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Friday, November 7, 2008

Does Ultrasound Miss Abdominal Lesions?

Of course it does. But big question is how often? Are some findings more or less reliable?

An interesting article in the recent JAAHA looks at the correlation of abdominal ultrasound findings with gross surgical exploration. Whenever I have access to the ex lap findings of a patient undergoing an explore after one of my ultrasounds, I am anxious to find out how my findings compare. We all fear a negative explore, although almost every patient I can think of who had a negative gross explore, had microscopic lesions that were helpful in patient management. Following up on the ultrasound findings is an essential part of the learning process for anyone performing ultrasound or ordering one for their patient.

This was a retrospective study looking at cases from The Queen Mother Hospital for Animals in the UK. The ultrasounds were performed by experienced radiologists or radiology residents. They looked at 100 cases who had an ex lap within 48 hours of an abdominal ultrasound. There were only 19 cats, so one has wonder whether this was an adequate sample size for this particular species. There were no stats looking at cats versus dogs. However, they did note that there was “no apparent relationship…detected between body size of animal and the sensitivity of ultrasound for the primary lesion.” I find cats much easier to ultrasound than similarly-sized dogs (perhaps that is my bias towards this fabulous species), but I do feel this is a weakness in the study.

Their results are similar to what I have found in my clinical practice:

100 primary lesions & 67 secondary lesions were found at surgery.

Ultrasound did not detect the primary lesion in 24 of these animals and secondary lesions in 11 animals.

“A total of 36 animals [out of 100] had discordant ultrasonographic and surgical findings of their primary and secondary lesions.”

Ultrasound detected peritonitis lesions in 89% of cases.

Ultrasound detected intestinal obstruction in 64% of cases.

Ultrasound detected hepatic or splenic nodules in 63% of cases.

GI lesions were most likely to be missed by ultrasound (perforations, ulcerations) followed by organomegaly.

Although not statistically significant, ultrasound missed 5 GI foreign bodies.

Gross visualization at surgery missed some lesions seen on ultrasound - prostatic cysts, renal lesions, bladder lesions, splenic/liver lesions, and a gall bladder polyp.

This study brings to light my own experience.

If I am presented with a persistently vomiting animal with radiographs that are very suspicious for a GI obstruction but my ultrasound findings do not suggest obstruction - I ALWAYS err on the side of suspecting obstruction. Depending on the status of the animal and the level of suspicion from the radiographs, the next step may be to continue supportive care and repeat rads in 6-12 hours or it may be an exploratory laparotomy. My own cat had a negative explore and a number of my patients have as well. We have always learned something from the biopsies obtained and I have been fortunate to never have an owner be angry about it. The possibility of a negative explore is an important part of my conversation with the owner prior to surgery.

When ultrasound is used as part of check for metastasis, again, I always warn owners that we may be missing something. Ultrasound is notoriously poor at seeing all lesions in a liver or spleen. It may miss a focal intestinal lesion. I cannot count how many times over the course of my residency that Mike Willard showed me pictures of horrid livers at laparoscopy that were deemed normal by very experienced radiologists. Likewise, as was seen in this study, ultrasound may be able to detect architectural irregularities in an organ (especially liver, spleen, kidney) that are not seen on the surface of the organ at surgery. In these cases, a biopsy of a “normal” organ may reveal significant pathology.

This is why I am an annoyance to the surgeons when they explore the abdomens of my patients. Ultrasound is so subjective. It helps to have the objective look at surgery (or necropsy) to verify what I have seen. I am quick to recommend surgery (unless it would be detrimental to the patient) when I have any doubt about what I am seeing with ultrasound or if the animal’s signs are worse than expected based on ultrasound. Until we get a hold of one of Dr. Crusher’s tricorders, we’re stuck with histopathology for a diagnosis in many patients.

Jennifer S. Fryer, DVM


Saturday, October 25, 2008

Introduction to Veterinary Answers, LLC

Veterinary Answers is a phone, fax, and email consultation service provided by specialist veterinarians to assist general practice veterinarians with their cases and practice. Our goal is to provide veterinarians with the information that will allow them to refer fewer patients and provide the highest standard of care available. We provide this service to licensed veterinarians only.

In addition to assistance with individual cases, we also provide article searches, we will set up hospital protocols for infection control or commonly encountered diseases, and answer any question you have in small animal veterinary medicine.

In this blog, we will review current literature and provide our assessment of recent articles that bring up clinically relevant or controversial topics.

Contact us with your questions or comments.
Toll Free Phone (877) 262-3024

Toll Free Fax (888) 496-4473

Email -

Monday, September 29, 2008

Managing Twins in the Mare

C. Scott Bailey, DVM, Dipl. ACT

Although twinning in the horse is a well-described condition academically, it remains a topic for which most horse-owners and many veterinarians feel inadequately prepared. Historically, twinning has been the most common cause of mid- to late-term pregnancy loss in mares; this is because the equine placenta requires a large surface area (the entire uterus) to supply sufficient oxygen and nutrients to the developing fetus in late gestation. Even a relatively small decrease in surface area will result in growth- retardation and a smaller and less thrifty foal at birth.

Physiologically, twins are most often the product of 2 asynchronous ovulations in a single cycle, which may be up to 5 days apart in the mare. For the first 16 days both developing embryos will be propelled around the uterus either adjacent to each other or separately, and they will then become fixed by muscular contraction between 16 and 17 days. In 80% of cases, the embryos are fixed together at the base of one horn, and in 20% of cases, they are each fixed in separate horns. In the latter case, there is no competition for nutrients in early gestation and the vast majority of cases result in late-term abortion. However, if the embryos are adjacent to each other, they may undergo spontaneous regression (70%) by day 40. Overall, in one study 64% of naturally occurring twins were found to undergo spontaneous regression, most before day 26. The likelihood of spontaneous reduction decreased thereafter until day 40. After day 40, 90% of twins will result in late-term pregnancy failure, either in the form of abortion of both fetuses, stillbirth and stunting of term foals or dystocia.

