTS)

(CARDIOLOGY)UNIVERSITY OF TENNESSEE VETERINARY MEDICAL CENTER

CARDIOLOGY DEPARTMENT

Outline

• What is taurine?• Dilated Cardiomyopathy• DCM & diet in dogs and cats• Current concerns about Diet and DCM

in dogs



2

Outline

• Testing taurine levels• FDA investigation/most recent statement• What to do…• Summary

So, what are you saying???

• GF/BEG Boutique, exotic-ingredient, & grain-free• CHF Congestive Heart Failure• FDA Food and Drug Administration• LV Left ventricle• TD Taurine Deficiency



3

So, what are you saying???

• Legumes-peas, beans, lentils, chickpeas, soybeans,peanuts

• Pulses-dry edible seeds of certain legume plants*EX-dried beans, dried peas, lentils, chickpeas(Not all legumes are pulses, but all pulses are legumes)

What is Taurine?

• One of the few known naturally occurring sulfonic acids

• In a strict sense, it is not an amino acid-

*lacks a carboxyl group



4

What is Taurine?

• Synthesized mainly in the liver and central nervous system from methionine and cysteine (dogs)

• Primarily found in body tissues and circulating in the blood

What is Taurine?

• In dogs, taurine is derived from methionine and cysteine.

(dogs don’t usually have a dietary requirement for taurine because they make their own)



5

What is Taurine?

• Methionine-must come from diet; plays a critical role in starting the process of making new proteins inside cells

• Cysteine-body can make it on its own

What is Taurine?

• Has many functions--Role in normal heart function

-Its presence as a component of bile acids



6

DCM• Characterized by-

-impaired myocardial contractility

-dilation of LV or both ventricles

http://feghalicardiology.com/dilated-cardiomyopathy/

DCM-echocardiogram

ABNORMAL

short axis m-mode-NORMAL



7

DCM• Tachyarrhythmias are

common

*Atrial fibrillation


DCM• Underlying disease

mechanisms are unclear

• In individual cases--altered gene expression-abnormal Ca++ flux-toxins http://feghalicardiology.com/dilated-

cardiomyopathy/



8

DCM-Biochemical or nutritional

deficiencies


DCM and diet in dogs & cats• *DCM used to be one of

the most common cardiac diseases in cats • Pion et al report 1987

*Pion PD, Kittleson MD, Rogers QR, et al.

Myocardial failure in cats associated with

low plasma taurine: a reversible cardiomyopathy. Science 1987;237;764-768

This Photo by Unknown Author is licensed under CC BY-SA



9

DCM and diet in dogs and cats

• Paper reported-DCM in cats was

associated with taurine deficiency and could be reversed by providing supplemental taurine.

• Taurine levels in cat food was increased

• Taurine deficiency-related DCM is now uncommon

• Home-prepared diets or commercial diets prepared with inadequate nutritional expertise or quality control

DCM and diet in dogs & cats• *1995 veterinary

cardiologists investigating the role of taurine deficiency in dogs with DCM suggested that certain breeds -Golden Retrievers -American Cocker Spanielsmay be predisposed to

taurine deficiency*Kramer GA, Kittleson MD, Fox PR, et al. Plasma taurine concentrations in normal dogs and in dogs with heart disease. J Vet Intern Med 1995; 9:253-258




10

DCM and diet in dogs & cats• 2005 paper-Involved 24 Golden retrievers with echo confirmed DCM and low plasma or whole blood taurine concentrations.

After switching diets and supplementation of taurine-reechoed 12-24 months later, showed substantial echocardiographic improvement

*Belanger MC, Ouellet M, Queney G, et al. Taurine-defiencydilated cardiomyopathy in a family of Golden Retrievers. J Am Anim Hosp Assoc 2005; 41:284-291


Current Concerns About Diet and DCM in Dogs• Beginning in the 2000’s-

the number of dog with TD and DCM appeared to decrease.

• In 2016, Dr. Josh Stern (UC Davis School of Vet Med) began to diagnose DCM in breeds not commonly known to have the disease.

• Dogs diets- same GF/BEG diet



11

Current Concerns About Diet and DCM in Dogs• Remove grains=must

replace with something else….

