The Itchy Dog: An Overview of Diseases

Chris Reeder, DVM, DACVD

Sometimes no matter how hard we try, a diagnosis of pruritic skin disease is frustrating.There are a few key questions and findings that may make life a little easier in dealing with the itchy dog.  The skin as an organ has incredible powers. Not mystical or magical, those are confined to brain along with neurologic pathways to control motion and physiologic/psychologic processes. No, the skin has its own special powers.  It acts as a physical barrier providing innate protection against the evils of the environment.  Skin stretches and can transition from taut to lose, thick to thin, it controls water loss and temperature regulation, it acts as a sensory organ and to many animals, camouflage to help hide from predators or stalk prey.  Skin truly is an incredible organ, though as incredible as it is, an Achilles’ heel does exist…..pruritus. 

Pruritus is derived from the Latin prurire meaning to “itch.”   It is defined as the desire or reflex to scratch.  Itching in the dog is one of the most common presenting complaints from owners to the general practitioner, yet one of the most frustrating and costly as well.  There is help, several key questions and findings may provide a starting point or diagnosis as to why a dog is itching.  Our first step is the question the owner about the dog’s condition:

-          Age of onset of the itching

-          Duration of the itching

-          Other animals in the household affected

-          Housed indoor, outdoor or both

-          Travel history

-          Current and previously fed diets (including human foods)

-          Seasonal history or exacerbations of itching

-          Previous medications, what worked and what didn’t work

-          Current flea/tick control products (other animals treated)

-          Number of bowel movements daily

-          Loose, runny stools or any vomiting

Many animals who have a food allergy will present as young dogs (<1 year of age) with loose or runny stools, >3 bowel movements daily and may be refractory to glucocorticoid use.  Other household animals are not affected and this is typically non-seasonal with itching as a constant feature.  Compare that to the typical dog with atopy (environmental allergies) and we see that most of those dogs present first between 1-4 years of age, have some seasonal pattern, respond to glucocorticoids with a reduction of pruritus and no other animals in the household are affected.  The author’s experience, along with many dermatologists, find that atopy is a much more common presentation than food allergy in roughly 90% to 10%, respectively.  We also see that food allergic dogs often have some compromise to the gastrointestinal barrier function.  This could be a history of intestinal parasites, Parvovirus enteritis, or any other disruption to the gut integrity.  What about a dog whose symptoms appears more atopic but is non-seasonal?  That could be a dog that is suffering from indoor allergens (dust mites, storage mites, human or cat dander, sheep wool, cotton, etc) which allergy testing may be a helpful tool in order to diagnose. 

Scabies can mimic food allergy and atopy very closely.  Other animals or even humans in the household may be affected with pruritus.  The typical approach to dogs with scabies is to identify a pinnal-pedal reflex.  This involves grasping the pinna between the thumb and forefinger of both hands and rubbing the skin together.  A positive response would involve the ipsilateral hind leg start scratching vigorously after a few seconds.  It has been reported that up to 80% plus of dogs with scabies exhibit a positive pinnal-pedal response and these are cases to empirical treat with an acaracidal therapy (e.g. Advantage-multi^® Bayer, Revolution^® Pfizer) which is usually an off-label dosing of one treatment every 2 weeks for 3 total doses.  Common areas affected with scabies infestation include: hocks, elbows, pinnae, groin and scrotum.  All animals in the household should be treated as some may serve as a reservoir even if not itching. 

Flea allergy is truly a hypersensitivity response. This appears as a dose-dependent phenomenon with the higher number of flea bites with salivary protein exposure thus resulting in an allergic response.  The number of bites to induce an allergic response varies with some animals showing no response even with hundreds of bites.  It is important to examine the dog, especially those with long coats, on the rump region.  A severe inflammatory response can be seen in dogs with a strong allergic response to fleas with moist pyoderma and excoriations predominantly over the dorsal lumbar region.  Another common finding in dogs with flea allergy is the discontinuation of flea control over the winter months.  Fleas overwinter indoors and continue to thrive, only at a slower rate than the warm and humid summer months.  Continued flea control for all animals in the household is a very effective means of controlling flea allergies.  Several topical formulations now have both flea prevention and heartworm prevention in a single dose application (e.g. Advantage-multi^® Bayer).  Bathing around the time of application of the topical spot-on formulations of flea preventative is another question to ask the owner.  Typical recommendations are to wait 48-72 hours after application to bathe a dog or use an oral flea preventative (e.g. Comfortis^® or Trifexis^® Elanco). 