Despite the high rate of pregnancy failure in mares carrying twins, the incidence of double-ovulations is high (20%) is some breeds. The very act of reducing twins results in increased numbers of horses that carry the genetic propensity for twinning. Likewise, inducing ovulation with exogenous hormones also increases the likelihood of double-ovulations. As a result, the use of ultrasound for early pregnancy diagnosis has become routine for many equine practitioners. At this stage, reduction of pregnancy by “pinching” one embryonic vesicle can be performed reliably and safely. This procedure is generally performed around 14-15 days of gestation – a time at which embryonic vesicles are readily detectable and are still mobile in the uterus, making it possible to move one embryo to the tip of a horn by manual trans-rectal manipulation. Once the vesicle is separated adequately from the remaining embryo, and is at the tip of a horn it can be “pinched” manually or with the ultrasound. This procedure has a 90-95% success-rate when performed by a skilled practitioner and can be performed early in pregnancy, at a time in which re-breeding the mare is possible if the procedure results in the loss of both embryos.

After this critical window, success-rates for various reduction methods are low. Between 17 and 26 days natural reduction with or without the benefit of energy deprivation by eliminating grain-based feed may be the most effective means of eliminating one twin. However, if twins are still identified after day 30, another means of reduction should be selected. Allowing the pregnancy to continue beyond day 35 will result in the development of endometrial cups and a loss of the remaining-breeding season if pregnancy is lost subsequently. Therefore, trans-vaginal ultrasound-guided twin reduction may be attempted at this time. A 5 - 7.5 MHz vaginal ultrasound probe with a needle-guide is used to visualize one embryo, which is held adjacent to the probe with one hand in the rectum. The needle is then punctured through the vaginal wall and uterus, and the fetal fluids are aspirated aggressively. This technique has been reported with a 30% success-rate for the production of one live foal in the case of unilateral twins, and up to 70% success-rate for the production of one live foal in the case of bilateral twins when performed between 30 and 36 days.

After 35-36 days of pregnancy, two procedures have been described for selective reduction of one twin.

Most recently, cranio-cervical dislocation of one fetus has been described by a practitioner in central Kentucky. While not widely available, this technique has been demonstrated to carry a relatively high success-rate of >60%. It can be performed trans-rectally or surgically by flank laparotomy, and has been described between 60 and 110 days. At this stage of gestation, the gender of each fetus can be determined, and the fetus is selected for reduction based on both gender and location in the uterus. In addition, this procedure can be performed before complete development of the placenta and may have a higher success-rate than later procedures due to the ability of the remaining fetus to form a fully functional placenta.

Alternatively, ultrasound-guided trans-abdominal cardiac puncture has been well-described in the literature, with a success-rate around 50%. For this procedure, the fetuses are identified by trans-abdominal ultrasound after sedation of the mare and one fetus is injected with KCl or procaine penicillin by intra-cardiac puncture using a spinal needle. The success of this procedure is operator-dependent, but is less invasive than the surgical procedure described above and requires little equipment other than a 3.5 MHz curvilinear probe. It is best performed between 115 and 130 days of gestation and as for the procedure above, both location and fetal gender may be used as criteria for selection. It should be noted that this procedure may result in the birth of a small and unthrifty foal. This is likely due to the fact that the placenta is largely developed by 120 days and the area of placenta which opposes that of the reduced twin remains unavailable for nutrient transfer for the remainder of gestation.

When all other procedures fail to achieve the goal of one developing fetus, abortion of both conceptuses is the single remaining option. Due to the risk of dystocia and periparturient complications to the mare and the low chance of achieving two live foals (1- 2%), allowing the pregnancy to be maintained naturally cannot be recommended. Chemical abortion can easily be achieved before formation of the endometrial cups (36-40 days) with a single dose of prostaglandin or prostaglandin analog, but may require multiple doses of a prostaglandin/ prostaglandin analog and/or oxytocin in later gestation. At this time, abortion should be performed in a hospital-setting, where the mare can be monitored carefully and where parturition can be attended.

Thus, while twins undoubtedly constitute a significant risk to equine pregnancy, there are many methods of managing them successfully. Indeed, the common use of ultrasound for early pregnancy diagnosis has been so successful that many practitioners now feel that double-ovulations are actually of benefit, because they increase the likelihood of fertilization and because any twins can readily be managed early in gestation.


Ginther OJ. Twin embryos in the mare: 1. From ovulation to fixation. Equine Vet J 1989; 21:166-70

Leadon DP, Rossdale PD, Jeffcot LB et al. A comparison of agents for inducing parturition in mares in the pre-viable and premature periods of gestation. J Reprod Fertil Suppl 1982; 32: 597-602

Macpherson ML, Homco LD, Varner DD. Transvaginal ultrasound-guided allantocentesis for pregnancy elimination in the mare Biol Reprod Monogr 1995; 1: 215-223

Rantanen NW, Kincaid B. Ultrasound guided fetal cardiac puncture. A method of twin reduction in the mare. Proc Am Assoc Equine Pract 1988; 34:173-79

Wolfsdorf KE. Management of postfixation Twins in Mares. Vet Clin Equine 2006; 22: 713-725

Practical Recent Abstracts

Edited by Jennifer S. Fryer, DVM

The influence of crystalloid type on acid-base and electrolyte status of cats with urethral obstruction

Drobatz KJ, Cole SG. JVECCS 2008; 18: 355 – 361.

To compare the effect of a balanced isotonic crystalloid solution with that of 0.9% sodium chloride on the acid[ndash]base and electrolyte status of cats with urethral obstruction. Randomized prospective clinical trial. Academic veterinary emergency room.