This Photo by Unknown Author is licensed under CC BY-NC


Current Concerns About Diet and DCM in Dogs• GF/BEG contained-

KangarooDuckBuffaloSalmonLambBisonVenison

LegumesPulsesFava beansBarleyPotatoes/Sweet potatoes



12

Current Concerns About Diet and DCM in Dogs• Began testing plasma

and whole blood taurine levels

• Some of the affected dogs had low taurine levels, some did not.

• Common factor-GF/BEG diet


Current Concerns About Diet and DCM in Dogs• Closer look at GF/BEG

diets-Exotic ingredients

• Different nutritional profiles & different digestibilitythan typical ingredients-potential to affect the metabolism of other nutrients



13

Current Concerns About Diet and DCM in DogsExample-

*Bioavailability of taurine-• Is different when included

in a lamb-based dietvs.

chicken-based diet

• Can also be affected by the amount and types of fiber in the diet.

*Ko Ks, Backus RC, Berg JR, et al. Differences in taurine synthesis rate among dogs related to differences in their maintenance energy requirement. J Nutr 2007; 137: 1171-1175

Current Concerns About Diet and DCM in Dogs• Taurine-why the

deficiency?-Could be related to:• *reduced synthesis of taurine resulting

from an absolute dietary deficiency of the taurine precursors methionine and cystine

This Photo by Unknown Author is licensed under CC BY

*Backus RC, Ko Ks, Fascetti AJ, et al. Low plasma taurine concentrations in Newfoundland dogs is associated with low plasma methionine and cyst(e)ine concentrations and low taurine synthesis. J Nutr 2006; 136: 2525-2533



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Current Concerns About Diet and DCM in Dogs

• *Reduced bioavailability of taurine, methionine, or cystine in the diet

• Abnormal enterohepatic recycling of bile acids because of fiber content in the diet

• Possible breed-related metabolic differences• Genetic factors

*Backus RC, Ko Ks, Fascetti AJ, et al. Low plasma taurine concentrations in Newfoundland dogs is associated with low plasma methionine and cyst(e)ine concentrations and low taurine synthesis. J Nutr 2006; 136: 2525-2533


• Research began in 2011-

*Exploring whether diet-associated DCM in dogs without taurine deficiency may be related to inclusion of a cardiotoxic ingredients, as with ingredients containing melamine-cyanuric acid that affected pet foods in 2007.

*Puschner B, Reimschuessel R. Toxicosis caused by melamine and cyanuric acid in dogs and cats: uncovering the mystery and subsequent global implications. Clin Lab Med 2011;31:181-199



15


• Could the cause be even more complicated?

*Interaction between gut microbiota and a dietary factor (eg. Trimethylamne N-oxide).

Tang WHW, Hazen SL. The gut microbiome and its role in cardiovascular diseases. Circulation 2017;135:1008-1010


• Could the cause be even more complicated?

*Intercaction between gut microbiota and a dietary factor (eg. Trimethylamne N-oxide).-a small colorless amine oxide generated from choline, betaine, and carnitine by gut microbial metabolism

Tang WHW, Hazen SL. The gut microbiome and its role in cardiovascular diseases. Circulation 2017;135:1008-1010



16

Testing Taurine Levels

What kind of samples to collect…

*2019 sample collection guidelines

• If DCM is diagnosed in a dog BEG,

vegetarian,vegan, or

home-prep diet.

• Measure plasma andwhole blood taurine concentrations



17

What kind of samples to collect…

• Why whole blood?Whole blood taurine concentrations may be used to substantiate a diagnosis of taurine deficiency when plasma concentrations are equivocal.

• Whole blood concentrations are only slightly altered after eating, whereas plasma taurine concentrations may change substantially in taurine-depleted animals.

UC DavisAmino Acid Laboratory

www.vetmed.ucdavis.edu/labs/amino-acid-laboratory

Where do I send the samples?



18

FDA Investigation• What is the FDA investigating

exactly?

