Our Consultants in Print
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.
Click Here to Read the Article
Effect of dietary protein content on the renal parameters of normal cats
Backlund B, Zoran DL, Nabity MB, Norby B, Bauer JE
Could it be Addison’s?
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. | ||||
Read About Us in Veterinary Practice News
It is always nice to start the year with some good press! Check out “Electronic Consultation: A Tool To Increase Pets’ Standard Of Care” in this month’s Veterinary Practice News.
PREGNANCY DIAGNOSIS AND TIMING ELECTIVE C-SECTIONS
C. Scott Bailey, DVM, MS, DACT
Consultant, Veterinary Answers
Veterinarians are often asked to perform pregnancy diagnosis and time a c-section with very little information from the owner. Often, the only information provided is the breeding-dates and occasionally even those are hard to come by. Consequently there is a need for veterinarians to be familiar different with methods of estimating gestational age. This is particularly important when an elective caesarean section is desirable. Elective c-sections can carry an excellent prognosis for maternal and fetal viability when timed correctly and may be less stressful to the bitch, puppies and attending veterinarian than waiting for a potential dystocia. Animals that are particularly good candidates are those with a history of dystocia or a c-section and animals that have small (less than 3 pups) or large (more than 8 pups) litter sizes. Dogs of certain breeds have a known predisposition to dystocia, such as Boxers, Bulldogs, Scottish Terriers, Great Danes and Bernese Mountain Dogs [1].
A number of factors play critical roles in the ultimate success-rate of elective c-sections, including fetal maturity, patient preparation, selection of anesthesia protocol and surgical technique as well as neonatal care of the pups. In this review we focus on only the first of these – Timing of c-section to maximize fetal maturity.
Three basic methods exist to predict parturition in the bitch:
Hormonal Assay
While the easiest methods for timing involve breeding management, breeding dates provided by owners are notoriously unreliable. Parturition may occur anywhere from 57 to 72 days after a single observed breeding [2]. On the contrary, the easiest and most accurate way to predict whelping is to diagnose or estimate the time of LH surge. Bitches reliably whelp 64-66 days post LH surge [2,3], which can be diagnosed by repeated LH assay (every 12 hours due to the short duration of the LH surge in the bitch). LH-peak may also be estimated by observing serum progesterone levels that achieve 2-3ng/ml and continue to rise thereafter [3,8]. Shortly after this period, vaginal cytology may be used to diagnose the onset of diestrus, occurring approximately 51-60 days before whelping [4].
Thereafter a variety of measures represent guides to estimate gestational stage within 2-3 days [4-6]. Further, equations have been developed to calculate gestational age in a variety of breeds [6,7].
A brief summary of useful ultrasonographic and radiographic markers of gestational age is listed below:
Ultrasonographic examination [5-8]
The fetal heartbeat is visible at approximately 22-26 days.
Limbuds, fetal movement and a fluid filled stomach may be seen on day 29, 30 and 33.
Fetal length exceeds chorionic width at approximately day 42.
Radiographic examination [5,7,9]
Pregnancy can first be reliably diagnosed radiographically day 45-48 post LH surge. More specific information is also available describing the appearance of specific structures in relation to whelping.
The scapula, humerus and femur are first detectable 17 days (15-18) prepartum.
The pelvis and 13 pairs of ribs are visible 11 days (9-13) prepartum.
Teeth are visible 4 days (3-8) prepartum.
During the final days of gestation, cortisol is produced and released from the maturing fetal adrenal gland in response to space-constraint and other physiologic stressors. This results in production of prostaglandin F2α in the placenta and endometrium, which in turn induces luteolysis and starts the cascade of events that ultimately result in fetal expulsion [10]. At the same time the cortisol also has critical effects on the fetus, resulting in rapid maturation of vital organ systems, including the musculoskeletal system, gastrointestinal system and lungs. Prior to these final maturation processes, puppy survival may be decreased due to weakness, poor mobility and respiratory distress after removal from the uterus. On the contrary, if these processes have occurred and the bitch experiences a dystocia, survival may also be decreased. Consequently, the goal of gestational timing should be to predict whelping accurately enough to intervene after final maturation has occurred but before the bitch is in active labor. To do this, repeated monitoring of hormone levels during the final week of gestation, in combination with fetal monitoring via ultrasound or tocometry, may improve fetal viability and prevent dystocias [11-13].
Progesterone [11]:
Progesterone measures below 2ng/ml indicate imminent parturition within 18-36 hours.