   

Ringworm, is neither a ring nor a worm, the saying goes “if it looks like ringworm, it’s probably not” in dogs holds true.  Dermatophytosis in dogs usually presents with pruritus, hair loss, erythema and scaling.  Rarely does ringworm present as focal, circular patches of alopecia in dogs.  Various forms of ringworm can be present in dogs, geophilic, zoophilic, anthrophilic with the geophilic (soil) or zoophilic (animal) forms most common.  Microsporum gypseum is a geophilic dermatophyte whereas Microsporum canis is a zoophilic dermatophyte and the most common species seen in the dog and cat.  Occasionally multiple animals in the household may be affected and about 10% of humans can also have lesions which are typically pruritic.  A dermatophyte test media (DTM) culture is ideal to diagnose and speciate the type of dermatophyte present.  Fluconazole (5-10 mg/kg po daily) is the author’s treatment of choice for dermatophytosis.  Terbinafine (Lamasil^®, 30-40 mg/kg po daily) may also be used for refractory cases. 

Pruritus also damages the cutaneous barrier function both as, what we think is, a genetic dysfunction of the intercellular cement along with direct excoriations of the integument. This barrier defect has led to the development of many good products to help control and restore function.  Wipes, shampoos, lotions, balms and sprays have all been recently developed an are on the maket to help restore or improve skin barrier function in animals.  Shampoos have technology to even prevent bacteria/yeast from adhering to the skin surface (Virbac glycotechnology).  Pro-ceramides have been incorporated into sprays and shampoos to help repair damaged skin (phytosphingosine, Douxo^® (Sogeval)). 

Pruritus may have developed due to an allergic response to food, parasites or the environment and taking the time and understanding what to look for in these cases can make for a much more rewarding treatment outcome.  Many dogs need ongoing management for their atopy, need to be on flea prevention every 3-4 weeks ongoing or must be maintained on certain diets if food allergic.  Scabies is curable, though we do occasional see reservoirs in other household dogs or wildlife making further questioning an important part of the treatment.  Asking the right questions along with a thorough history and physical exam may help increase the correct diagnosis and decrease frustrations levels for the itchy dog. 

Pregnancy Termination in Companion Animals

by C. Scott Bailey, DVM, DACT

Despite much of discussion on the subject, there is still a great disparity in treatment protocols for mismated companion animals in the USA and elsewhere. Numerous treatment protocols are available. Ovariohysterectomy has the advantage of permanently removing the risk of an unwanted pregnancy. Medical treatments have varying side effects depending on the protocol selected, and depend on owner vigilance to prevent future pregnancies. Medical treatment is most often performed in early gestation or mid gestation. Pregnancy termination after fetal ossification (45 days) results in abortion of non-viable or poorly viable fetuses.

            Treatment choices should be guided by an animal’s actual risk of pregnancy. In dogs, a vaginal swab and cytologic evaluation provide 2 key pieces of information: 1) Detection of sperm heads on cytology can confirm exposure to a male, and 2) determination of estrus stage at the time or presentation. In a study involving 16 females with known breeding histories, Whitacre and coworkers demonstrated that sperm could be seen microscopically in 100% of cases within 24 hours of breeding and in 75% of cases within 48 hours of breeding, using a modified sampling technique. Determination of estrus stage is also a key component of determining the risk of pregnancy. Bitches with known or suspected exposure to a male during proestrus are at much lower risk of pregnancy than those exposed during estrus. Cytologic diagnosis of proestrus can be further confirmed with serum progesterone concentrations of <2ng/mL. As cats are induced ovulators, serum progesterone will likely be low in unexposed cats (<2ng/mL) and would rise after coitus in exposed cats.

Prior to any treatment, it is important to carefully consider options for treatment. Animals that are not intended to be breeding animals, do not have high risk-factors for spay-associated disease and which are not in show, should undergo ovariohysterectomy in early diestrus/pregnancy. This will prevent future unwanted pregnancies and may decrease the animals’ risk of several diseases, including pyometra, mammary and ovarian neoplasia. Animals which cannot be spayed may be treated medically with a variety of protocols.