July 2018-FDA announcement:*“…begun investigating reports of canine dilated cardiomyopathy in dog eating certain pet foods, many labeled as “grain-free,”…

*http://www.fda.gov/animal-veterinary/news-events June 27, 2019

FDA Investigation• What is the FDA investigating

exactly?

…which contained a high proportion of peas, lentils, other legume seeds (pulses), and/or potatoes in various forms (whole, flour, protein, etc.) as main ingredients.”




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FDA Investigation• What do they consider “main

ingredients?”

“…the first 10 ingredients in the ingredient list, before vitamins and minerals.”


FDA Investigation


Between January 1, 2014 and April 30, 2019, the FDA received

524 reports of DCM

• 515 canine reports• 9 feline reports



20

FDA Investigation


FDA Investigation


• Forms of diet reported



21

FDA Investigation


• Most reported brands reported

FDA Investigation


• Ingredients or characteristics



22

FDA Investigation


• Animal proteins reported

FDA Investigation


• Taurine and Amino Acids• *Nutritional research

indicates that taurine-not considered an essential amino acid for dogs(can synthesize taurine from

cysteine and methionine)



23

FDA Investigation

*http://www.fda.gov/animal-veterinary/news-events

AAFCO Official Publication

• Taurine and Amino Acids• *Nearly all the grain-

free products had methionine-cysteine values above the minimum nutritional requirement of 0.65% for adult maintenance food for dogs

FDA Investigation

*http://www.fda.gov/animal-veterinary/news-events

• What’s next?• * “FDA is continuing to investigate

and gather more information in an effort to identify whether there is a specific dietary link to development of DCM and will provide updates as information develops.”



24

What to do…

• If DCM is diagnosed in a canine patient that is eating a BEG, vegetarian, vegan, or home-based diet:

1. Change diets2. To test or not to test taurine levels…3. Begin taurine supplementation ( 1 gm POBID-TID for large breeds, 500mg PO BID-TID

smaller breeds)

4. Follow up *If taurine responsive, should see echocardiogram evidence within 3-6 months

What to do…

• If DCM is diagnosed in a canine patient that is eating a BEG, vegetarian, vegan, or home-based diet:

5. Report to the FDA /animal-veterinary/report-problem/how-report-pet-food-complaint



25

Summary• Pet food marketing has outpaced science• Owners want to do the best for their pets

• *Although there appears to be an association between DCM and feeding BEG, vegetarian, vegan, or home-prepared diets in dogs, a cause-and-effect relationship has not been proven, and other factors may be equally or more important.

*Freeman L, Stern J, Fries R, Adin D, Rush J. Diet-associated dilated cardiomyopathy in dogs: what do we know? JAVMA Dec 2018;1390-1394

Summary• Diet-induced DCM is not limited to grain-free

foods and certainly not all grain-free diets have been associated with the disease.



26

Summary• While dogs do not usually have a dietary

requirement for taurine, higher dietary fiber and increased concentrations of plant-based protein sources may lead to inadequate concentrations of taurine precursors.

Summary• How do we help owners?

§ ????? connection between DCM dogs and dietThe formulation of pet foods is a complicated

process involving the interaction of many ingredients.

Whether a diet contains grains or not, it’s important to feed diets from reputable companies with experienced pet food formulators.



27

Summary• How do we help owners?

If there isn’t a medical benefit to feeding grain free, help them find a food that they will feel comfortable feeding their pet and that their pet likes.

May be able to save them $$$$$$

Questions?



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1Diabetic Ketoacidosis: More Than Just "The

Sugars"

Eric Hilton, BSc, RVT, LVMT, VTS (ECC)

[email protected] of Tennessee Veterinary

Medical CenterSmall Animal Clinical Sciences

Intensive Care Unit

What is Diabetes Ketoacidosis (DKA)?

• Complication of diabetes mellitus (DM) resulting from an insulin deficiency or insulin resistance (cats)

• Complicated network of fluid and electrolyte abnormalities

• Involves multiple body systems

• Is a medical emergency and requires immediate attention



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2

DKA Is The Most Common Endocrine Emergency!