A temperature drop by 1-3F from previous measures occurs in 75-85% of bitches within 8-18 hours prior to parturition.
Fetal heart-rate can accurately diagnose fetal distress during late gestation [12,13]
Normal late pregnancy: 200 beats/min
Fetal Stress: 180 beats/min – Values in this range indicate readiness for parturition
Fetal distress: 150 beats/min – values of 150 or below indicate the urgent need for emergency intervention to save the puppy.
References:
1) Bergström A, Nødtvedt A, Lagerstedt AS, Egenvall A. Incidence and breed predilection for dystocia and risk factors for cesarean section in a Swedish population of insured dogs. Vet Surg 2006 Dec;35(8):786-91.
2) Concannon PW, Whaley S, Leid D, Wissler R. Canine Gestation length: vacioation related to time of mating and fertile life of sperm. Am J Vet Res 1983;44:1819-21.
3) Cohen JA, Holle DM, Meyers-Wallen VN. Accuracy of canine parturition date prediction from LH peak. Clin Theriogenology 2009;1:570
4) Holst PA, Phemister RD. Onset of diestrus in the Beagle bitch: definition and significance. Am J Vet Res 1974;35:401-6
5) Aissi A and Slimani C. Ultrasonographic appearance of the gestational structures throughout pregnancy in bitches. Am J Anim Vet Sciences 2008;3(1):32-35
6) Yeager AE and Concannon PW. Association between preovulatory LH surge and the early ultrasonographic detection of pregnancy and fetal hearteats in beagle dogs. Theriogenology 1990;34:655-665.
7) Lopate C. Estimation of gestational age and assessment of canine fetal marutation using radiology and ultrasonography: A review. Theriogenology 2008;70:397-402
8) Luvoni GC and Beccaglia M. The Prediction of Parturition Date in Canine Pregnancy. Reprod Dom Anim 2006;41:27-32.
9) Rendano VT. Radiographic evaluation of fetal development in the bitch and fetal death in the bitch and queen. In: Current veterinary therapy vol VIII. WB Saunders Co 1983; 947-52
10) Concannon PW, Butler WR, Hansel W, Knight PJ, Hamilton JM. Parturition and lactation in the bitch: serum progesterone, cortisol and prolactin. Biol Reprod 1978 Dec;19(5):1113-8.
11) Verstegen-Onclin K, Verstegen J. Endocrinology if pregnancy in the dog: A review. Theriogenology 2008;70:291-199.
12) Verstegen JP, Silvia LDM, Onclin K, Donnay I. Echocardiographic study of heart rate in dog and cat fetuses in utero. J Reprod Fertil Suppl 1993;47:174-80
13) Zone MA and Wanke MM. Diagnosis of canine fetal death by ultrasonography J. Reprod Fertil 2001;57:215-9.
Recall of Merrick Pet Treats
The FDA has announced a recall of Merrick Jr Texas Taffy Pet Treat TEXAS (ITEM # 27077, ALL LOTS UP TO AND INCLUDING 10364) due to possible Salmonella contamination.
Recalls – Horse Feed
This weekend, the FDA announced a recall of a single lot (1006) of Family Farm Complete Horse 10 horse feed, UPC 0 95668 90151 6, packaged in 40 lb. bags because it may contain monensin sodium (Rumensin). Monensin sodium is a medication approved for use in some livestock and poultry species, but can be fatal to horses if fed at sufficiently high levels.
Cool Abstracts
The prevalence of hypocobalaminaemia in cats with spontaneous hyperthyroidism
Novel gastroretentive controlled-release drug delivery system for amoxicillin therapy in veterinary medicine
Influence of blood collection technique on platelet function and coagulation variables in dogs
Evaluation of orally administered famciclovir in cats experimentally infected with feline herpesvirus type-1
Effects of isoflurane anesthesia on cerebrovascular autoregulation in horses
In Print – Mary Nabity, DVM, PhD, DACVP
Vet Clin Pathol. 2009 Mar;38(1):113-20.
B-cell lymphoma with Mott cell differentiation in two young adult dogs.
Stacy NI, Nabity MB, Hackendahl N, Buote M, Ward J, Ginn PE, Vernau W, Clapp WL, Harvey JW.
Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610, USA.
