Clarifications regarding veterinary school accreditation

The recent commentary by Dr. Robert R. Marshak¹ regarding veterinary school accreditation requires clarification on the roles played in the accreditation process by the AVMA, the AVMA Council on Education (COE), and the schools and colleges of veterinary medicine (CVMs) that are full members of the Association of American Veterinary Medical Colleges.

Accreditation through the COE is a standards-driven, evidence-based process relying on key quality-control features, many of which are embodied in the COE Policies and Procedures Manual. The standards adopted by the COE are such that COE-accredited CVMs are considered the gold standard of veterinary medical education around the world. The CVMs are not compared with each other during the accreditation process. Rather, their programs are assessed against clearly articulated standards through the use of appropriate data sets analyzed by means of processes detailed in the Policies and Procedures Manual. It is important to remember that these standards are under constant review and that the deans of the COE-accredited CVMs regularly have opportunities to comment on the COE standards.

The COE accreditation process constantly evolves to meet changing societal and professional needs. The accreditation standards and the accreditation process must necessarily change to address new ideas and approaches in education. These standards serve as the guidelines by which the COE reviews each CVM during its accreditation review every seven years. Also, each CVM informs the COE every year of changes in program status or any planned changes for the future.

The COE operates under the guidelines of the US Department of Education and the Council on Higher Education Accreditation. The composition of the 20-member COE represents the broad spectrum of stakeholders in the profession. The council includes nine faculty members or administrators from US CVMs, seven veterinary practitioners, three public members, and one member from the Canadian Veterinary Medical Association. Of the nine members currently representing CVMs on the COE, two are deans and two are associate deans; one public member is from a medical school. The AVMA as an association does not control or interfere with the COE accreditation process.

All members of the COE must have their credentials reviewed by the Candidate Qualification Review Committee before they are eligible to be elected to the council. Members of the COE make recommendations on changes to the standards that are forwarded to the CVM deans for their comments. The comments are carefully evaluated by the COE before any changes are finalized. Our academic colleagues are encouraged to step up as leaders of the profession to review and comment on proposed changes to the standards and to consider serving on the COE. Despite the best and most thorough review, we recognize that the COE and the profession as a whole may determine at a later time that a specific change was not helpful, but the accreditation process also allows for the correction of such events.

Gerhardt Schurig, dvm, phd

President

Association of American Veterinary

Medical Colleges

Dean's Office

Virginia-Maryland Regional College of Veterinary Medicine

Virginia Polytechnic Institute and State University

Blacksburg, Va

Ovariectomy during early pregnancy

I enjoyed reading the commentary by Drs. DeTora and McCarthy regarding the use of ovariohysterectomy versus ovariectomy for elective sterilization of female dogs and cats.¹ One question I have that did not seem to be answered in this article or in other articles I have read is in regard to the possible consequences for a dog or cat that undergoes ovariectomy while in the very early stages of pregnancy. Many of the dogs we spay are from animal shelters and have unknown histories, and I am sure that at least some of them have been recently bred but pregnancy has not advanced enough to be grossly identifiable.

Phillip Henderson, dvm

Ponder Veterinary Hospital

Ponder, Tex

The authors respond:

Thank you for your inquiry in regard to our recent commentary on the use of ovariohysterectomy versus ovariectomy for elective sterilization of female dogs and cats.¹ You bring up an interesting point regarding the effects of ovariectomy during the early stages of gestation, before development of grossly identifiable feti. We recognize that in shelter medicine and in private practice there is variability in pregnancy status when elective sterilization is performed. It is important to remember that in both dogs and cats, the ovaries are the major source of progesterone required to maintain pregnancy, whereas only a nominal amount is produced by the placenta.² Ovariectomy before the development of grossly identifiable feti would remove the source of progesterone required to maintain pregnancy and result in resorption or abortion. As a result, performing ovariectomy during the earliest stages of pregnancy should not cause a clinical issue.