Early pregnancy termination

            Several protocols have been proposed to medically treat bitches as soon as a mismating occurs. This approach is attractive, but may pose a greater risk to the animal and have lower success rates than other protocols. As a result, most reviewers have recommended against these treatment regimens.

            Estrogens have been widely used for this purpose in the past, but potentially severe side-effects should raise concerns. Several reports indicate significant health risks associated with estrogen treatment in dogs and cats, including an increased risk of pyometra, infertility and toxicity.

Pregnancy termination in mid-gestation

            In the dog, pregnancy can be readily diagnosed by palpation approximately 30 days after mating, whereas ultrasonographic examination can confirm pregnancy as early as 15-18 days after the LH surge (~10-20 days after mating). Embryos are easily detectable between day 22 and 25 after LH surge. In the queen, ultrasonographic pregnancy diagnosis can be achieved as soon as 11 days after mating and the embryo becomes visible by 14 or 15 days after mating.

            At this stage, embryonic fluids and tissues are resorbed by the uterus and few clinical signs are expected in response to medical intervention. A bloody discharge may be seen in bitches and queens after approximately 30 days. Abortion (fetal expulsion) occurs after 40-45 days, when fetal ossification is underway.

Prostaglandins

Natural prostaglandins can be used to terminate pregnancy beginning 5 days after ovulation, however prior to 25 days, higher doses are required than later in gestation. Hospitalization and careful monitoring of animals are recommended to control side-effects, which tend to be more severe early and diminish during the course of treatment. Side effects may be minimized by using low doses of prostaglandin, or by starting with a lower dose and gradually increasing it. It should be noted that low doses may not induce permanent luteolysis, resulting in loss of only some pups or fetal death followed by mummification. The synthetic prostaglandin cloprostenol has also resulted in effective pregnancy termination, with few side effects.

Dopamine Agonists

            In both the bitch and queen, prolactin plays a necessary luteotrophic role in pregnancy maintenance. Progesterone can be reduced or eliminated during late pregnancy by administering a dopamine agonist, which inhibits endogenous prolactin secretion.³² However, treatment success for pregnancy termination has been inconsistent in both dogs and cats and dopamine agonists alone are rarely used in companion animals.

Combined Prostaglandin/Dopamine Agonist Regimen

            Extensive work by Verstegen and coworkers, demonstrated that a dual approach to pregnancy termination results in reliable efficacy in mid gestation. Low doses of either natural or synthetic prostaglandins result in luteolysis, while dopamine agonists inhibit prolactin release. In a series of studies, administration of cabergoline and cloprostenol resulted in fetal resorption with minimal discharge or unwanted drug-effects in both dogs and cats. Treatment was continued until ultrasonographic confirmation of fetal demise. The above protocol has several distinct advantages over other protocols described: Both prostaglandins and dopamine agonists are readily available in the USA. The combined luteolytic and antiluteotrophic mechanisms decrease dosages of each drug, substantially reducing side effects. The protocols can be instituted around day 25 and result in resorption prior to fetal ossification, when most animals would abort formed fetuses. The use of orally administered dopamine agonists and long-acting, synthetic prostaglandins eliminates the need for frequent examination and hospitalization.

Conclusions

In conclusion, risk for pregnancy should be determined at the time of mismating and ideally pregnancy should be confirmed prior to treatment in order to avoid unnecessary and potentially harmful medical side effects. Treatment choices should be based on the animal’s stage of gestation and availability and should be tailored to minimize side effects as much as possible. A treatment onset between 25 and 30 days and combination of two drugs, including a prostaglandin and dopamine agonist minimize drug dosage and side effects while inducing fetal resorption rather than abortion.

 

September Case of the Month - Intermittent Low Grade Colic

History: “Samson” Donovan, a 10-year-old Oldenberg gelding, presented on 8/24/12 for intermittent low-grade colic consisting mostly of parking out from discomfort, with no decline in condition or performance as a low-level dressage horse.  The owners report that he has also been gassy.  Physical examination and rectal exam were within normal limits and results of a sand flotation test are pending.  His colic episodes generally self-resolve or resolve with the aid of 5cc of Banamine.  He was recently started on the Succeed Digestive Conditioning Program and he is insured.