Sixty-eight cats with naturally occurring urethral obstruction. Cats were randomized to receive either a balanced isotonic crystalloid solution (Normosol-R, n=39) or 0.9% sodium chloride (n=29) for fluid therapy. Baseline venous blood gas and blood electrolyte values were obtained at the time of admission and at intervals during the course of therapy. Baseline values were similar between groups.

Cats receiving Normosol-R had a significantly higher blood pH at 12 hours, a significantly greater increase in blood pH from baseline at 6 and 12 hours, as well as a significantly higher blood bicarbonate concentration at 12 hours and a significantly greater increase in blood bicarbonate from baseline at 6 and 12 hours. Conversely, the increase in blood chloride from baseline was significantly higher at 2, 6, and 12 hours in cats receiving 0.9% sodium chloride. There were no significant differences in the rate of decline of blood potassium from baseline between groups. Subgroup analysis of hyperkalemic cats (K+>6.0 mmol/L) and acidemic cats (pH<7.3) style="font-weight: bold;">Efficacy and tolerability of once-daily cephalexin in canine superficial pyoderma: an open controlled study

Toma S, Colombo S, Cornegliani L, Persico P, Galzerano M, Gianino MM, Noli C. Journal of Small Animal Practice 2008; 49: 384 – 39.

Objectives: The aims of this study were to evaluate the efficacy and tolerability of oral cephalexin given at 30 mg/kg once daily in dogs with superficial pyoderma and to compare them with those of oral cephalexin given at 15 mg/kg twice daily.

Methods: Twenty dogs with superficial pyoderma were treated with cephalexin at 30 to 60 mg/kg orally once daily (group A) and compared with 20 dogs treated at a dose of 15 to 30 mg/kg orally twice daily (group B). Dogs were treated until 14 days after clinical remission. Type and distribution of lesions, pruritus and general health status were assessed every 14 days using a numerical scale until 14 days after treatment discontinuation. Total scores for each evaluation day were compared between the two groups as well as time to obtain resolution and percentage of relapses.

Results: Resolution of superficial pyoderma was obtained in all dogs in 14 to 42 days (median 28 days for both groups), with no difference between groups. Six dogs experienced vomiting or diarrhoea but did not require discontinuation of the treatment. Only one dog (in group A) relapsed nine days after treatment discontinuation.
Clinical Significance: Once-daily cephalexin is as effective as twice-daily cephalexin in the treatment of canine superficial pyoderma.

Evaluation of antibodies against feline coronavirus 7b protein for diagnosis of feline infectious peritonitis in cats

Kennedy MA, Abd-Eldaim M, Zika SE, Mankin JM, Kania SA. AJVR 2008; 69: 1179-1182.

Objective—To determine whether expression of feline coronavirus (FCoV) 7b protein, as indicated by the presence of specific serum antibodies, consistently correlated with occurrence of feline infectious peritonitis (FIP) in cats.

Sample Population—95 serum samples submitted for various diagnostic assays and 20 samples from specific-pathogen–free cats tested as negative control samples.

Procedures—The 7b gene from a virulent strain of FCoV was cloned into a protein expression vector. The resultant recombinant protein was produced and used in antibody detection assays via western blot analysis of serum samples. Results were compared with those of an immunofluorescence assay (IFA) for FCoV-specific antibody and correlated with health status.

Results—Healthy IFA-seronegative cats were seronegative for antibodies against the 7b protein. Some healthy cats with detectable FCoV-specific antibodies as determined via IFA were seronegative for antibodies against the 7b protein. Serum from cats with FIP had antibodies against the 7b protein, including cats with negative results via conventional IFA. However, some healthy cats, as well as cats with conditions other than FIP that were seropositive to FCoV via IFA, were also seropositive for the 7b protein.

Conclusions and Clinical Relevance—Expression of the 7b protein, as indicated by detection of antibodies against the protein, was found in most FCoV-infected cats. Seropositivity for this protein was not specific for the FCoV virulent biotype or a diagnosis of FIP.

Monday, July 7, 2008

Small Animal Test Guide

In this guide, we answer the following questions on all the most common small animal tests:
Why do it?
What samples do I need and at what time should they be collected?
Does the animal need to be fasted?
What unique things should I know about this test?

ACTH Stimulation Test
B12/Cobalamin & Folate
Bile Acids Test
Bromide Concentration
Digoxin Concentration
High-dose Dexamethasone Suppression Test
Endogenous ACTH
Free T4 by Equilibrium Dialysis
Low-Dose Dexamethasone Suppression Test
Parathyroid Hormone
Phenobarbital Concentration
PLI or cPL
T3 Suppression Test
Urine Cortisol:Creatinine Ratio
Urine Protein:Creatinine Ratio
von Willebrand's Factor

Monday, June 30, 2008

More Consultants, More Species, More Specialties

Veterinary Answers is growing by leaps and bounds. We now have consultants to cover almost all the species and organ systems you will encounter in practice.

Jennifer S. Fryer, DVM - Internal Medicine

Courtney Baetge, DVM - Anesthesia

Georgina Barone, DVM, DACVIM - Neurology

Terri Bonenberger, DVM, DACVD - Dermatology

Natalie Carrillo, DVM, DACVIM - Large Animal Internal Medicine

Curtis W. Dewey, DVM, MS, Diplomate ACVIM (Neurology) and Diplomate ACVS

Joan Dzeizyc, DVM, DAVCO - Ophthalmology

Carol Gamble, DVM, Diplopmate ABVP - Avian

Michael Garvey, DVM, DACVIM - Small Animal Internal Medicine
DACVECC - Small Animal Critical Care

Chelsea Greenberg, DVM, MS - Oncology

John Hintermeister, DVM, Board Eligible ACVIM - Oncology

Eric Klaphake, DVM, Diplomate ACZS and Diplomate ABVP - Avian

Nicholas Millichamp, Bsc, PhD, DACVO - Ophthalmology

Christal Pollock, DVM, DAVBP - Avian

Jeffery P. Simmons, DVM, MS, DACVECC

Ian Spiegel, DVM, MPH, Diplomate ACVD

Thursday, June 26, 2008

RSS feeds for Veterinary Journals

Last year, during the food recall, it seemed like new foods were being added to the recall list on a daily basis and I had great difficulty keeping up. In fact, when my own cat had eaten recalled food, I did not find out until VetCentric called me at home and at the office to alert me. It was then that I discovered the FDA's RSS feed on recalls. Every day, I would check my RSS reader for the latest on recall alerts and I was no longer in the dark when new recalls were announced.