§ Affects both cats and dogs§ Involves a wide array of derangements including:

§ Electrolyte Derangements: sodium, potassium, bicarbonate, phosphorus, magnesium

§ Metabolic Derangements: moderately to severely increased blood glucose and blood ketones

§ Acid‐Base Derangements:moderate to severe metabolic acidosis

§ Osmolality (amount of dissolved substances in the blood): Moderately to severely hyperosmolar

• Diabetes occurs in 1‐5 out of every 100 dogs and cats

• Dogs are generally between the ages of 4 and 14, with a peak incidence between 7 to 9 years old• Occurs twice as often in females than in males

• Can occur at any age in cats, but they are generally >6 years old• Twice as likely to occur in neutered male cats

Signalment for Diabetics



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3

History and Physical Exam Lethargy/weakness Polyuria/Polydipsia (PU/PD) Dehydration Hyporexia or anorexia Tachypnea Nausea Vomiting "Sweet‐smelling" breath (acetone)

Physical Exam Continued

• Cats may exhibit a diabetic neuropathy known as plantigrade stance/posture

• May have an onset of acute abdominal pain and possible abdominal distention



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4

• DKA is not a Primary Disease Process!

• Patient must be a diabetic in order to develop DKA!

• DKA is a complication of a concurrent disease process• Pancreatitis, urinary tract infection, sepsis, pneumonia, hyperadrenocorticism (Cushing's) hepatic lipidosis (cats), chronic kidney disease (cats), or congestive heart failure

• Consider running a T4 for cats• Corticosteroid use is also a predisposing factor

Diagnosis of DKA• Diagnosis is supported by clinical history as well as an increased resting (fasted) hyperglycemia• May be a stress hyperglycemia, so this is not diagnostic by itself

• Also requires the presence of urine and blood ketones!



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5

Urine Ketone Reading

Blood Ketone Reading (mmol/L)

Action Required

Negative < 0.6 Normal readings – continue to monitor. No other action needed.

Trace ‐ Monitor frequently – trace can increase rapidly. See information below.

Small to Moderate 0.6 ‐ 1.5 URINE• Small: test often. If any change,

or your cat starts acting lethargic or showing other symptoms, take your cat to the vet.

• Moderate: take your cat to the vet immediately

BLOOD• Towards the Lower End: monitor

frequently

• If the reading increases or if your cat is acting lethargic or showing other symptoms, take your cat to the vet immediately.

Large to Very Large >1.6 Your cat is at risk of or has developed DKA – get your cat to the vet immediately. This is a medical emergency.

PRO TIP!!!• Urine ketone strips do NOT detect β‐hydroxybutyrate (BHB), but ketosis cannot occur without the presence of it.

• Add a drop or two of hydrogen peroxide to the patient's urine that has tested negative for ketones, but you are strongly suspicious of ketonuria/ketonemia

• The addition of hydrogen peroxide to β‐hydroxybutyrate converts it to acetoacetic acid (AOA) that can be detected by the urine strip!



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6

Other Diagnostic Tests• Performed to assess the level of severity of DKA andto diagnose the underlying, predisposing disease

• The minimum data base (MDB) for a DKA patient should include:• Blood Chemistry Panel – assessing liver and kidney

function, pancreatic enzymes• Electrolytes and Venous Blood Gas – assessing for

acidemia, dehydration, and any electrolyte abnormalities

• Complete Blood Count (CBC) – assessing for dehydration, infection, or inflammation

• Urinalysis and Urine Culture – assessing for dehydration, renal insult, urinary tract infection, glucosuria/ketonuria

Bloodwork Abnormalities

• Hyperglycemia (>300mg/dL) with concurrent glucosuria• BG >500mg/dL can indicate severe dehydration

and/or renal insufficiency

• Increased liver values (ALT, ALP, and cholesterol in dogs; AST and cholesterol in cats)

• Increased Packed Cell Volume (PCV) or Hematocrit (Hct) ‐ patient is generally dehydrated• May be falsely elevated due to level of dehydration (patient may actually be anemic)

• Increased Total Solids (TS) or Total Plasma Protein (TPP) ‐ generally due to dehydration

• Increased Blood Urea Nitrogen (BUN) and Creatinine ‐ can be secondary to dehydration, or primary renal insult• More common in cats