Labwork analysis:

1.      CBC/chemistry panel: Bloodwork was unremarkable, with insignificant changes in Cl and GGT.

2.      Fecal egg count: Fecal egg count was negative for parasites.

3.      Fecal occult blood: Fecal occult blood was negative for blood.

Diagnosis: Chronic colic, open.

Common causes of chronic intermittent colic include gastric ulceration, sand impaction, and enterolithiasis. 

Gastric ulcers are prevalent in horses, with statistics ranging from 58% of showhorses and 70% of Thoroughbred broodmares to 86% of racehorses.  Due to vague clinical signs and large variation in treatment dosage and duration using GastroGard, the gold standard method of diagnosis remains gastroscopy.  Alternative methods include the Succeed fecal blood test (limited in accuracy), urine sucrose, and blood sucrose.  The procedure for urine sucrose concentration for detecting gastric ulcers is documented in the paper: Evaluation of urine sucrose concentration for detection of gastric ulcers in horses.  O'Conner MS et al. Am J Vet Res. 2004 Jan;65(1):31-9.  In this study, horses were fed 1kg concentrate (Purina Horsechow 100) and intubated with 454g sucrose (10% solution in water).  Urine sucrose was collected 2h and 4h following the intubation.  Sucrose concentration is higher in horses with gastric ulceration, with a sensitivity of 83% and specificity of 90% using a cut-off of 0.7mg/ml.  The procedure for blood glucose can be found in the paper: Sucrose concentration in blood: a new method for assessment of gastric permeability in horses with gastric ulceration.  Hewetson M, Cohen ND, Love S, Buddington RK, Holmes W, Innocent GT, Roussel AJ.  J Vet Intern Med. 2006 Mar-Apr;20(2):388-94.  In this procedure, horses are withheld from feed for 20h, intubated with 250g sucrose, and serum sucrose was significantly elevated 45min later in horses with moderate to severe gastric ulceration. 

The definitive diagnosis for sand impaction and enterolithiasis is through abdominal radiography.   If the sand flotation that was performed by the owner is negative, the test can be improved by administering psyllium (Sand Clear instructions are 5oz daily for 7 days) and performing the sand flotation during and after the treatment.  Psyllium may also have some GI benefits of aiding in mucosal repair.

Recommendation:

1.      Diagnostics: I would recommend doing additional diagnostics, including gastroscopy.  If the gastroscopy is not possible, urine/blood sucrose or empirical treatment (take note GastroGard takes 3-5 days to take effect) can be used to indicate the presence of gastric ulcers.  If he is negative for ulcers, you may wish to consider referral for abdominal radiographs and/or a trial with psyllium and repeated fecal sand flotation.

2.      Treatment: For discomfort due to bloating, you may wish to consider administration of a proven prebiotic such as Saccharomyces boulardii (10 billion organisms PO BID).  All other treatments could be pursued based on the results of additional diagnostics.

Jean-Yin Tan, DVM, DACVIM (Large Animal Internal Medicine)

Palladia (Toceranib phosphate)

by Cheryl Harris, DVM, DACVIM (Oncology and Small Animal Internal Medicine)

Palladia (toceranib phosphate) was the first FDA-approved antiangiogenic and antiproliferative cancer treatment specifically for dogs. It is manufactured by Pfizer and was released for use by veterinary oncologists in 2009 for the treatment of Patnaik grade II or III, recurrent cutaneous mast cell tumors with or without regional lymph node involvement in dogs. It has been a remarkable adjunct for the treatment of canine mast cell tumors (MCT) and is now being used for a variety of canine and even feline tumors. It is now available for widespread use by all licensed veterinarians.

Palladia is a receptor tyrosine kinase (RTK) inhibitor. Inhibition of RTKs on endothelial cells, pericytes, and tumor cells disrupts multiple processes necessary for tumor growth. Palladia inhibits the activity of VEGFR-2, an RFK expressed on endothelial cells. It inhibits the activity of PDGFR-B, an RTK expressed on pericytes and inhibits the RTK KIT on tumor cells. KIT is commonly dysregulated in canine MCT.

The original clinical field study using toceranib phosphate was a multi-center, double-blind, placebo-controlled trial conducted at 10 oncology referral centers and included 151 dogs with MCT. In dogs treated with Palladia, approximately 60% of MCT disappeared, regressed, or stabilized.