Since then, I have found RSS feeds to be a helpful way of keeping up with the latest veterinary literature. I read through the abstracts as soon as they are published online & then determine if I want to read the entire article. Many US veterinary college libraries allow veterinarians in their state to request individual articles for free or a reduced fee. You can also order individual articles through the Veterinary Information Network (VIN). The Royal College of Veterinary Surgeons subscribes to many veterinary journals and any veterinarian (whether in the UK or abroad) can become a member for a very reasonable price. This keeps printed journal subscriptions to a minimum and means less paper waste. And you can keep a pdf of each article on file in your computer, rather than paper files which take up so much space and time to maintain. You can also have a separate drive or an online service like Carbonite to back up your files, so that all your journal articles are still accessible if your computer is lost, stolen, destroyed, or self-destructs.

There are numerous RSS readers out there. I like Google Reader, as it is easy to read and is incorporated in to my Google account. Yahoo has a nice reader as well.

There are also services which will search newly released articles for parameters you set and either send you an email, or place it in a mailbox for you to check when you next login. PubMed's MyNCBI and Highwire both offer these services. On the human side, Amedeo will send you a weekly list of abstracts on the subject of your choice (from a menu) and journal of your choice (from a menu). I am trying to convince Amedeo to start a veterinary journal alert service. I will let you know if I am successful. Google recently added Google Alerts, which will send you email alerts when new entries for a specific search term come up. However, you cannot limit the search to journals - so lots of useless stuff may come up.

I have found lists of human medical journal RSS feeds, but have yet to find something similar in Veterinary Medicine. So here are the ones I have found so far. Please feel free to comment if you find additional links or have a problem with a link.

RSS FEEDS - Look for the orange symbols above to find the link for the RSS feed
American Journal of Animal and Veterinary Sciences
American Journal of Veterinary Research
Anatomia, Histologia, Embryologia: Journal of Veterinary Medicine
Australian Veterinary Journal
Brazilian Journal of Veterinary Research and Animal Science
Equine Veterinary Education
Equine Veterinary Journal
Journal of Small Animal Practice
Journal of the American Medical Association
Journal of the American Veterinary Medical Association
Journal of Veterinary Cardiology
Journal of Veterinary Emergency and Critical Care
Journal of Equine Veterinary Science
Journal of Veterinary Internal Medicine
Journal of Veterinary Pharmacology & Therapeutics
The Lancet
Medical and Veterinary Entomology
New England Journal of Medicine
New Zealand Veterinary Journal
Onderstepoort Journal of Veterinary Research (must scroll down list to find it)
Preventive Veterinary Medicine
Research in Veterinary Science
Topics in Companion Animal Medicine
Transboundary and Emerging Diseases
Tropical Animal Health and Production
Veterinary and Comparative Oncology
Veterinary Anaesthesia and Analgesia
Veterinary Dermatology
Veterinary Economics - free content
Veterinary Immunology and Immunopathology
The Veterinary Journal
Veterinary Medicine - free content
Veterinary Microbiology
Veterinary Ophthalmology
Veterinary Parasitology
Veterinary Pathology - free content
Veterinary Radiology and Ultrasound
Veterinary Research
Veterinary Research Communications
Veterinary Surgery
Zoonoses & Public Health

Australian Equine Veterinarian
Indian Journal of Veterinary Pathology
Indian Journal of Veterinary Surgery
In Practice - British Veterinary Association
Journal of the American Animal Hospital Association
Journal of Animal Husbandry and Veterinary Medicine in Tropical Countries
Journal of Veterinary Behavior
Journal of Veterinary Diagnostic Investigation
Journal of Veterinary Medical Education
NAVC Clinician's Brief - Free registration & content
Veterinary and Comparative Orthopaedics and Traumatology
Veterinary Clinics of North America: Equine Practice
Veterinary Clinics of North America: Exotic Animal Practice
Veterinary Clinics of North America: Food Animal Practice
Veterinary Clinics of North America: Small Animal Practice
Veterinary Health and Safety Digest
The Veterinary Record

Canadian Journal of Veterinary Research
Canadian Veterinary Journal
Compendium: Continuing Education for Veterinarians
Compendium Equine
Exotic DVM - free subscription for vets, techs, students
Flemish Veterinary Journal
Online Journal of Veterinary Research
The Pig Journal
Review of Medical and Veterinary Entomology
Review of Medical and Veterinary Mycology
Standards of Care
Veterinary Bulletin
Veterinary Clinical Pathology
Veterinary Focus - free subscription for vets, techs, students
Veterinary Forum
Veterinary Technician
Veterinary Therapeutics

British Veterinary Dental Association Journal
The International Journal of Applied Research in Veterinary Medicine
The Irish Veterinary Journal
Israel Journal of Veterinary Medicine
Japanese Journal of Veterinary Research
The Journal of Veterinary Medical Science (Japanese Society of Veterinary Science)
Journal of Veterinary Science
Turkish Journal of Veterinary and Animal Sciences
Veterinary Neurology and Neurosurgery
Veterinary Practice News
The Veterinary Quarterly
Veterinary Review

AVMA Directory - need AVMA membership
Canadian Compendium of Veterinary Products - need annual subscription
Compendium of Veterinary Products - need AVMA membership
FDA - News, Recalls, Drug shortages, etc.
Material Safety Data Sheets - need AVMA membership
Merck Veterinary Manual - Free Content
Veterinary Biologic Products - Licensees and Permittees -USDA- December 2007

Tuesday, April 29, 2008

EHV-1 the neuropathogenic strain

by Natalie Carrillo, MV, DVM, Dip ACVIM-LA

Recent outbreaks of myeloencephalopathy caused by equine herpesvirus (EHV-1) have generated new research that provides better information about diagnosis, treatment and outbreak management. The objective of this article is to summarize this information in a practical and applicable manner.

