VetCom April 2010

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We’re Hitting

tHe road See uS in a townnear you

tHe LetHargiC

igUana a CaSe StuDy ByMarK a. MitCHeLL,

DVM, MS, PhD

tHe anorexiC

and ListLess

PatienttHe neeD to aSSeSS PatientS

witH CoMPreHenSiVein-HouSe BLooD worK

sPeak UP we want to HearfroM you

Publications

APRIL 2010


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The Need to Assess Patients with Comprehensive

In-House Blood Work 4

Where to Find Us 11

Full Recovery for This Foal 12

Renal Failure in a Green Iguana 13

Let Us Hear From You 16

dateLine 4.1.10

Welcome to VetCom Publications, a bi-monthly newsletter availableboth in print and online. VetCom Publications offers readers case studies,practice tips from a clinical and cost savings perspective as well as

educational opportunities. This issue also includes a forum for Veterinarianto Manufacturer communication and so much more.

As an introductory note to this issue I want to highlight that Abaxis,Inc. has experienced incredible growth despite the economic downturnimpacting many companies in a wide variety of industries. Abaxis, Inc.,a point of care diagnostic company, has experienced an increase inveterinary instruments and consumable revenue for the nine monthsending December 31, 2009 in the North America Animal Health segmentof 23% year over year. While many companies are downsizing, Abaxishas increased our head count by nearly 4% and our facilities at ourworldwide corporate headquarters have grown by 27%.

We don’t take our growth for granted; on the contrary, Abaxis is focused

on research and development, exemplary products, sales, marketing,services and support in every sense of the word. Because of that focus ourcustomers have come to know Abaxis for our superior quality products andservices, ultimately reflected in the company's strong balance sheet.

Please note our growth is a direct result of VetScan® products like thenewly released VetScan i-STAT® 1, a handheld analyzer, and the muchanticipated Canine Wellness Profile with a built in heartworm antigentest which changes the paradigm of wellness testing.

The addition of these products to the portfolio of products that includethe VetScan VS2 chemistry analyzer, VetScan HM2 hematology analyzer,VetScan HM5 hematology analyzer, VetScan VS pro coagulation andspecialty analyzer and the Canine Heartworm Rapid Test allows yourpractice to meet all of your in-house testing needs.

Enjoy this issue and I look forward to your feedback, comments andcustomer advice in this exciting field of Animal Health.

Sincerely,

Valerie Goodwin-AdamsDirector of MarketingAbaxis, Inc.

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tHe Case for

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froMyou

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The owners are faithful clients and are

concerned because Chance is suddenlydepressed, weak, lethargic, and has not eaten

for the last two days. There has been no

overall change in her history, no known toxins

or poisons that she could have gotten into,

and the other pets in the household are ne.

The veterinarian evaluates Chance and nds

that her body temperature is 102.3 degrees

Fahrenheit. She has a strong 120 pulse rate,

04 Apri l 2010

The Need

to AssessPatients withComprehensiveIn-House

Blood WorkContributing Authors:

Andrew J. Roseneld, DVM, ABVP

Sharon Dial, DVM, ACVP

40 respiration rate, light pink mucus membranes,

a two second capillary rell time, and normalhydration. She appears weak and possibly

slightly painful in her caudal abdomen; no

palpable abnormalities can be detected. All

other elements of her physical examination

are within normal limits.

The veterinarian discusses the concerns

with the owners and outlines the diagnostic

recommendations, which include a complete

Case Example

General and emergency practitioners have all faced the enigma of the

anorexic, listless patient. For example, Chance Murphy, a 6-year-old

66-pound female spayed black lab mix, walks in the practice door.


http://slidepdf.com/reader/full/vetcom-april-2010 5/162010 Apri l 05

Test Finding Normal

HCT 26% (l) 35–55%

WBC 19,250 (h) 6,000–17,000

Platelet 125,000 (l) 200,000–500,000

Albumin 2.5 mg/dl 2.5–3.5 mg/dl

Test Canine Normal

PT 25 s 12–17 s

aPTT 180 s 90–110 s

The differential list for this patient includes

Disseminated Intravascular Coagulopathy

(DIC) / Atraumatic Bleed of the Abdomen,

Intestinal Disease / Chronic GI Ulceration, Liver

Disease, Infectious Disease (i.e. Ehrlichiosis),Toxin / Poison, and Neoplasia.

The primary concern for this patient is whether

Chance has a non-regenerative anemia such

as anemia of chronic disease, has a chronic

bleeding issue (i.e. gastrointestinal ulceration),

or has an acute blood loss anemia. At this point

an in-house coagulation prole is necessary to

help determine if there is a coagulation concern

suggesting a life-threatening problem. The clotting

prole shows:

With the observed prolonged clotting times

and evidence of anemia and thrombocytopenia

acute internal bleeding must be a primary

concern. Ultrasound evaluation showed a

moderate amount of free uid in the abdomen

which when tapped produced non-clotting

blood with a packed cell volume of 32%. An

emergency exploratory laparotomy revealed

a small, irregular spleen with multiple nodules.

The spleen was successfully removed and the

bleeding resolved.

blood count, chemistry prole, urinalysis and

chest and abdominal radiographs. The owners

agree to the initial diagnostic plan, and the

medical team takes Chance to the back for

radiographs and lab work.

Thoracic lms show a possible microcardia

with no signicant changes in the lungs,

diaphragm and trachea. Abdominal lms

suggest a slight loss of contrast in the ventral

abdomen. Blood is collected and mild bruising

is noted on Chance’s hind limb venipuncture

site. In-house lab work is completed, and

except for the following changes in the blood

work; all other parameters are unremarkable.