Abstract
Two young adult dogs with gastrointestinal signs were each found to have an intra-abdominal mass based on physical examination and diagnostic imaging. On exploratory laparotomy, small intestinal masses and mesenteric lymphadenopathy were found in both dogs; a liver mass was also found in dog 1. Cytologic and histologic examination of intestinal and liver masses and mesenteric lymph nodes revealed 2 distinct lymphoid cell populations: lymphoblasts and atypical Mott cells. With Romanowsky stains, the atypical Mott cells contained many discrete, clear to pale blue cytoplasmic inclusions consistent with Russell bodies that were positive by immunohistochemistry for IgM and CD79a in both dogs and for IgG in dog 2. The Mott cells and occasional lymphoblasts stained strongly positive with periodic acid-Schiff. Using flow cytometric immunophenotyping in dog 1, 60% of peripheral blood mononuclear cells and 85% of cells in an affected lymph node were positive for CD21, CD79a, IgM, and MCH II, indicative of B-cells. With electron microscopy, disorganized and dilated endoplasmic reticulum was seen in Mott cells in tumors from both dogs. Antigen receptor gene rearrangement analysis of lymph node and intestinal masses indicated a clonal B-cell population. Based on cell morphology, tissue involvement, and evidence for clonal B-cell proliferation, we diagnosed neoplasms involving Mott cells. To the authors’ knowledge, this is the second report of Mott cell tumors or, more appropriately, B-cell lymphoma with Mott cell differentiation, in dogs. More complete characterization of this neoplasm requires further investigation of additional cases. This lymphoproliferative disease should be considered as a differential diagnosis for canine gastrointestinal tumors.
In Print – Stephen Mehler, DVM, DACVS
J Small Anim Pract. 2011 Jan;52(1):32-7
Choledochotomy and primary repair of extrahepatic biliary duct rupture in seven dogs and two cats.
Baker SG, Mayhew PD, Mehler SJ.
Abstract
OBJECTIVE: To report clinical findings and outcome in dogs and cats undergoing choledochotomy or primary repair of extrahepatic biliary duct rupture.
METHODS: Retrospective study of dogs (n=7) and cats (n=2) that had choledochotomy or primary bile duct repair.
RESULTS: Extrahepatic biliary obstruction was confirmed at surgery in all cases. The underlying cause in four dogs and both cats was choledocholithiasis, two dogs had gall bladder mucocoeles with associated bile duct rupture, and one dog had inspissated bile obstructing the bile duct secondary to gall bladder carcinoid tumour. Three dogs and both cats had choledochotomies performed to relieve extrahepatic biliary obstruction, and four dogs with bile duct rupture underwent primary repair of the defect. One dog with a bile duct rupture was re-explored four days postoperatively and had suffered dehiscence of the repair; this rupture was re-repaired. All animals were discharged from the hospital, and did not have clinical recurrence of extrahepatic biliary obstruction.
CLINICAL SIGNIFICANCE: Choledochotomy and primary repair of extrahepatic biliary duct rupture were associated with low perioperative morbidity and no mortality in this small cohort of cases. These techniques are reasonable options either alone or in conjunction with other procedures when bile duct patency cannot be re-established by catheterisation or bile duct discontinuity exists.
In Print – Stephen Mehler, DVM, DACVS
J Am Vet Med Assoc. 2009 Jan 15;234(2):236-9.
Use of a balloon-expandable metallic stent to relieve malignant urethral obstruction in a cat.
Newman RG, Mehler SJ, Kitchell BE, Beal MW.
Abstract
CASE DESCRIPTION: A 19-year-old neutered male domestic shorthair cat was evaluated because of signs of urinary tract obstruction.
CLINICAL FINDINGS: Physical examination findings were consistent with urethral obstruction, and a mass could be palpated in the region of the bladder neck. Abdominal ultrasonography and thoracic radiography revealed a mass in the trigone of the urinary bladder and a solitary mass in the left caudal lung lobe. Cytologic examination of the urine sediment, samples obtained by means of traumatic urethral catheterization, and fine-needle aspirates of the bladder mass did not result in a diagnosis.
TREATMENT AND OUTCOME: A balloon-expandable metallic stent was placed in the proximal portion of the urethra to relieve the malignant obstruction. After stent placement, the cat had signs of urinary incontinence and detrusor atony, both of which resolved with medical treatment. The cat was euthanized 1 month after stent placement because of progressive azotemia. Histologic examination of necropsy samples revealed grade III urothelial carcinoma and papillary pulmonary adenocarcinoma.
CLINICAL RELEVANCE: Findings suggested that stent placement may be a viable palliative treatment in cats with malignant urinary obstruction.