Michael DeTora, dvm

Robert J. McCarthy, dvm, ms, dacvs

Department of Clinical Sciences

Cummings School of Veterinary Medicine

Tufts University

North Grafton, Mass

Corrections regarding hyperkalemia pathophysiology

The Anesthesia Case of the Month article¹ in the December 1, 2011, issue of the JAVMA has what appears to be an incorrect statement regarding hyperkalemia. The statement indicates that “[h]yperkalemia decreases the cell membrane resting potential (ie, makes it more negative) and hyperpolarizes the cells, reducing their ability to conduct impulses.”

It is true that hyperkalemia decreases the membrane potential, but this actually makes the membrane potential less negative. Potassium ions cannot escape the cell owing to the high extracellular potassium concentrations, and the cell interior becomes more positive (not hyperpolarized). This results in a membrane potential closer to the threshold potential, so it becomes easier to trigger an action potential in this situation.

Ralph E. Werner, vmd

Richard Stockton College of New Jersey

Galloway, NJ

In the Anesthesia Case of the Month article published in the December 1, 2011, issue of JAVMA,¹ there appear to be 2 incorrect descriptions regarding the effects of hyperkalemia and the administration of calcium gluconate on the resting membrane potential. First, the article states that “[h]yperkalemia decreases the cell membrane resting potential (ie, makes it more negative) and hyperpolarizes the cells, reducing their ability to conduct impulses.” Hyperkalemia does decrease the cell membrane potential as stated, but this makes the resting membrane potential less negative, which in turn makes cells more, not less, excitable.² As hyperkalemia progresses, resting membrane potential will eventually become less than the threshold potential. Once this occurs, cells can no longer repolarize, which removes their ability to depolarize. This can be appreciated by examining the Nerst equation: E_m = −61 × log₁₀ K⁺_I/K⁺_O, where E_m is resting membrane potential, K⁺_I is intracellular potassium concentration, and K⁺_O is extracellular potassium concentration. Increasing extracellular potassium concentration results in a less negative resting membrane potential.

Second, the article states that “[b]y administering calcium gluconate, the cardiac cell threshold potential is decreased, thus normalizing the difference between resting and threshold potentials….” With hyperkalemia, administration of calcium causes the membrane threshold to be increased, increasing the difference between resting and threshold potentials. This will allow the cell to repolarize and depolarize once again.

Bradley Simon, dvm

Hiroki Sano, bvsc

School of Veterinary Medicine

University of Pennsylvania

Philadelphia, Pa

The author responds:

Thank you for your comments regarding the Anesthesia Case of the Month article in the December 1, 2011, issue of JAVMA.¹ The authors understand the letter writers' concerns and agree with the information in these letters. In particular, we agree that hyperkalemia causes cells to be less hyperpolarized and makes the membrane potential less (not more) negative, making the cells more excitable.

Another important point we would like to emphasize is that human RBCs are very different from canine RBCs, and with the exception of RBCs from dogs of certain breeds, potassium concentration in canine RBCs is not as high as the concentration in human RBCs. The cause of the hyperkalemia in the dog described in our report can't solely be attributed to the rapid blood transfusion, even if all the transfused blood had been completely hemolyzed. Most likely, a combination of factors, including acidosis, hypovolemia, tissue trauma, and the transfusion, was the culprit.

Again, we would like to thank the letter writers for taking the time to address (and correct) this important point regarding hyperkalemia pathophysiology.

Andre Shih, dvm, dacva

Department of Large Animal

Clinical Science

College of Veterinary Medicine

University of Florida

Gainesville, Fla

Question about fish oil dosages

I found the recent Timely Topics in Nutrition article “Therapeutic use of fish oils in companion animals”¹ to be extremely useful and interesting, and I plan on greatly increasing my use of omega-3 polyunsaturated fatty acids in my practice after reading this review. However, I found the dosage information provided in Table 1 to be confusing. Do the dosages given on a mg/kg basis represent the combination of eicosapentaenoic acid and docosahexaenoic acid or are these the dosages for each compound individually? Also, the approximate doses listed for a 10-kg (22-lb) dog do not seem to equate to the mg/kg dosages given. Can the author please clarify?