Most oncologists are no longer using the label dose of 3.25 mg/kg, but instead use dose ranges between 2.5 to 2.75 mg/kg, EOD or on a MWF basis. This appears to be associated with better tolerability while maintaining efficacy. Prednisone or NSAIDs can be used on alternate days. Many dogs are receiving Cytoxan in addition to Palladia as part of a metronomic therapy. Dogs are started on Cytoxan 10-12 mg/m2 (EOD or T/Th/Sat/Sun) and famotidine for 2 weeks prior to initiation of Palladia. Palladia should be given with food.

All dogs should have a baseline CBC, chemistry profile, urinalysis and fecal occult blood prior to starting Palladia. Owners must observe carefully for loose stools, anorexia or lethargy. For dogs that develop diarrhea, loperamide is used SID/BID and continued during therapy. For dogs with decreased appetite, add canned food to the diet and use metoclopramide, ondansetron or Cerenia.

Dogs are rechecked weekly with CBC and hemoccults for the first 2-4 weeks and body weight should be monitored very closely. It is then recommended to monitor at least monthly with hemoccult, CBC and chemistry panels. Neutropenia can occur but is tolerable as long as neutrophils stay above 1500. If they are lower than 1500, a drug holiday is recommended until the neutrophil count is normal, then the dose is modified. The same holds true for muscle cramping and lameness, an occasionally reported side effect of the drug. Newly reported side effects are elevations in ALT and ALP, protein-losing nephropathy, hypertension and pancreatitis.

The following guidelines on treatment of MCT are based on the Ohio State University treatment experience and that of Dr. Cheryl London who has participated in much of the original research using Palladia.

Palladia is usually incorporated into treatment protocols for Grade III MCT and any Grade II MCT with negative prognostic indicators (mitotic index >5, recent rapid growth, recurrence following surgery, positive lymph nodes.) In general, Palladia is part of a treatment protocol that includes surgery +/- radiation therapy and chemotherapy. It is usually not used as a single agent unless the dog has failed these modalities or it is the only treatment available. For dogs with gross disease, every attempt is made to downstage the cancer prior to initiation of Palladia therapy. If surgery is not possible, dogs can receive vinblastine/prednisone chemotherapy for 2-6 weekly treatments prior to Palladia or receive radiation therapy or a combination of chemotherapy and radiation therapy.

All MCT patients are started on famotidine and Benadryl in addition to prednisone. Any dog with positive hemoccult tests at the start of treatment is pretreated with omeprazole and sucralfate for 1-2 weeks prior to Palladia. Dogs with significant mast cell tumor burden are at high risk for developing side effects from Palladia, particularly if they are already sick. H1 and H2 blockers should always be used in dogs with gross MCT.

It is usually recommended to give Palladia for 30 days to see the full response but some responses are dramatic and seen in the first 7 days. It is unknown how long to treat dogs who are having a good response but many will have their disease recur if Palladia is discontinued. If they are tolerating the drug well, it is currently recommended to keep them on the drug on a M/W/F basis indefinitely.

Other types of tumors which have demonstrated response to Palladia include anal sac adenocarcinomas, metastatic osteosarcomas, thyroid carcinomas, nasal carcinomas, melanomas, squamous cell carcinomas, multiple myeloma and transitional cell carcinomas.

Palladia is very well tolerated in cats. The recommended starting dosage is 2.8 mg/kg EOD. Compounding is recommended to get accurate dosing. Responses have been seen in mast cell tumors, squamous cell carcinomas and vaccine-associated sarcomas. GI toxicity and myelosuppression should be monitored.

Palladia is supplied in 10, 15 and 50 mg tablets and are packaged in 30 count bottles. The tablets should not be split or crushed and should be handled with gloves. A chemical hood such as is used for administration of chemotherapy is not required. The tablets should not be handled by pregnant women.

For more information on the use of Palladia in treating tumors in dogs and cats, please feel free to call the oncologists at Veterinary Answers.

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Mary B. Nabity, DVM, PhD, DACVP

Proteomic analysis of urine from male dogs during early stages of tubulointerstitial injury in a canine model of progressive glomerular disease.

Nabity MB, Lee GE, Dangott LJ, Ciancolo R, Suchodolski JS, Steiner JM.

