This month’s survey question
Thank you for responding to our January survey! Here are the results:
All signs point to an increase in in-house diagnostics
Of those who responded to our January survey on in-house diagnostics, a full 66% expressed high
interest in increasing their in-house diagnostic capabilities. Another 31% of respondents were also interested,
leaving only 4% satisfied with their current level of in-house capabilities.
Current trends are toward increasing in-house diagnostic capabilities for more immediate
information. Quick and easy access to diagnostic results allows practitioners to provide their patients
and clients with more immediate answers and to begin treatment during the first visit to the
clinic. This kind of service makes life easier for everyone—especially for the patients whose care
can begin right away. In-house diagnostics also allow practices to easily perform rechecks and
monitor their patients’ treatments to ensure dosages and medicines are working as expected.
There are many options for in-house diagnostics, and IDEXX has a full range of diagnostic
instruments and services. The IDEXX
VetLab® Suite offers comprehensive capabilities, including
hematology, chemistry, electrolytes, urinalysis, endocrinology, blood gases and infectious
diseases. IDEXX also offers world-class customer and technical service, educational services and
help from expert pathologists for consultations on difficult cases.
To learn more about the IDEXX VetLab Suite and other services, call us at
1-800-355-2896 or visit us on the Web at
www.idexx.com/vetlab.
Chemistry • Hematology • Urinalysis • Electrolytes • Endocrinology • Coagulation • Blood Gas
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Featured case study: 4-year-old neutered
male shar-pei, Raisin by
Suzanne M. Pratt1, DVM, DABVP; John A.
Christian1, DVM, PhD; Rose E. Raskin1,
DVM, PhD, DACVP; Margaret A. Miller1, DVM, PhD; and Anne E.
Brown2, Department of Comparative Pathology1
and Clinical Sciences2, Purdue University School of Veterinary Medicine,
West Lafayette, Indiana
Detailed history Two days prior to
presentation to the PUVTH, the owner noticed that the dog’s skin was yellow. The referring
veterinarian performed blood work that revealed elevated liver enzymes and renal parameters
(specifics unknown) and referred the client. There is no history of abnormal urination or
drinking, although the dog is a picky eater and has only one meal per day in the evening.
Approximately once a month the dog has soft stools. The dog is on monthly heartworm preventive
(Interceptor) year-round. Vaccination history is reportedly up-to-date. There is no history of
travel and there are no other pets in the home. Recently, the dog has shown a decreased activity
level.
Physical exam Raisin was slightly
dehydrated and no other significant physical exam abnormalities were identified beyond the
clinical icterus.
Differential diagnoses With the relatively
sudden onset of icterus, the initial diagnostic list is focused on primary and secondary hepatic
disease as well as possible acute hemolytic disease.
Plan Because of the limited clinical
picture, collection of a minimum data base with a complete blood count (CBC), clinical chemistry
profile and urinalysis was deemed essential to help localize primary and potential secondary organ
system involvement. These data will influence further diagnostic testing decisions.
Laboratory data
Morphology comments: Adequate platelets, enlarged platelets, anisocytosis 1+, slight icterus
Erythron—There is a very mild increased RBC count associated
with a slightly decreased MCV (microcytosis). Microcytosis is most commonly seen with developing
or well-established iron deficiency anemia as well as with hepatic insufficiency. The lack of any
significant polychromasia and low normal to decreased hematocrit suggest underlying liver disease.
No significant morphologic change such as acanthocytosis is seen for further support.
Leukon—Normal.
Thrombon—There is no quantitative platelet abnormality, but
the presence of enlarged platelets may suggest a bone marrow response to a peripheral demand for
platelets. Consideration for shortened platelet lifespan, as might be seen with peripheral
consumptive processes (inflammation, coagulation, etc.), should be made.
Morphology comments: Moderate icterus
Kidney panel—There is mild azotemia (decreased GFR) with
inadequate urine concentration (SG = 1.014 indicating tubular dysfunction) consistent with renal
azotemia. There is potentially a mild prerenal component to the azotemia contributed by
dehydration (hyperproteinemia, high normal albumin and sodium). There is no evidence to support a
postrenal mechanism.
Electrolyte and acid-base profiles—Most electrolytes are within
reference values. However, the mild elevation of TCO2 and moderate decrease in chloride relative
to sodium provides evidence of metabolic alkalosis. Relative chloride loss is most commonly due to
upper GI loss or sequestration, although there is no current clinical support for this. Loss
secondary to renal disease should also be considered.