Clinical signs

The onset of EHV-1 myeloencephalopathy is characterized by a biphasic fever. In several outbreaks2 it has been observed that only horses younger than 5 years displayed fevers and respiratory signs, whereas the older horses were febrile, but had no signs of respiratory disease. It has also been observed that older horses develop neurologic deficits more frequently and of greater severity than younger horses (<5> 2. The reason for this bias is unknown, but may be explained by the role the horse’s immune system plays in the extent and severity of vasculitis and vascular thrombosis2.

The neurologic deficits appear approximately 4-6 days after the onset of fever2 and develop as the result of vasculitis, thrombosis and secondary ischemic degeneration of the neuropil1. The neurologic signs reflecting spinal cord involvement range from mild ataxia to recumbency, the pelvic limbs are more frequently involved and bladder atony is common. The brainstem may also be affected and therefore deficits of the cranial nerves may also be observed.

Epidemiology and outcome

The clinical signs are of rapid onset, but they also stabilize quickly. Most non recumbent animals do well, but the prognosis for recumbent horses is poor. In an outbreak of EHV-1 approximately 20-30 % of horses will be affected by the neuropathogenic strain, and of these the mortality will be approximately 30%1, 2.


If you suspect a horse has EHV-1 due to an unexplained fever after being at an event, for example. A nasal swab and an EDTA purple top tube should be collected and submitted on ice packs overnight for real-time TaqMan® PCR on both samples to diagnose and differentiate the neuropathogenic vs non neuropathogenic strains. Results will be ready in 24h post arrival3. (See references for mailing addresses).

Outbreaks and treatment

In the event of a suspected outbreak there are guidelines on the AAEP website that pertain to biosecurity and quarantine. They are to extensive to cover, and are not the objective of this article. What I do want to incur into are treatment guidelines.

On the onset of fever of a suspected animal:

First implement biosecurity measures including stall confinement. Collect pertinent samples for diagnosis and then initiate therapy with NSAIDs such as flunixin meglumine 1.1 mg/kg or phenylbutazone 4.4mg/kg to manage the fevers.

Once the disease is confirmed or clinical signs of the disease progress to a working diagnosis of EHV-1, then more aggressive therapy and prophylaxis of surrounding animals should be initiated. All animals possibly exposed should be treated with Valacyclovir (Valtrex®) 205-403 mg/kg PO every 8 hours. Acyclovir despite clinical reports of effectivity2 has shown not to reach adequate serum levels to inhibit viral replication6 therefore should not be the first drug of choice. Valtrex® is an expensive drug and this option should be thoroughly discussed with the owner.

Management for the horses displaying clinical signs of the neuropathogenic form of EHV-1:

NSAIDs - continue flunixin meglumine 1.1mg/kg for 10 d (monitor serum creatinine every 3-5d depending on hydration status of the horse).

DMSO (if you are a believer) 1g/kg at 20% sol IV every 24h for 3 days, as a free radical scavenger.

Valacyclovir (Valtrex®) 205-403 mg/kg PO every 8 hours for 10 days or until clinical signs stabilize.

Vitamin E 10.000 IU PO every 24h for 10 days7 as an antioxidant.

Dexamethasone 0.1 mg/kg IV for 3 days then taper for a total of 10d. This therapy is controversial. On one hand it is a potent anti-inflammatory, but on the other it does suppress the immune system at these doses. And never forget the potential for laminitis. I would reserve this choice of therapy for horses showing neurological deficits, I would not administer to horses with just a fever, even if it is a confirmed case.

If at any point a horse should become recumbent or needs assistance standing, or in general deteriorates to the point of requiring constant monitoring please talk to the client about referral to a hospital with facilities for critical care.

Vaccination in an outbreak


On premises with confirmed clinical EHV-1 infection, booster vaccination of horses likely to be exposed is not recommended.

Non-exposed horses or horses that have to enter the premises should have a booster vaccination if they have not been vaccinated within the past 90 days. This does not guarantee protection against the disease; the hope is that reduced nasal shedding of infectious EHV-1 by these horses will help reduce the magnitude of challenge experienced by other horses and potentially help reduce spread.

A current publication8 showed that recent vaccination with Rhinomune (modified live vaccine) may provide some protection against EHV-1 myeloencephalopathy. These results should be interpreted with caution because the number of animals used in the study was small.

Vaccines that provide the highest levels of viral neutralizing titers are Pneumabort, Prodigy, Calvenza and Rhinomune. The high levels of antibodies have been shown to reduce viral shedding. It is important to warn clients of the potential side effects of the modified live vaccine such as swelling of the injection site, fever and swelling of the limbs.

I hope this article has been helpful, if you should have any further questions about a case please do not hesitate to contact me.


1.- Julia H. Kydd and K.C. Smith, Equine Herpesvirus Neurologic Disease: Reflections from across the pond. J Vet Intern Med. 2006 May-June;20(3):467-68.

2.- Henninger RW, et al, Outbreak of neurologic disease caused by equine herpesvirus-1 at a university equestrian center. J Vet Intern Med. 2007 Jan-Feb;21(1):157-65.

3.- Allen GP, Development of a real-time polymerase chain reaction assay for rapid diagnosis of neuropathogenic strains of equine herpesvirus-1.J Vet Diagn Invest. 2007 Jan;19(1):69-72. M.H. Gluck Equine Research Center, Department of Veterinary Science, University of Kentucky, Lexington, KY 40546.