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Effect of dietary protein content on the renal parameters of normal cats

Backlund B, Zoran DL, Nabity MB, Norby B, Bauer JE

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Could it be Addison’s?

Linda E. Luther, DVM

Diplomate ACVIM (SAIM)

Many cases presented for evaluation of vague symptoms end up having hypoadrenocorticism.

Can you spot the classic cases?

Can you spot the not-so-classic cases?

Hypoadrenocorticism, or “Addison’s” disease, results from atrophy of the adrenal cortex, and often presents as a diagnostic challenge. Clinical signs can vary from subtle signs to acute collapse, and the clinical course is often waxing and waning. Untreated collapsed dogs may die, so identifying dogs affected with this disease early is optimal. Types of hypoadrenocorticism include the ‘classic’ glucocorticoid & mineralocorticoid deficient patient, and the more subtle, glucocorticoid deficient patient.

Clinical signs of classic hypoadrenocorticism may include vomiting, diarrhea, lethargy, collapse, bradycardia, abdominal pain, polyuria, polydipsia, or being “just not right”. Physical examination findings are often nonspecific. Laboratory findings in a classic case may include hyponatremia, hyperkalemia, decreased Na/K ratio, azotemia (with or without an inappropriate specific gravity), hypoalbuminemia, hypoglycemia, hypercalcemia, nonregenerative anemia. The lack of a stress leukogram is common; a normal to elevated lymphocyte count, and normal to elevated eosinophil count in a sick dog are frequent, subtle findings.

The not-so-classic case will often present with more subtle clinical signs. They will have normal electrolytes, and will often have a lack of a stress leukogram. They may also have a low normal hematocrit or a non-regenerative anemia, a low to borderline albumin, hypoglycemia and hypercalcemia. These cases are commonly missed. How can you ensure that you spot these? Look at the CBC carefully. Is there a stress leukogram? Look at the albumin level. Is it decreased or in the low normal range? Consider the history. Consider the lack of other obvious disease, and don’t forget to IGNORE the normal electrolytes. If there are enough consistent findings in a dog with vague symptoms, test for hypoadrenocorticism!

Once you suspect hypoadrenocorticism, confirmation historically has been done with an ACTH stimulation test. However, a recent study showed that if a dog had a baseline cortisol level that was greater than 2.0 ug/dL, they were very unlikely to have hypoadrenocorticism. If the baseline cortisol is less than 2.0 ug/dL, hypoadrenocorticism is not ruled out, and an ACTH stimulation test should be done.

But I thought she was in renal failure…

Cases of hypoadrenocorticism can mimic acute renal failure in that clinical signs are similar, and azotemia with an inappropriate urine specific gravity may exist. How does the astute clinician differentiate the two? Questions to ask include: Is there a stress leukogram? Was the resolution of severe azotemia very rapid? Did the patient act like a ‘brand-new dog’ after just a day of fluids?

Let’s compare “Maggie”, a 7-year-old Fs Collie that presented with vomiting and lethargy, to “Bailey”, a 12-yr-old Mn Cocker that presented in lateral recumbancy (see Table 1). Both dogs had severe azotemia with an inappropriate urine specific gravity. “Maggie” lacked a stress leukogram. The electrolyte findings in both dogs were suggestive of hypoadrenocorticism, but this finding is not pathognomonic for the disease. “Maggie” turned out to have hypoadrenocorticism. “Bailey”, did not, and he was diagnosed with renal failure (see Table 3). Because “Maggie” had an abnormal ACTH stimulation test as well as abnormal electrolytes, she had glucocorticoid and mineralocorticoid deficient hypoadrenocorticism.

Therapy for “Maggie” started with intravenous fluid therapy. The hyperkalemia was treated with the fluids, as well as intravenous sodium bicarbonate therapy (1 mEq/kg, slow IV). Glucocorticoids were given, initially using dexamethasone sodium phosphate (0.1-2 mg/kg IV). Chronic glucocorticoid therapy with physiologic dose of prednisone (0.1-0.2 mg/kg/day, doubled when she was stressed) was initiated. She was also given mineralocorticoid therapy using Percorten®-V (Desoxycorticosterone pivalate or DOCP, 2.2 mg/kg IM or SQ q. 25 initially). Florinef ® (fludrocortisone acetate, 0.01-0.02 mg/kg/day initially), which also has glucocorticoid effects, could have been used instead of Percorten®.