Additionally, the anion gap is mildly elevated, which suggests a titrational metabolic acidosis;
however, the TCO2 is not decreased accordingly. This suggests that the alkalosis is predominant.
An increase in uremic acids (renal azotemia) is the most likely cause of the increased anion gap.
Other major differentials for a high anion gap include lactic acidosis, ketoacidosis and ethylene
glycol or salycilate intoxication. None of these are likely, based on laboratory and clinical
information.
The urine pH (6.5) in the face of a predominant metabolic alkalosis (based on elevated TCO2) raises
concern that there may be a paradoxical aciduria. Additional support for this concern includes a
mild state of dehydration providing a drive to retain sodium in combination with a relative
decrease in chloride. When chloride is depleted, the kidneys reabsorb bicarbonate in place of
chloride, leading to lowering of urine pH. Although serum potassium is within reference limits,
serum values are often a poor reflection of intracellular stores. It is possible that alkalosis
could be driving potassium intracellularly leading to an increase in extracellular hydrogen ions.
Hydrogen ions could then be excreted in the urine instead of potassium.
Hepatobiliary profile—A mild increase in ALT indicates
hepatocellular injury. The moderate increase of ALP could indicate cholestasis or induction of the
glucocorticoid isoenzyme. There is no other evidence to support a glucocorticoid response (normal
leukogram, normoglycemia) and no history of steroid or anticonvulsant administration. Additionally,
the moderate bilirubinuria (2+, SG = 1.014) supports cholestasis. The total bilirubin is mildly
elevated and attributed mostly to an elevation of the delta bilirubin, which provides evidence
for previous cholestasis.
Most parameters affected by functional hepatic mass are unremarkable. These include urea
(increased), glucose, albumin, cholesterol and unconjugated bilirubin. In addition, no coagulation
parameter (PT, PTT) abnormalities were observed. However, microcytosis without other clinical or
laboratory evidence for iron depletion raises some concern for decreased functional mass.
Protein profile—There is a mild increase in total protein. In
light of the mild clinical dehydration noted and the finding of a high within reference interval
albumin and sodium, dehydration may be contributing to this increase. However, the degree of
increase in globulin along with a low within reference interval albumin:globulin ratio are
supportive of systemic antigenic stimulation/inflammation. A combination of processes is likely.
Interpretations
- Renal azotemia (± prerenal due to dehydration)
- Mixed acid-base disorder with a predominant metabolic alkalosis and titrational metabolic
acidosis (secondary to azotemia)
- Possible paradoxical aciduria
- Mild hepatocellular injury, cholestasis and subtle evidence for decreased functional mass
Additional tests to be considered
- Blood gas analysis to better characterize the acid-base disturbance
- Additional evaluation of hepatic function:
- Ammonia level determination would be ideal, with consideration for conducting an ammonia
challenge test
- Bile acids may be difficult to interpret due to concurrent cholestasis
- Serum protein electrophoresis to allow accurate assessment of protein changes
- Leptospirosis titers since both renal and hepatic disease are suggested
- Fine needle aspirates and/or biopsies of liver and/or kidney
Primary differential—For a young shar-pei with
evidence of hepatorenal disease, systemic amyloidosis, familial or reactive, is the working
differential.
Further diagnostics
Diagnostic imaging findings—Hepatosplenomegaly was revealed
with abdominal radiographs. No ultrasound abnormalities were observed and a guided liver biopsy
was collected.
Diagnostic cytology—Impression smears of liver biopsy were
highly cellular and primarily contained blood and hepatocytes that often had intracytoplasmic
bluish-black pigment material consistent with lipofuscin. Benign hepatocellular hyperplasia was
suggested based on the finding of mild to moderate anisocytosis, anisokaryosis and variation in
N:C ratios. Occasional binucleation is seen. There are several bile canalicular casts between
hepatocytes. Intermixed between hepatocytes there are moderate to abundant quantities of
a bluish amorphous to fibrillar product consistent with amyloid. No infectious agents, significant
inflammatory process or evidence of neoplasia is seen.