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7

Bloodwork Abnormalities

• Electrolyte Abnormalities – may be hypo or hypernatremic, hypo or hyperkalemic, hypophosphatemic, hypomagnesemic

• Urine Abnormalities – may have an increased urine specific gravity (USG) if dehydrated (pre‐renal azotemia) or a low‐to‐normal USG (renal azotemia)

• CBC Abnormalities – usually a stress leukogram, or evidence of inflammation and a nonregenerative anemia

• Heinz bodies may be seen on a blood smear



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8Potassium

• Patient may present with an initial hyperkalemia• Usually secondary to dehydration and decreased

renal excretion as well as impaired insulin release/function

• After fluid therapy begins, patient will develop hypokalemia secondary to renal excretion and potassium binding to ketoacids• Insulin therapy will further exacerbate hypokalemia

• All DKA patients will require potassium supplementation!• Can be supplemented as potassium chloride and/or potassium

phosphate

What's The Deal with Ketones, Anyway?!

• Ketones are a naturally occurring product of fatty acid metabolism in the liver

• Cells can use ketones as a short‐term source of energy in the absence of glucose

• Ketones are a source of "fuel" for the brain and the heart



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9Ketone Body Metabolism

• Acetate and carbon dioxide are the biproducts of the metabolism of AOA• Acetate has a high vapor pressure, so the body can rid itself of this via exhalation

• Over‐production, and the body's inability to utilize β‐hydroxybutyrate and acetoacetic acid, depletes the body's reserve of buffers (bicarbonate) thus causing ketoacidosis

Side Effects of Acidosis (Acidemia)

• When the body is unable to adequately rid itself of excess acid, this can lead to decompensatory shock• Tachypnea gives way to Kussmaul breathing (deep, labored breathing)• As pH decreases, the affinity of hemoglobin for oxygen also decreases leading to tissue hypoxia

• As oxygen delivery decreases, anaerobic metabolism increases, exacerbating an acidemic state (lactic acidosis)

• As pH decreases, cellular enzyme activity also becomes impaired• As pH decreases, mental acuity also decreases

• Patient may become stuporous to comatose



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1 0

Oxygen‐Hemoglobin Dissociation

Curve

Treatment for DKA

Identifying the underlying, primary disease process is paramount to successful treatment of DKA

Usually requires at least 36‐48 hours of hospitalization (can be seven days or greater)

Involves labor‐intensive nursing care and serial monitoring of vitals and blood work

Fluid therapy and insulin therapy are the mainstays for the management of DKA

• Depending on level of dehydration, electrolyte abnormalities and acid‐base status, any number of crystalloid fluids can be used including Normosol‐R, Plasma‐Lyte, Lactated Ringers (controversial) or Normal Saline.



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1 1

Fluid Therapy

• Maintenance fluid rate• 60mL/kg/day (dogs)• 40mL/kg/day (cats)

• Estimate percentage dehydration (fluid deficit)• Fluid deficit should be replaced over 12‐24 hours

Physical Findings in DehydrationDehydration (%) History of Fluid

LossDry Mucous Membranes

Tachycardia Decreased Skin Turgor

Decreased Pulse Pressure

Shock

< 5 + ‐ ‐ ‐ ‐ ‐

5‐6 + + ‐ ‐ ‐ ‐

7 + + + + ‐ ‐

10 + + + + + ‐

12 + + + + + +

Fluid Calculation Example

• A 30 kg mixed‐breed dog presents with an estimated 7% dehydration. Your doctor asks you to calculate a rehydration rate to replace that 7% dehydration over 24‐hours.

• What will your HOURLY fluid rate be for the first 24 hours?



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1 2

Survey Says...

