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Small Animal Test Guide

July 7, 2008 Leave a comment


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
Fructosamine
High-dose Dexamethasone Suppression Test
Endogenous ACTH
Free T4 by Equilibrium Dialysis
Insulin/Glucose
Low-Dose Dexamethasone Suppression Test
Parathyroid Hormone
Phenobarbital Concentration
PLI or cPL
T3 Suppression Test
TLI
Urine Cortisol:Creatinine Ratio
Urine Protein:Creatinine Ratio
von Willebrand’s Factor

Emergency Management of the Blocked Ferret

April 29, 2008 Leave a comment

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

Diet

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

Crystalluria

Radiographs

Unremarkable

Radiopacity

Ultrasonography

Prostatomegaly

Adrenomegaly

—–

· 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.

Emergency Management of the Blocked Ferret

April 29, 2008 Leave a comment
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

Diet

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

Crystalluria

Radiographs

Unremarkable

Radiopacity

Ultrasonography

Prostatomegaly

Adrenomegaly

—–

· 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.

Calcitriol?

January 2, 2008 Leave a comment

One of the most common diseases we treat as small animal veterinarians is renal failure and renal insufficiency in cats and dogs. We are desperate to do more for these patients – to keep them eating and comfortable with minimal intervention for as long as possible. In the past 10 years, there has been much controversy regarding the use of calcitriol (1,25 dihydroxyvitamin D) to slow the progression of renal failure in cats and dogs.

In lab animal research and years of human use, calcitriol has been used to reduce renal secondary hyperparathyroidism. However, evidence suggests that it is most effective before the onset of excess parathyroid hormone secretion and the hyperphosphatemia that results. Newer synthetic vitamin D analogs may have other actions besides vitamin D receptor activation that benefit ill kidneys, although their injectable, short-acting formulations limit their use in veterinary medicine. A recent study of calcitriol use in cats showed no decrease in PTH concentrations in either normal or renal failure cats. This suggests that if the goal is to reduce PTH, the doses used in this study were not adequate, the sample size was too small, or the trial length too short.

 

The key question for veterinarians and clients, is whether the use of calcitriol will benefit an individual patient. While mulling over this question, the motto “DO NO HARM” lurks inevitably in the foreground. I have seen many patients, particularly cats, who lived far long and better on calcitriol than expected. Although the same can be said of some animals with renal failure NOT on calcitriol, especially those on a phosphorus-restricted renal diet.

 

What are the risks?

· Animals can become hypercalcemic at any time during therapy (days, weeks, months, years). Since this cannot be predicted, frequent blood calcium & phosphorus monitoring is essential. Once detected, stopping calcitriol and later reducing the dose typically resolves the hypercalcemia. However, if the animal has had a Ca x P > 60 for a prolonged period this may result in permanent dystrophic mineralization and reduced GFR.

· Dystrophic mineralization is also a risk for patients who are hyperphosphatemic.

 

What are the benefits?

· Delayed onset of renal secondary hyperparathyroidism and signs of uremia.

· Improved quality of life.

 

Which animal is a candidate?

· Renal failure or insufficiency with normal total and ionized calcium and phosphorus < 6 mg/dl.

· The animal must have an owner willing to commit to the time and expense of frequent monitoring – q 1 week initially, then q 1-2 months for the duration of Calcitriol therapy.

o I typically Rx only 1 month’s worth of calcitriol at a time. I put no refills on the 1st Rx and only 1 refill on subsequent Rx’s to encourage the owner to return for recheck blood work. No refills will be given until the patient returns.

o Warn owners of the potential for hypercalcemia and worsening of renal disease, even despite close monitoring.

 

Monitoring

· Obtain baseline chemistry panel (must include total calcium, phosphorus, BUN, creatinine) and baseline PTH and ionized calcium.

· Start calcitriol at the low end of the dose if PTH is elevated. Recheck calcium, phosphorus, BUN, creatinine in 1 week. If values are stable, continue for 3 more weeks.

· At 1 month, repeat chemistry panel (must include total calcium, phosphorus, BUN, creatinine) and baseline PTH and ionized calcium.

· If PTH is within normal limits, continue at the same dose of calcitriol and recheck q 1-2 months. If PTH remains above normal limits, increase the dose (up to 3.5 ng/kg/day) and recheck in 1 week and in 4 weeks.