Lindsay Warner, dvm

Mebane Veterinary Hospital

Mebane, NC

The author responds:

Thank you for your letter and renewed interest in incorporating omega-3 fatty acids into your practice. I am happy to additionally clarify how the dosing information in Table 1 should be used. The dosages listed in Table 1 are not given on a mg/kg of body weight basis but on a mg/kg of metabolic body weight basis. Food dosages for dogs and cats are typically calculated on the basis of metabolic body weight.

This means that the amount that should be administered is not directly related to body weight per se but is calculated according to body weight raised to some exponential power value. This phenomenon is especially important given that body weights of dogs can range from 1 to 90 kg (2.2 to 198 lb) or more. For dogs, this exponent is 0.75 (ie, kg^0.75) and for cats it is 0.67 (ie, kg^0.67). These exponents are more fully described in the National Research Council Nutrient Requirements of Dogs and Cats.¹

In the article, use of metabolic body weights for dosage calculations is described in the section “Therapeutic Use of Fish Oils for Clinical Disorders in Dogs” and in the footnote to Table 1. Use of metabolic body weights also enables one to determine from the label information the milligrams of omega-3 fatty acids a dog or cat consumes when fed a commercial diet and to compare amounts administered with the reported safe upper limit.

Dosages reported in Table 1 represent eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) combined. Thus, to calculate the approximate dosage of EPA plus DHA (combined) to use from the values listed in Table 1, it is necessary to first determine the dog's body weight in kg, raise this value to the 0.75 power, and then multiply this result by the dosage listed in Table 1 for a particular condition. For example, the metabolic body weight of a 10-kg (22-lb) dog is 10 kg^0.75, or 5.62 kg (12.364 lb). Thus, the dose of EPA and DHA combined for a 10-kg dog with kidney disease would be 5.62 kg × 140 mg/kg, or 787 mg of EPA and DHA combined. For a 10-kg dog with a cardiovascular disorder, the dose would be 5.62 kg × 115 mg/kg, or 646 mg of EPA and DHA combined. Values in Table 1 have been rounded up or down to the nearest 5 mg. Fish oil preparations typically list the amounts of EPA and DHA in milligrams on their labels, so the number of capsules to feed can be calculated from the approximate dose.

I trust that the above information clarifies your questions regarding the dosage calculations and hope to have assisted others with similar concerns with my response.

John E. Bauer, dvm, phd, dacvn

Department of Small Animal

Clinical Sciences

College of Veterinary Medicine and Biomedical Sciences

Texas A&M University

College Station, TX

Use of dexmedetomidine and ketamine in combination with opioids

I am grateful for the physiologic data presented in the study “Evaluation of dexmedetomidine and ketamine in combination with various opioids as injectable anesthetic combinations for castration in cats.”¹ I have been using dexmedetomidine combined with ketamine and either morphine or buprenorphine for more than five years in the context of a high-volume spay-neuter practice. I developed my protocol with the assistance of Dr. Richard Bednarski, an anesthesiologist at The Ohio State University College of Veterinary Medicine. Morphine is used for patients more than 12 weeks old, and buprenorphine is used for pediatric patients.