4.- Garré B, et al, Pharmacokinetics of acyclovir after intravenous infusion of acyclovir and after oral administration of acyclovir and its prodrug Valacyclovir in healthy adult horses. Antimicrob Agents Chemother. 2007 Dec;51(12):4308-14. Epub 2007 Sep 10.

5.- BG Bentz, et al, Pharmacokinetics of Valacyclovir in the adult horse. Abstract #108 J Vet Intern Med. 2007 May-June;21(3):601.

6.- BG Bentz et al, Pharmacokinetics of Acyclovir after Single Intravenous and Oral Administration to Adult Horses. J Vet Intern Med. 2006 May-June;20(3):467-68.

7.- J.K. Higgins, et al, Vitamin E levels in serum and cerebrospinal fluid of healthy horses following oral supplementation. Abstract #340 J Vet Intern Med. 2007 May-June;21(3):666.

8.- Goodman LB, et al, Comparison of the efficacy of inactivated combination and modified-live virus vaccines against challenge infection with neuropathogenic equine herpesvirus type 1 (EHV-1).

Vaccine. 2006 Apr 24;24(17):3636-45. Epub 2006 Feb 13.

Emergency Management of the Blocked Ferret

By Christal Pollock, DVM, DABVP-Avian

Diagnosis of urethral obstruction in the male ferret is rarely a diagnostic challenge, but the need to place a urinary catheter in a 1-kg patient can be intimidating.

Urinary catheter placement can be challenging in the male ferret because of its small size and its J-shaped os penis. Locate the prepuce on the ventral abdomen just caudal to the umbilicus. The os penis is palpable. After gently extruding the penis, it may help to grasp the base with a gauze square. Aseptically prepare the penis, and use a 24-gauge catheter with the needle removed to find and dilate the urethral opening. The urethral opening is located on the ventral surface of the penis just proximal to the J-shaped curve.

After the urethral opening is found and dilated, pass a urinary catheter. A 3.5 Fr red rubber catheter may be used in a very large male, however most individuals require a smaller tube. A 3-Fr 11-in urinary catheter specifically designed for ferrets is available (Slippery Sam, Global Veterinary Products; New Buffalo, MI) or a 22- or 20-gague jugular catheter may be used. Pre-measure red rubber catheters and jugular catheters. Leave the jugular catheter stylet in place to facilitate passage, but manipulate the catheter carefully. Resistance most often occurs as the catheter travels around the pelvic flexure. Gently flush the urethra with sterile saline to facilitate catheter passage.

· Anesthesia is required for adequate muscle relaxation. Most individuals should be intubated and maintained on isoflurane or sevoflurane when anesthetized for extended periods. Avoid ketamine in ferrets with urethral obstruction.

· When urinary catheterization proves difficult, remove a small amount of urine once via cystocentesis to reduce pressure and allow passage of the urinary catheter. Repeated cystocentesis is not recommended because of thin bladder wall. In rare cases, percutaneous cystostomy may be performed when catheter placement fails.

· Suture butterfly tape strips near the prepuce to secure the catheter. Use tape to fasten the catheter or attached tubing to the tail base to minimize tension on the line. Bandaging the abdomen may also minimize the risk of rotation. Create a closed collection system by attaching a small intravenous bag and monitor urine production. The average 1-kg ferret produces 26-28 ml of urine over a 24-hour period (range: 8-48 ml).

· To catheterize the female ferret, place her in ventral recumbency and elevate the rear with a rolled towel. Aseptically prepare the vulva and perivulvar region, and then insert a sterile vaginal speculum or otoscope. Locate the urethral opening on the vestibule floor 1-cm cranial to the clitoral fossa. Insert a 3.5-Fr red rubber catheter, which may be fitted with a wire stylet.

The most important cause of dysuria or stranguria in the male ferret is prostatomegaly secondary to adrenal disease. Struvite urolithiasis may also cause urethral obstruction, however the incidence is relatively low now that ferret food is commercially available. (Cystitis and prostatic abscesses are uncommon but potential causes of stranguria and dysuria in the ferret). History and physical examination may provide clues to the underlying cause of urethral obstruction, but signalment is not particularly helpful. Most affected ferrets are middle aged to older, although any age may be affected.

Adrenal disease

Struvite urolithiasis


Good diet (Animal protein-based)

Bad diet (Plant protein-based)

Exam findings

Dorsal symmetrical alopecia


Laboratory results

+/- Urinary tract infection

Non-regenerative anemia

Urinary tract infection









· Ferret adrenal disease is associated with an elevation in sex steroid hormones, and elevated androgen levels can leads to prostatomegaly. Dorsal symmetrical alopecia is also a common clinical sign.

· Ferrets require high quality, animal-based dietary protein. Therefore a low quality, plant protein-based diet promotes development of alkaline urine and struvite crystalluria.

· Ferrets normally have relaxed abdomens that are easy to palpate. Although pain will cause the abdominal muscles to tense, the over distended bladder is still palpable. There may also be evidence of urine dribbling and the prepuce may be red from excessive licking.

· Normal ferret biochemistry is similar to that in other mammals with a few exceptions. Creatinine in the ferret generally ranges from 0.1-0.3 mg/dL with values almost always less than 0.5 mg/dL. Creatinine from 0.7-1.0 mg/dL signifies azotemia.

· Obtain whole body survey radiographs using tabletop technique, high-speed film, and fine screen cassettes. Contrast radiography may be useful in identifying urethral stones. Enlarged adrenal glands are rarely visible on radiographs, and ultrasonography is needed. Note that renal cysts are a common incidental finding.

· Ferrets are relatively stoic animals, but do not ignore pain management. Provide preemptive analgesia, and monitor ferrets carefully for signs of discomfort. Signs of pain may include anorexia, lethargy, crying, stiff movements, squinting, and an inability to sleep in a natural, curled position.