· If hypercalcemia occurs, stop calcitriol and recheck total calcium, phosphorus, BUN, creatinine in 1 week. If the hypercalcemia has resolved and phosphorus remains below 6 mg/dl, consider restarting calcitriol at 50% the previous dose. Others discontinue calcitriol altogether at this point.

 

Jennifer S. Fryer, DVM

Calcitriol?

January 2, 2008 Leave a comment
By Jennifer S. Fryer, DVM

One of the most common diseases we treat as small animal veterinarians is renal failure and renal insufficiency in cats and dogs. We are desperate to do more for these patients – to keep them eating and comfortable with minimal intervention for as long as possible. In the past 10 years, there has been much controversy regarding the use of calcitriol (1,25 dihydroxyvitamin D) to slow the progression of renal failure in cats and dogs.

In lab animal research and years of human use, calcitriol has been used to reduce renal secondary hyperparathyroidism. However, evidence suggests that it is most effective before the onset of excess parathyroid hormone secretion and the hyperphosphatemia that results. Newer synthetic vitamin D analogs may have other actions besides vitamin D receptor activation that benefit ill kidneys, although their injectable, short-acting formulations limit their use in veterinary medicine. A recent study of calcitriol use in cats showed no decrease in PTH concentrations in either normal or renal failure cats. This suggests that if the goal is to reduce PTH, the doses used in this study were not adequate, the sample size was too small, or the trial length too short.

The key question for veterinarians and clients, is whether the use of calcitriol will benefit an individual patient. While mulling over this question, the motto “DO NO HARM” lurks inevitably in the foreground. I have seen many patients, particularly cats, who lived far long and better on calcitriol than expected. Although the same can be said of some animals with renal failure NOT on calcitriol, especially those on a phosphorus-restricted renal diet.

What are the risks?

· Animals can become hypercalcemic at any time during therapy (days, weeks, months, years). Since this cannot be predicted, frequent blood calcium & phosphorus monitoring is essential. Once detected, stopping calcitriol and later reducing the dose typically resolves the hypercalcemia. However, if the animal has had a Ca x P > 60 for a prolonged period this may result in permanent dystrophic mineralization and reduced GFR.

· Dystrophic mineralization is also a risk for patients who are hyperphosphatemic.

What are the benefits?

· Delayed onset of renal secondary hyperparathyroidism and signs of uremia.

· Improved quality of life.

Which animal is a candidate?

· Renal failure or insufficiency with normal total and ionized calcium and phosphorus

· The animal must have an owner willing to commit to the time and expense of frequent monitoring – q 1 week initially, then q 1-2 months for the duration of Calcitriol therapy.

o I typically Rx only 1 month’s worth of calcitriol at a time. I put no refills on the 1st Rx and only 1 refill on subsequent Rx’s to encourage the owner to return for recheck blood work. No refills will be given until the patient returns.

o Warn owners of the potential for hypercalcemia and worsening of renal disease, even despite close monitoring.

Monitoring

· Obtain baseline chemistry panel (must include total calcium, phosphorus, BUN, creatinine) and baseline PTH and ionized calcium.

· Start calcitriol at the low end of the dose if PTH is elevated. Recheck calcium, phosphorus, BUN, creatinine in 1 week. If values are stable, continue for 3 more weeks.

· At 1 month, repeat chemistry panel (must include total calcium, phosphorus, BUN, creatinine) and baseline PTH and ionized calcium.

· If PTH is within normal limits, continue at the same dose of calcitriol and recheck q 1-2 months. If PTH remains above normal limits, increase the dose (up to 3.5 ng/kg/day) and recheck in 1 week and in 4 weeks.

· If hypercalcemia occurs, stop calcitriol and recheck total calcium, phosphorus, BUN, creatinine in 1 week. If the hypercalcemia has resolved and phosphorus remains below 6 mg/dl, consider restarting calcitriol at 50% the previous dose. Others discontinue calcitriol altogether at this point.

Canine Adrenal Testing – Which Test Should I Run?