The investigators encountered problems such as an inability to quickly intubate patients and a lack of surgical anesthetic depth in some of the cats in the study. To circumvent these problems, the doses I use are higher than those used in the study. In my practice, male cats that will not be intubated receive an IM injection of dexmedetomidine (40 μg/kg [18.2 μg/lb]) and ketamine (8 mg/kg [3.6 mg/lb]) with either morphine (0.33 mg/kg [0.15 mg/lb]) or buprenorphine (22 μg/kg [10 μg/lb]). They also receive an intratesticular nerve block with bupivacaine and lidocaine prior to surgery. Female cats that are to be intubated receive an IM injection of dexmedetomidine (50 μg/kg [22.7 μg/lb]) and ketamine (11 mg/kg [5 mg/lb]) with morphine (0.33 mg/kg) or buprenorphine (22 μg/kg). Following laryngeal application of a topical lidocaine gel, female cats are intubated easily, usually within 10 minutes after the initial injection. Intubated patients receive oxygen and isoflurane (typical delivered concentration is 0.5%). In all patients, anesthetic effects are reversed with atipamezole administered IM at a dose equal to half the volume of dexmedetomidine administered. Postoperative analgesia is supplemented with a single dose of meloxicam (0.1 mg/kg [0.045 mg/lb], IM), and most feline patients are sent home with three days of buprenorphine for oral administration. Owner reports of painful cats following surgery are extremely rare.

There are a few cautions associated with use of this combination protocol. The cats must be watched closely after the IM anesthetic injection is given and cats are placed back in their cages. Deleterious body postures that result in nasal occlusion or kinking of the trachea can develop as sedation develops and could obstruct airflow. Rarely, cyanosis can occur either as a result of hypoxia secondary to hypoventilation and breathing room air or as a result of peripheral vasoconstriction caused by dexmedetomidine. Oxygen supplementation via face mask or endotracheal tube easily resolves this.

The doses I currently use were developed through trial and error as I dealt with the same problems of inability to intubate and lack of anesthetic depth. In a high-volume spay-neuter clinic, such delays substantially disrupt the surgical workflow. I monitor the patients' heart rate, respiratory rate, oxygen saturation, and end-tidal partial pressure of carbon dioxide and am confident in the safety of this protocol. Nevertheless, the study's more in-depth analysis of physiologic data is reassuring. I hope to see more such studies, especially at higher doses such as those used by my spay-neuter clinic.

Danielle N. Rastetter, dvm

Pets In Stitches, LLC

Miamisburg, Ohio

The study “Evaluation of dexmedetomidine and ketamine in combination with various opioids as injectable anesthetic combinations for castration in cats” by Ko et al¹ provides interesting information on the use of these drugs in cats. However, it appears all of these combinations resulted in a relatively deep plane of anesthesia that required intubation for a surgical procedure involving a site accessible for local anesthesia.

In contrast, in my practice, I administer a combination of acepromazine maleate and ketamine, IV, at approximately a quarter of the doses used for IM injection, and then inject each testicle with a local anesthetic such as 2% lidocaine until the testicle feels hard. This results in rapid sedation, early recovery, and excellent postoperative analgesia.

M. Gregory Carbone, dvm

Arlington, Va

Veterinary school class size and job outlook

I read with a great deal of interest and concern the JAVMA News article regarding Virginia-Maryland Regional College of Veterinary Medicine's building project.¹ To help fund this project, the dean estimates an increase in class size by 20 to 25 students, most coming from out of state.

I personally believe there are sufficient data to conclude that there is a surplus of practicing veterinarians in the United States, although it seems that few within the profession want to discuss this. Wise and Kushman² in a synopsis of a veterinary workforce study published back in 1985 concluded that schools and colleges of veterinary medicine in the United States would need to decrease the number of graduates by 20% to balance workforce supply and demand. Since then, we have, instead, added new veterinary programs and increased class sizes. I believe that this continual disregard for supply and demand is having and will continue to have disastrous consequences for our profession.

Is it responsible, or even ethical, to increase the number of graduates given the already unstable job market? Is it in the best interest of students or the profession to do so? I would argue that it is not.

I urge the leadership of the AVMA to issue a statement with regard to job market outlook, starting salaries, and return on investment of a veterinary degree. Our future colleagues need honest, accurate information before they should be expected to take on the burden of veterinary school debt. Perhaps our universities should be discussing closures and mergers rather than increases in class size.

Greg Nutt, dvm

Canton, Ga