References & Further Reading

Castanheira de Matos RE, Morrisey JK. Common procedures in the pet ferret. Vet Clin North Am Exot Anim Pract 2006; 9: 347-365.

Esteves MI, Marini RP, Ryden EB, et al. Estimation of glomerular filtration rate and evaluation of renal function in ferrets (Mustela putorius furo). Am J Vet Res 1994;55:166-172.

Pollock CG. Emergency medicine of the ferret. Veterinary Clinics of North America: Exotic Animal Practice. 10(2): 463-500, 2007.

Quesenberry KE, Carpenter JW, eds. Ferrets, rabbits, and rodents: clinical medicine and surgery. 2nd ed. St. Louis: WB Saunders Co, 2003: 2-134.

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Courtney S. Baetge, DVM – Board Eligible in Anesthesia


Terri Bonenberger, DVM, DACVD

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Large Animal Internal Medicine

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Jennifer S. Fryer, DVM – Board Eligible in Internal Medicine

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Wednesday, March 12, 2008

Disorders of the Brain Part I: Update on current trends, diagnostic tools, and treatments of congenital encephalopathies

By Georgina Barone, DVM, DACVIM (Neurology)

Canine congenital encephalopathies comprise a broad range of developmental disorders. Clinical signs are dependent upon the area of the brain affected and may indicate whether the patient has focal, multifocal, or diffuse disease. A thorough neurologic examination is essential to determine neuroanatomic localization and make appropriate diagnostic and treatment recommendations. It is also imperative that other diseases that may contribute to neurologic deficits be ruled out such as hypoglycemia, porto-systemic shunts, infectious diseases, and inborn errors of metabolism. When evaluating a dog with a suspected intra-cranial developmental anomaly, the veterinarian should consider the following factors. First, is the abnormality of clinical significance? Some anomalies do not produce clinical signs and must be interpreted in light of the patient’s condition. Second, the animal must be evaluated for other malformations. Embryologic development of the brain is closely related to that of the spine and other tissues. Critical evaluation of all organ systems is essential to determine the viability of the dog as a pet. Heritability of the problem is also of key importance to the breeder, although many anomalies occur as sporadic occurrences. Lastly, treatment options and quality of life concerns must be addressed as many anomalous conditions of the CNS carry a guarded to poor prognosis with them.

This article will provide information on some of the more common congenital anomalies seen in our canine patients. Acquired disorders will be addressed in a future newsletter.

Quadrigeminal cysts (QC) are widely believed to be developmental anomalies that arise in close proximity to an intra-cranial arachnoid cistern, most commonly the quadrigeminal cistern located above the cerebellum. They represent accumulation of cerebrospinal fluid between sheets of the arachnoid layer of the meninges and lack an epithelial lining, thus are considered “pseudo-cysts”. Once thought to be rare, these anomalies are increasingly being recognized, most likely due to the greater availability of advanced imaging such as CT and MRI.

Small-breed dogs, particularly brachycephalic breeds (especially Shih-tzu’s) and male dogs are over-represented. Although clinical signs can be variable, one of the most common signs are generalized seizures, likely due to the pressure on the occipital lobes of the cerebrum by pressure from the cystic mass. Additionally, ataxia, intention tremors, paresis, and head tilt have all been reported. Support for the developmental nature of this disease stems from the fact that most patients are young (<1> Occasionally, QC’s are found as incidental findings, either on necropsy or brain imaging.

fig-1-crop.jpg Figure 1 – Arachnoid Cyst

fig-2-crop.jpg Figure 2 – Arachnoid Cyst

Diagnosis of arachnoid cysts requires advanced imaging, preferably MRI or 3-D CT scanning. MRI (see Figures 1 & 2) will reveal a mass lesion rostro-dorsal to the cerebellum and caudal to the occipital lobes. The lesion appears hyper-intense on T2 images and hypointense on T1 images and is non-contrast enhancing. The quality of the lesion is virtually indistinguishable from cerebrospinal fluid. Variable degrees of compression and distortion of the adjacent cerebellum and cerebrum can be observed. Concurrent hydrocephalus has been reported, but this is likely a breed-related variant of ventricle size and unlikely to be of clinical significance. QC must be differentiated from cystic neoplasia or cysts associated with infectious disease (e.g. hydatid cyst).

Treatment of QC’s include surgery (fenestration, shunting, or marsupialization) or medical management (e.g. corticosteroids and carbonic anhydrase inhibitors), but controversy still remains over the preferred treatment. Prognosis must be considered guarded and the majority of dogs require life-long anticonvulsant therapy, even if surgical correction is performed.

Hydrocephalus refers to an increased volume of cerebrospinal fluid within the ventricular system and is most commonly recognized within the first few months of a dog’s life. The pathophysiology of congenital hydrocephalus is complex and mutifactorial but may be associated with fusion of the rostral colliculi, pre-natal infections causing stenosis of the mesencephalic aqueduct, compromise of cerebral vasculature, and intrauterine toxicity. Breeds at risk include Chihuahua’s, Yorkshire Terrier’s, Poodle’s, and a variety of brachycephalic breeds. Clinical signs generally are apparent prior to 6 months of age and are highly variable but usually include evidence of a prosencephalic disturbance. Abnormal mentation, visual deficits, circling, poor response to training, head pressing, seizures, and pacing have all been reported. Occasionally, hindbrain signs will predominate with ataxia, head tilt, abnormal nystagmus, and balance loss. Physical examination may reveal a large, dome-shaped head (Figure 3), calvarial defects, or an open fontanelle. Bilateral ventrolateral strabismus (“sunset eyes”) is seen as a sequelae to the skull malformation rather than as an indication of a vestibular disturbance.