November 28, 2007 2 comments

By Dr. Jennifer S. Fryer

Urine Cortisol:Creatinine Ratio:

· Screening test for Hyperadrenocorticism (Cushing’s or HAC)

· Low Cost, Easy to collect (voided morning urine at home)

· Normal value rules out Hyperadrenocorticism

· Elevated values can indicate stress or Hyperadrenocorticism & adrenal function testing is necessary.

Baseline Cortisol:

· Screening test for Hypoadrenocorticism (Addison’s)

· Values >2 mcg/dl rule out Hypoadrenocorticism (Addison’s)

· Cannot be used to diagnose Hyperadrenocorticism (Cushing’s)

ACTH Stimulation Test:

· Test of choice to diagnose Hypoadrenocorticism (Addison’s)

· Screening test for Hyperadrenocorticism (Cushing’s)

· Used to monitor Trilostane or Lysodren Therapy

· Can be used to differentiate spontaneous vs. iatrogenic HAC

· 60-85% of dogs with HAC will have a positive result on this test.

· 85-90% of dogs without HAC will have a negative result on this test.

· Advantages:

o Can be completed in 1 hour

o No special handling of samples

o Submit for extended Adrenal Panel to document Atypical HAC

· Disadvantages:

o High cost of Cosyntropin

o Low Sensitivity (false negatives are possible)

Low-Dose Dexamethasone Suppression Test:

· Screening test for Hyperadrenocorticism (Cushing’s)

· Helps differentiate pituitary vs. adrenal origin

· 85-95% of HAC dogs have a positive result.

· 70-75% of dogs without HAC have a negative result.

· 40% of dogs with PDH and all adrenal tumor dogs have dexamethasone resistance and will require another differentiating test.

· Advantages:

o Low cost

o Higher sensitivity than ACTH Stim

o No special handling of samples

· Disadvantages:

o All day test requiring three blood samples at 0, 4, 8 hours

o The dog should be kept as minimally stressed as possible during this 8 hour period

High-Dose Dexamethasone Suppression Test:

· Theoretically helps differentiate Hyperadrenocorticism of pituitary vs. adrenal origin.

· Similar results to Low-Dose Dexamethasone Suppression Test at 8 hours.

· Rarely performed.

Endogenous ACTH Measurement:

· Helps differentiate pituitary vs. adrenal HAC

· Single plasma sample required

· Sample handling is difficult & critical to accurate measurement.

· With proper sample handling, this test is very reliable at differentiating pituitary vs. adrenal HAC.

Abdominal Ultrasound:

· Helps differentiate pituitary vs. adrenal HAC.

· May identify adrenal tumor, local invasion or metastasis.

· High cost

· Adrenals can be normally sized in PDH

· Adrenals can be difficult to visualize in some animals

· Ultrasound does not always accurately identify extent of metastasis or local invasion of an adrenal tumor

Computed Tomography (CT Scan):

· Screening test for Pituitary Tumor or Primary Adrenal Tumor and abdominal metastasis &/or local invasion

· Brain CT is not indicated unless a macroadenoma is suspected.

· Very high cost.

· Requires anesthesia.

· Cannot detect 50% of pituitary masses.

· Cannot differentiate between functional and non-functional tumors. Adrenal function tests are still required.

Brain Magnetic Resonance Imagine (MRI):

· Screening test for Pituitary Tumor

· Brain MRI is not necessary unless a macroadenoma is suspected.

· More reliable than CT at detecting small pituitary masses.

· Very high cost.

· Requires anesthesia.

· Not indicated unless a macroadenoma is suspected.

· Cannot differentiate between functional and non-functional tumors. Adrenal function tests are still required.

 

 

References

Lennon EM, Boyle 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(3):413-6.

Nelson RW, Turnwald GH, Willard MD. Endocrine, Metabolic, and Lipid Disorders. In: Willard MD and Tvedten H, eds. Small Animal Clinical Diagnosis by Laboratory Methods. 4th edition. St. Louis: Elsevier Saunders, 2004:165-207.

Reusch, CE. Hyperadrenocorticism. In: Ettinger SJ and Feldman EC, eds. Textbook of Veterinary Internal Medicine. 6th edition. St. Louis: Elsevier Saunders, 2005:1592-1611.

 

Canine Adrenal Testing – Which Test Should I Run?