• Maintenance Fluid Rate = 60 mL/kg/day• = 60 x 30kg/day• = 1800 mL/day• 1800 mL/24hrs = 75 mL/hr

• Calculate Fluid Deficit:• 7% dehydrated = 0.07 (7% as a decimal)• 0.07 x 30kg = 2.1 liter deficit• 2.1 L = 2100 mL – correct over 24 hours

• 2100 mL/24hr = 87.5 mL/hr

• 75 mL/hr + 87.5 mL/hr = 162.5 mL/hr for the first 24 hours

Fluid Therapy

Fluid diuresis alone will decrease blood glucose levels via renal excretion, but it WILL NOT decrease blood ketones• Insulin therapy is required to decrease ketogenesis, thus correcting acidosis/acidemia

Fluid therapy should be viewed as a "fluid" therapy, not a "one‐size‐fits‐all" therapy• Fluid rates and additives(potassium and phosphorus) need to be reassessed and adjusted as needed, especially after insulin therapy begins



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1 3

Insulin Therapy: GAME CHANGER!!

• How does insulin promote the uptake of glucose by the cell?

• What else does insulin promote the uptake of by the cell?

• How does insulin administration help correct acidemia?

Retrospective comparison of early‐ versus late‐insulin therapy regarding effect on time to resolution of diabetic ketosis and ketoacidosis in dogs and cats: 60 cases

(2003‐2013).J Vet Emerg Crit Care (San Antonio). 2016 Jan‐Feb;26(1):108‐15. doi: 10.1111/vec.12415. Epub 2015 Nov 9.

• Retrospective study done at Cornell University looking at the initiation of insulin administration for DK(A) patients• Is delaying insulin therapy necessary until patients are properly rehydrated in order to avoid serious electrolyte abnormalities and changes in osmolality?

• Insulin is required to stop the production of ketone bodies and facilitate ketone body metabolism as well as promote the utilization of glucose at the cellular level

• "Early administration of short‐acting insulin was associated with a more rapid resolution of DK/DKA without an increase in complication rates"



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1 4

Effects of Insulin Therapy

• Causes the uptake of glucose by cells

• Causes the uptake of ketones by cells

• Decreases hepatic glucose production (gluconeogenesis)

• Prevents lipolysis and ketogenesis, and allows for metabolism of ketoacids, thus correcting both ketonemia and acidemia

Methods of Administration: Intramuscular

• Intermittent intramuscular (IM) injections of insulin is one method of insulin administration• Advantages:

• Does not require a dedicated line/catheter• May be less cost‐prohibitive

• Disadvantages:• Pain associated with each injection• Increases possibility of dosing errors



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IM Insulin Therapy

• Dosing will vary depending on BG• But usually ranges from 0.05 U/kg ‐ 0.20 U/kg

• BG should be checked hourly with the IM therapy technique

• Preferred site of injection is a back leg as to avoid injecting into adipose tissue

Methods of Administration: Constant Rate Infusion

• An insulin constant rate infusion (CRI) is another method of insulin administration for dog and cats• Advantages

• Easy to change rate of administration based on current BG• Better option for severely dehydrated patients when insulin

therapy is initiated at an early onset• Multilumen jugular catheters may be beneficial in cases

with prolonged hospitalization

• Disadvantages• Should have a dedicated line/catheter and proper aseptic

technique must be used with catheter placement (especially central lines)

• Managing too many fluid lines, catheters, and pumps



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How to Prepare an Insulin CRI

• 2.2 U/kg for dogs or 1.1 U/kg for cats of Humulin R (Regular Insulin) is added to a 250 mL bag of 0.9% NaCl

• 50 mL of fluid is run through the line due to insulin's ability to bind to plastic

• Leave the bag to sit for 30 minutes before administration

• Bag and line are replaced every 24 hours

Handy Insulin CRI Protocol(Courtesy of Dibartola)

Blood Glucose Concentration (mg/dL)

Intravenous Fluid Solution IV Insulin Solution Rate (mL/hr)

> 250 0.9% saline 10200‐250 0.9% saline, 2.5% dextrose 7150‐200 0.9% saline, 2.5% dextrose 5100‐150 0.9% saline, 5% dextrose 5< 100 0.9% saline, 5% dextrose stop the insulin



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Why Dextrose Supplementation?

• Patients will usually be anorexic at presentation and initially during hospitalization

• Administration of insulin will drive glucose intracellularly, thus increasing the odds of a Somogyi effectIsomers!