Figure 3 – Dome-shaped head in Hydrocephalus

Diagnosis is generally straightforward and is based on signalment, clinical signs, physical exam findings, and confirmation of ventriculomegaly. It must be understood that enlargement of the ventricles and the presence of an open fontanelle are not necessarily of any clinical significance. The patient must demonstrate signs of a brain disorder in the absence of any concurrent, active causal disease that may be responsible (e.g. encephalitis, metabolic encephalopathy). In patients with a patent fontanelle, the diagnosis may be confirmed with ultrasonography. Advanced imaging (CT, MRI) is the preferred method for imaging and confirming the diagnosis and for ruling out any concurrent disorders. MRI (Figure 4) will reveal dilation in the ventricular system and loss of the adjacent parenchyma.


Figure 4 – Hydrocephalus MRI

Treatment is aimed at reducing CSF volume and production. Prednisone or carbonic anhydrase inhibitors have been used with variable success. Surgical intervention is the treatment of choice and is aimed to divert CSF away from the ventricular system to the peritoneal cavity, pleural space, or right atrium. Ventriculoperitoneal shunting is the most common, technically feasible procedure done in domestic animals and can be done even on very small patients, such a Chihuahua’s. Prognosis is highly variable and depends on the degree of pre-operative neurologic dysfunction, chronicity, and avoidance of complications (infection, occlusion) associated with the shunt. Success rates as high as 90% have been reported with ventriculoperitoneal shunts, but owners must be advised that long-term prognosis for full return to function is guarded.

Chiari-Like Malformation (Caudal Occipital Malformation Syndrome or “COMS”) is a developmental anomaly that is being increasingly recognized as advances in neuroradiology are made. Anatomic abnormalities of the skull, specifically the occiput, result in compression of the structures of the caudal fossa and lead to cerebellar herniation. Consequently, there is alteration in the dynamics of cerebrospinal fluid flow and pressure on the cranial aspects of the spinal cord. Pressure gradients resulting from altered CSF flow as well as constriction of the cervicomeduulary junction at the foramen magnum result in the development of excessive fluid buildup within the spinal cord, either confined to the central canal (hydromyelia) or within the neuroparenchyma (syringomyelia). Collectively, the condition is referred to as syringohydromyelia (SM).

COMS is most often diagnosed in small breed dogs, especially Cavalier King Charles Spaniels. Other breeds being seen with increasing regularity include the Pomeranian, Pug, and other brachycephalic breeds. Affected animals can display a wide array of clinical signs including cerebellovestibular dysfunction, seizure activity, cervical/cranial hyperesthesia, or persistent scratching at the neck and shoulder region. Although it is considered to be a developmental disorder (most are diagnosed by 3 years), age at diagnosis can vary and clinical signs may not be evident until the animal is several years old. This is likely due to the fact that syringomyelia may take years to develop; the author has observed dogs that did not begin to display clinical signs until 7 or 8 years of age.

fig-5-crop.jpg Figure 5 - MRI of COMS & SM

fig-6-crop.jpg Figure 6 – MRI of COMS & SM

MRI is considered to be the diagnostic tool of choice to confirm COMS and SM (Figures 5 & 6). MRI findings in this condition include rostral displacement of the cerebellum by the occiput, obliteration of the dorsal subarachnoid space at the cervicomedullary junction, and cervical syringohydromyelia. Ventriculomegaly can also be observed but may be a normal variant in brachycephalic breeds and must be interpreted with caution. Additional diagnostics are currently being evaluated by researchers and include spiral CT scanning and brain-stem auditory evoked responses (BAER).

Medical management is directed toward relieving pain and decreasing CSF production. Commonly prescribed drugs include corticosteroids, narcotics, gabapentin, pregabalin, and carbonic anhydrase inhibitors. While medical therapy may effectively alleviate discomfort, long term prognosis is poor if the underlying anomaly is not addressed and treated. Progression of SM leads to pressure on the spinal cord parenchyma leading to permanent nerve damage and eventually intractable pain and paralysis. The treatment of choice in humans with COMS is Foramen Magnum Decompression (FMD) and the majority of human patients that undergo FMD either experience a halt in the progression or improvement in clinical signs. There is increasing evidence that FMD is the preferred method of treatment in dogs as well. Without surgery, more than 1/3 of dogs will be euthanized due to chronic severe pain and quality of life concerns. FMD allows for removal of hyperplastic occipital bone and relieves pressure on the underlying parenchyma. Often, SM will resolve or improve after the procedure, as evidenced by serial MRI exams. Unfortunately, in humans and animals, recurrence rate is high due to formation of scar tissue at the previous surgical site which in essence, recreates the original defect. A modification of the FMD in which titanium is placed over the defect created by the FMD to prevent excessive scar tissue has shown great promise with significantly fewer animals requiring re-operative procedures.

Other brain anomalies: Many other anomalies of the brain have been reported sporadically in dogs and should be considered when evaluating a pediatric patient with intracranial signs. Hydranencephaly has been reported in Labrador Retriever puppies and results from in utero destruction of previously viable neocortex during a critical period of development. Unlike hydrocephalus, the cranial cavity is of normal configuration. Imaging findings are similar to those seen with hydrocephalus but prognosis is extremely guarded. Lissencephaly (Figure 7) occurs when the normal cerebrocortical folds fail to develop, leading to an absence of gyri and sulci of the cerebral hemispheres. Lhasa Apso’s are most commonly affected, but the disease has also been reported in Irish Setters and Wire Hair Fox Terriers. Clinical signs include aggression, blindness, poor training ability, and generalized seizures. Seizures often do not occur until the animal is greater than 1 year of age and tend to be refractory to standard anticonvulsants. Prognosis is grave. Other defects in neuroparenchymal development (Figure 8 ) are seen infrequently and are poorly understood.

fig-7-crop.jpg Figure 7 – Lissencephaly

fig-8-crop.jpg Figure 8 – Defect in neuroparenchymal development