November 28, 2007 Leave a comment

By Jennifer S. Fryer, DVM

Urine Cortisol:Creatinine Ratio:

· Screening test for Hyperadrenocorticism (Cushing’s or HAC)

· Low Cost, Easy to collect (voided morning urine at home)

· Normal value rules out Hyperadrenocorticism

· Elevated values can indicate stress or Hyperadrenocorticism & adrenal function testing is necessary.

Baseline Cortisol:

· Screening test for Hypoadrenocorticism (Addison’s)

· Values >2 mcg/dl rule out Hypoadrenocorticism (Addison’s)

· Cannot be used to diagnose Hyperadrenocorticism (Cushing’s)

ACTH Stimulation Test:

· Test of choice to diagnose Hypoadrenocorticism (Addison’s)

· Screening test for Hyperadrenocorticism (Cushing’s)

· Used to monitor Trilostane or Lysodren Therapy

· Can be used to differentiate spontaneous vs. iatrogenic HAC

· 60-85% of dogs with HAC will have a positive result on this test.

· 85-90% of dogs without HAC will have a negative result on this test.

· Advantages:

o Can be completed in 1 hour

o No special handling of samples

o Submit for extended Adrenal Panel to document Atypical HAC

· Disadvantages:

o High cost of Cosyntropin

o Low Sensitivity (false negatives are possible)

Low-Dose Dexamethasone Suppression Test:

· Screening test for Hyperadrenocorticism (Cushing’s)

· Helps differentiate pituitary vs. adrenal origin

· 85-95% of HAC dogs have a positive result.

· 70-75% of dogs without HAC have a negative result.

· 40% of dogs with PDH and all adrenal tumor dogs have dexamethasone resistance and will require another differentiating test.

· Advantages:

o Low cost

o Higher sensitivity than ACTH Stim

o No special handling of samples

· Disadvantages:

o All day test requiring three blood samples at 0, 4, 8 hours

o The dog should be kept as minimally stressed as possible during this 8 hour period

High-Dose Dexamethasone Suppression Test:

· Theoretically helps differentiate Hyperadrenocorticism of pituitary vs. adrenal origin.

· Similar results to Low-Dose Dexamethasone Suppression Test at 8 hours.

· Rarely performed.

Endogenous ACTH Measurement:

· Helps differentiate pituitary vs. adrenal HAC

· Single plasma sample required

· Sample handling is difficult & critical to accurate measurement.

· With proper sample handling, this test is very reliable at differentiating pituitary vs. adrenal HAC.

Abdominal Ultrasound:

· Helps differentiate pituitary vs. adrenal HAC.

· May identify adrenal tumor, local invasion or metastasis.

· High cost

· Adrenals can be normally sized in PDH

· Adrenals can be difficult to visualize in some animals

· Ultrasound does not always accurately identify extent of metastasis or local invasion of an adrenal tumor

Computed Tomography (CT Scan):

· Screening test for Pituitary Tumor or Primary Adrenal Tumor and abdominal metastasis &/or local invasion

· Brain CT is not indicated unless a macroadenoma is suspected.

· Very high cost.

· Requires anesthesia.

· Cannot detect 50% of pituitary masses.

· Cannot differentiate between functional and non-functional tumors. Adrenal function tests are still required.

Brain Magnetic Resonance Imagine (MRI):

· Screening test for Pituitary Tumor

· Brain MRI is not necessary unless a macroadenoma is suspected.

· More reliable than CT at detecting small pituitary masses.

· Very high cost.

· Requires anesthesia.

· Not indicated unless a macroadenoma is suspected.

· Cannot differentiate between functional and non-functional tumors. Adrenal function tests are still required.

References

Lennon EM, Boyle 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(3):413-6.

Nelson RW, Turnwald GH, Willard MD. Endocrine, Metabolic, and Lipid Disorders. In: Willard MD and Tvedten H, eds. Small Animal Clinical Diagnosis by Laboratory Methods. 4th edition. St. Louis: Elsevier Saunders, 2004:165-207.

Reusch, CE. Hyperadrenocorticism. In: Ettinger SJ and Feldman EC, eds. Textbook of Veterinary Internal Medicine. 6th edition. St. Louis: Elsevier Saunders, 2005:1592-1611.