Goals of Insulin Therapy

• The main goals of insulin therapy are to decrease blood glucose by 50‐100 mg/dL/hr and to decrease/stop ketogenesis

• Decreasing BG too rapidly with insulin administration can lead to a rapid intracellular shift of glucose and electrolytes (potassium and phosphorus), and a rapid change in osmolality, leading to cerebral edema

• Decreasing BG too rapidly can also cause a Somogyi effect (AKA rebound hyperglycemia)

• Resolving ketogenesis can take 72 to 96 hours (or more!)



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Other Therapies to Consider• Pain Management:

• Especially in cases of pancreatitis, pyelonephritis, or sepsis

• Consider the use of opioid analgesics (Fentanyl, Hydromorphone, Methadone, Buprenorphine)

• If patient does not start eating, consider placement of a nasogastric (NG tube)• NG tube feedings must be started slowly (~¼ RER for the first 24 hours)

• Can do bolus feedings or a CRI• Formulated liquid diet

• Perative (vegetarian formulation), Clinicare, RC Recovery, Vivonex

• Oral medications can go through the tube• Antibiotic therapy may or may not be warranted

Additional Therapies

• Antiemetics (Maropitant) may be warranted in many cases when patient is nauseated or vomiting• Has secondary analgesic properties

• Prokinetics (Metoclopramide) may be warranted in cases of GI ileus• If NG tube in place, can monitor for ileus by aspirating NG tube!



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• Electrocardiograms (either intermittent or continuous) may be warranted if concerns for tachycardia, and can show signs of certain electrolyte changes

• Doppler blood pressure every 4‐8 hours, depending on how critical the patient is

When To Switch to Long‐Acting Insulin• Vomiting and nausea have resolved• Patient is eating and drinking reliably on his or her own

• Ketoacidosis has resolved (as indicated by urine or blood ketone level)

• Continue to monitor BG for 24‐48 hours after clinical signs and symptoms have resolved• "At‐home" insulin dosing may need to be adjusted with a BG curve



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• The prognosis for a DKA patient is fair to guarded• The mortality rate is 30‐40%• Prognosis depends on severity of clinical signs and symptoms at presentation as well as underlying etiology• Mortality rate can be higher in certain cases, such as severe pancreatitis, sepsis, or pyelonephritis• Management of DKA as a sequela of heart failure is very difficult to manage and prognosis is guarded to poor

QUESTIONS??



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References

• Abrahms‐Ogg, Anthony and Karol Matthews. "Diabetic Ketoacidosis" in Veterinary Emergency and Critical Care Manual 2nd ed. Pp 263‐9: Lifelearn Inc; Guelph: 2006.

• Hess, Rebecca S. "Diabetic Ketoacidosis" in Small Animal Critical Care Medicine 2nd ed. Pp 343‐6. Elsevier Saunders; St Louis: 2015.

• Plunkett, Signe J. "Diabetic Ketoacidosis" in Emergency Procedures for the Small Animal Veterinarian 3rd ed. Pp 325‐30. Saunders Elsevier; Edinburgh: 2013.

• Randells, Angela. "Endocrine and Metabolic Emergencies" in Study Guide to the AVECCT Examination. Rene Scalf ed. Pp 238‐43. Np. 2014