Interpretation
Extracellular proteinaceous product most consistent with amyloid, mild hepatocellular hyperplasia, cholestasis.
| Figure 1: Impression
smear from a shar-pei with hepatic amyloidosis. Bluish amorphous to fibrillar
material in the center and top center is amyloid. The dark black-green material is
bilirubin accumulation due to the cholestasis. The binucleate cells are consistent with
hyperplasia. Few cells contain dark pigment consistent with lipofuscin. Wright’s stain,
100x objective field of view |
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Histopathology findings—Hepatic amyloidosis
Clinical case outcome This dog had been
diagnosed with shar-pei fever at 12 weeks of age based on episodic fevers with swollen hocks and
an arched back. The patient was discharged from the PUVTH with prescriptions for colchicine to
slow the progression of the disease and deracoxib (Deramaxx) for periodic fever and swollen joints.
Blood work performed by the referring DVM one month postdischarge showed moderately elevated
alkaline phosphatase similar to the PUVTH results. He also had a minimally elevated creatinine
(1.9, reference interval 0.5–1.8 mg/dL) and urea within the reference interval (15, reference
interval 7–27 mg/dL). The dog has been on a low-protein diet, which could explain the urea value
being relatively lower than the creatinine.
During the nine months postdischarge, the dog has had one notably bad episode of fever and swollen
hocks at four months and weekly fever/swollen hock episodes once a week for the last four weeks.
The referring veterinarian has increased the minimal Deramaxx dosage. Additional blood work is
planned during the dog’s annual exam within the next six months unless there is a more immediate
need prior to that.
References
- DiBartola SP, Tarr MJ, Webb DM et al. Familial renal amyloidosis in Chinese Shar Pei dogs.
J Am Vet Med Assoc. 1990;197:483–487.
- May C, Hammill J, Bennett D. Chinese Shar Pei fever syndrome: a preliminary report.
Research in Veterinary Science 1992;53:319–320.
- Loeven KO. Hepatic amyloidosis in two Chinese Shar Pei dogs. J Am Vet Med Assoc.
1994;204:1212–1216.
- DiBartola SP, Tarr MJ, Parker AT et al. Clinicopathologic findings in dogs with renal
amyloidosis: 59 cases (1976–1986). J Am Vet Med Assoc. 1989;195:358–364
- Flatland, B., Moore, R. R., Wolf, C. M., Yeomans, S. M., Donnell, R. L., Lane, I. F., Fry,
M. M. VCP, 2007; 36: 105-108. Liver aspirate from a Shar Pei dog
Tell us what you think of this case, or let us know if you have a case that
you would like to submit. E-mail us at
diagnosticedge@idexx.com to get the process started.
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Spotlight on Nicki Brentin, LVT
A three-time weekly winner in our Suite Stories contest for her stories about
Zena the cat,
Chewy the rottweiler and
Bailey the schnauzer,
Nicki also became a finalist for her Zena story!
Nicki has been a technician for five and a half years. She currently works at the Puget Sound
Veterinary Referral Center/Animal Emergency Clinic, which employs 12 veterinarians and more than
25 full- and part-time technicians. It’s a busy place, and even busier during the evenings and on
weekends, with anywhere from 5 to 25 patients coming in during each shift.
Nicki feels that without a doubt, her clinic will increase its use of in-house diagnostics over the
next few years. “The demand for in-house diagnostic work is becoming huge. If an animal comes in
at 2:00 a.m., we want to know what’s wrong by 3:00 a.m. The more we can do in-house, the better we
can serve our patients and clients.”
Nicki feels that pet owners compare their pets’ care to the care people get when they go to their
own doctors. “You get everything done right away in human medicine, so clients expect to be able
to get everything done for their pet in one building and get everything back quickly. In-house
diagnostics allow us to offer better, higher quality service. It helps our reputation, too. A
higher level of patient care makes clients happy, and happy clients tell their friends.”
“In-house diagnostics make our business more profitable, too. We can offer better, higher quality
service and we can charge for it. We generally use outside laboratories for pathology,
histopathology, etc. Our board-certified surgeons will send out tissue samples and our neurologist
sends out cerebral spinal fluid for analysis. The doctors may occasionally do a recheck, too. But
we rarely send out panels—we do them in-house because we can.”
Nicki describes herself as “one of those crazy vet techs whose life revolves around her pets,” all
of which were owner-relinquished or abandoned at the clinic. Her lucky pets include Eddy, a
five-year-old rottweiler mix; Isadora “Dori,” a four-year-old terrier mix; Murray, an
eight-year-old border collie mix; and a few cats to round out the household.
Visit
suitestories.com to read Nicki’s stories as well as other finalists’ stories.
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