Could he be an Addisonian?

Some Addisonian dogs have very subtle symptoms. “Max” is a 7-yr-old Mn Labrador retriever that presented for a blood panel to monitor carprofen therapy that was chronically administered to treat degenerative joint disease (see Table 2).

“Max’s” blood panel revealed significant anemia. Upon further questioning, the owner thought that he had been quieter lately. He really was not all that sick though. Besides the anemia, the blood work showed a lack of a stress leukogram, his electrolytes were normal, and there was no azotemia. An ACTH stimulation test was done (see Table 3), and “Max” indeed was an Addisonian! Since “Max” had normal electrolytes, he had glucocorticoid deficient hypoadrenocorticism, and he was not mineralocorticoid deficient. Chronic glucocorticoid therapy with a physiologic dose of prednisone (0.1-0.2 mg/kg/day, doubled when he was stressed), was started. Mineralocorticoid therapy was not indicated in this dog. Some glucocorticoid deficient cases eventually develop mineralocorticoid deficiency, thus periodic monitoring of electrolytes was indicated.

In summary, hypoadrenocorticism can be a challenging disease to diagnose. Suspicion of the disease in dogs with vague symptoms is recommended, even in dogs that have normal electrolytes.

Disclaimer: Please verify all drug dosages before administering.

References:

Scott-Moncrieff JCR. Hypoadrenocorticism. In Ettinger SJ, Feldman EC (eds.) Textbook of Veterinary Internal Medicine, 7th ed. Saunders Elsevier, St. Louis, 2010, 1847-1857.

Lennon EM, Boyce TE, Hutchins RG et al. Use of basal serum or plasma cortisol concentrations to rule out a diagnosis of hypoadrenocorticism in dogs: 123 cases (2000-2005). J Am Vet Med Assoc 2007;231:413-416.

Thompson AL, Scott-Moncrieff JC, Anderson JD. Comparison of classic hypoadrenocorticism with glucocorticoid-deficient hypoadrenocorticism in dogs: 46 cases (1985-2005). J Am Vet Med Assoc 2007;230:1190-1194.

Table 1.	“Maggie”	“Bailey”	Normal values
White blood cells, #/μL	12,880	28,290	5,500-16,900
Neutrophils, #/μL	7,670	24,750	2,000-12,000
Lymphocytes, #/μL	2,710	490	500-4,900
Monocytes, #/μL	1,550	2,370	300-2,000
Eosinophils, #/μL	890	520	100-1,490
Platelets, # x 103/μL	299	431	175-500
BUN, mg/dL	130	130	7-27
Creatinine, mg/dL	7.7	7.7	0.5-1.8
Calcium, mg/dL	13.8	5.5	7.9-12
Phosphorus, mg/dL	14.6	16.1	2.5-6.8
Na, mmol/L	136	145	144-160
K, mmol/L	9.0	9.0	3.5-5.8
Cl, mmol/L	103	111	109-122
Na/K	15.1	16.1	< 27
Urine specific gravity	1.015	1.015

Table 2.	“Max”	Normal values
Hematocrit, %	23.6	37-55
White blood cells, #/μL	2,500	5,500-16,900
Neutrophils, #/μL	1,840	2,000-12,000
Lymphocytes, #/μL	340	500-4,900
Monocytes, #/μL	110	300-2,000
Eosinophils, #/μL	190	100-1,490
Platelets, # x 103/μL	325	175-500
BUN, mg/dL	35	7-27
Creatinine, mg/dL	1.3	0.5-1.8
Albumin, mg/dL	1.2	2.3-4
Na, mmol/L	152	144-160
K, mmol/L	5.5	3.5-5.8
Cl, mmol/L	123	109-122
Na/K	27.6	< 27

Table 3.	“Maggie”	“Bailey”	“Max”	Normal values
Pre-ACTH cortisol, ug/dL	< 0.5	8.0	< 0.5	> 2.0
Post-ACTH cortisol, ug/dL	< 0.5	N/A	< 0.5	> 8.0
* Note that “Bailey’s” baseline cortisol adequately ruled out hypoadrenocorticism. “Maggie” and “max” had baseline cortisol values < 2.0 ug/dL, thus an ACTH stimulation was needed to rule in the disease.