PRACTICEMANAGEMENT


PROCEEDINGS



Wellness Rocks! A Circle of Life Introduction to Wellness in Veterinary Medicine Becky Jones, LMSW, BCC Presentation description: Self-care is mandatory, in any helping profession. True self-care requires investing in yourself so you can ultimately help others. Using a nationally recognized health and wellness coaching system, this class will walk you through a personal assessment of your current self-care practices and create a step-by-step process for improving your life, in and out of the veterinary clinic. Regardless of where you are on your journey towards improving your life, you will leave this class with tips and tricks to make real lasting changes in your personal development and self-care practice. Problem addressed in this class Stress and overwhelm seem to direct our life in ways that impact us from all sides. Helping professionals are good at teaching others the importance of self-care but appear to be poor practicers of what they preach. Veterinarians and animal related professionals are no different in their lack of self-care practices or, at best, lack consistency. While engaging with veterinarians, vet students, faculty and staff, I have come to realize that it is imperative to introduce areas of life that are impacted and how it “shows up” at home, the office or within our personal relationships. This class will offer solid, actionable and sustainable options on how to address overwhelm in the moment, develop a long-term practice for increased personal life satisfaction, improved overall health and wellbeing. We will also explore ways to identify what stressors exist and how they affect you. Methods for solution Self-care demands attention and intention. It takes work. It takes practice. One reason is that (although happily things are changing) engaging in self-care goes against the grain of the veterinary culture of sacrifice. To say, “I can’t take that afterhours case because if I don’t go to my exercise class, I will get depressed,” is hard. It's even harder to say simply “No” as if “No” is a complete sentence… which it is! There is a misconception that self-care is self- indulgent, but self-care is really doing things like being on top of your finances, not dealing with your stress by the 1-click feature on Amazon.com or too much tequila. It’s having hard conversations with family members and figuring out how to take action on the things that keep you up at night in a mixture of paralysis and anger. Self-care is about really taking a hard, clear look at your life and seeing where the energy is draining out of your life and then taking action to plug the hole. Easy? No….and not for the faint-hearted. Recommended action steps In this class we will use the Circle of Life Model to assess our level of self-care in 12 domains.

● Nutrition: (Keywords- Diet) The kind, quality and quantity of food and drink you consume; How (fast, slow), why (hungry, bored, sad) and when (before bed, while driving) you eat. Your knowledge of the right diet that you will need to meet your goals.

● Exercise: (Keywords- Fitness) Your knowledge of the exercise or fitness program that is appropriate for you to meet your goals. The kind of exercise you do (aerobic, strengthening, flexibility), how often and for how long you exercise.

● Stress Mastery: (Keywords- Stress Management) Your knowledge, skills and integration of stress management practices such as deep breathing, positive self-talk, relaxation techniques, etc. Assessment of your current life stresses and how you cope with them.

● Relationships: (Keywords- Communication, Sex, Family, Social) Your social connections, communication, conflict resolution family and parenting skills. Evaluation of the quality of your relationships: are they “draining” – or healthy, honest, loving and supportive?

● Finances: (Keywords- Money) Your ability to create the financial resources that you need, as well as your awareness of feelings and beliefs about money. Reflection on your money management skills and your financial planning for the future.



● Work: (Keywords- Career, Jobs) (paid and volunteer) Rating of your work or career satisfaction, as well as evaluating your satisfaction with the organization, management and interactions with your co-workers and supervisor.

● Play: (Keywords- Creativity, Humor, Play) can refer to your sense of humor, as well as how much time you spend doing what you enjoy. It can also mean creativity (i.e., how much creative energy you allow to be expressed in your home, in the arts, at work or in your daily life.)

● Healthcare: (Keywords- Medical or Complementary Medicine, Wellness) Health screenings, prevention, education and treatment in any area (e.g., dental, eye / ear care, counseling, acupuncture, massage, physical therapy, chiropractic, naturopathy, etc.)

● Environment: (Keywords- Nature, Home and Office, Environmental Work) Larger environment (ecosystem) and smaller environments (home and office) Reflection on how your actions affect the ecosystem (which in turn affects your life and health.) Evaluation of your environments in terms of order, beauty, health and harmony.

● Life Purpose: (Keywords- Service, Contribution) Living and fulfilling your reason for being here. Your way of being (supportive, positive, spiritually-focused, high integrity, etc) or working from a life calling, passion or gift. Can refer to service or contributions you make to the world around you.

● Self-Esteem: (Keywords- Emotions, Attitudes, Self-Acceptance) Your level of self-esteem (i.e., your self-acceptance, self-love and self-respect) Can refer to what your beliefs and perceptions are about yourself and about life in general. Also refers to your attitude or relationship with your feelings: Are you driven by emotions? How do cope with your feelings?

● Spirituality: (Keywords: Intuition, Faith) This refers to the fulfillment of your spiritual life, and the frequency and quality of your spiritual practices (meditation, prayer, spiritual gatherings, selfless service, connection to nature, time with spiritually focused people, spiritual reading, etc.). Intuition measures your ability to “tune into” your deeper self and listen to its messages.

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