The medical team evaluates a blood

film and a wet slide prep of Chance’s

blood. The technician team member

finds no obvious agglutination onthe wet prep, and a blood film that

shows normal red and white blood

cell morphology. The medical team

agrees that the platelet number

appears slightly decreased and sees

no overall sign of a regenerative red

blood cell response.

THE PRACTICAL NEED TO ASSESS COAGULATION IN THE PATIENT



Endothelial cells line all blood vessels.

When injured, the endothelial cell retracts to

expose proteins present in the tissue deep

to the vessel wall or interstitium that interact

with platelets to promote their adhesion.

Further, these sites release molecules thatpromote activation of the clotting factors. The

blood vessel wall plays a major role in both

coagulation and brinolysis.

There is no laboratory testing that can

evaluate the function of endothelial cells.

There are diseases that can interfere with

the function of the endothelial cells. In most

cases, abnormal endothelial cells result in

abnormal clot formation because they do not

maintain their anticoagulant nature. Sepsis and

metabolic diseases such as diabetes can result

in pro-coagulant changes in endothelial cells

throughout the body.

Platelets are essential for primary hemostasis;

the formation of the initial primary platelet

plug. The injured endothelial cells promote

the adhesion, aggregation, swelling and

secretion by platelets (activation). Activated

platelets also promote the activation of other

platelets. When platelets are activated, they

release factors that promote activation of

the coagulation cascade. In addition to the

Figure 1

Damage to the endothelial cells exposes

receptors (von Willebrand factor),

and platelets adhere to the wall of the

vessel covering the defect. The platelets

become activated, undergo a shape

change and begin to aggregate to form

a plug at the injury. The platelets secrete

substances and provide tissue factor for

activation of the clotting factors. Once

the coagulation pathways are activated,

prothrombin is converted to thrombin;

thrombin converts brinogen to brinand the brin “glues” the platelets

together into a stable clot sealing off

the injury1.

The three primary elements of hemostasis are

the endothelial cells that line the wall of the

blood vessels, platelets and clotting factors

(See Figure 1). Each of these elements must

function appropriately for normal hemostasis.

Defects in any of these three participants can

result in abnormal bleeding or inappropriate

clot formation.

• Constriction of the injured vessel

• Formation of the “primary platelet plug”

• Stabilization of the primary platelet plug

by deposits of brin through activation

of clotting factors

A Review of Coagulation

In this case, as with many other cases, the need to evaluate the clotting abilityof the patient is essential. There are several principle events that are involved

in coagulation:

1. Image courtesy of Clinical Pathology for the Veterinary Team, Rosenfeld, A & Dial, S.Wiley, Ames Ia, 2010.

06 Apri l 2010



Secondary hemostasis is the process of

stabilizing the platelet plug by formation of

fbrin, the mortar that holds the platelets

together. The processes of primary and

secondary hemostasis occur simultaneously.

The formation of stable brin is the result of

activation of numerous circulating clotting

factors and enzymes or enzyme complexes that

form the coagulation cascade. The coagulation

secreted factors, platelets provide a surface for

the clotting process and the cellular mass that

will form the clot. Defects in primary hemostasis

can occur due to decreased numbers of

circulating platelets (thrombocytopenia) orplatelet dysfunction.

Thrombocytopenia is the most common defect

in primary hemostasis. The platelet count is

the most common test to evaluate platelet

number. In general an animal will not begin to

spontaneously bleed until platelet number is

less than 40,000 / µL.

Platelet function tests should be performed

in the bleeding patient with normal platelet

numbers and coagulation times. There aresensitive tests for platelet function that

require submission of a sample to a specialty

laboratory. However, there are in-house

tests that can be done to identify patients

with possible defects in platelet function; the

most reliable is the buccal mucosal bleeding

time. The buccal mucosal bleeding time is commonly done to screen dogs for von

Willebrand’s disease. A small shallow cut is

made in the mucosal surface of the upper lip

and the time from the initial cut to cessation

of bleeding is recorded. It is very important to

perform this test in a standard and consistent

manner. A standard procedure for this test is

outlined in Figure 2. Normal buccal bleeding

times are 1.7 to 4.2 minutes with a mean of

2.6 minutes. If there is a prolonged buccal

mucosal bleeding time, further laboratorytests are required to determine the cause of

the platelet dysfunction.

2. Image courtesy of Clinical Pathology for the Veterinary Team, Rosenfeld, A & Dial, SWiley, Ames Ia, 2010.

Figure 2

Step I: With the patient anesthetized, fold the upper lip up and secure loosely with a gauze tie. The tie must be loose to allow normal blood ow.

Step 2: Make a reproducible 1/8 – 1/4 inch stab wound using a #11 surgical blade. The depth of the wound can be determined by marking the blade.

Step 3: Gently remove the blood drops with lter paper without touching the wound. Measure the time it takes to stop bleeding2.

Step I Step 2 Step 3


cascade depends on many cofactors such

as calcium and multiple feedback loops that

accelerate and inhibit the process. If there

is a deciency in the coagulation cascade,

the primary plug will degrade prematurely

and bleeding will resume. The common tests

for defects in secondary hemostasis are the

Prothrombin Time (PT) and the activated

Partial Thromboplastin Time (aPTT).



A prolonged PT and normal aPTT indicate

a defect in the extrinsic pathway, while a

prolonged aPTT with a normal PT indicates a

defect in the intrinsic pathway. If both tests are

prolonged, there may be a combined pathway

disorder, such as Vitamin K antagonism due

to warfarin toxicity or liver disease, or DIC, or

there may be a common pathway disorder

such as an inherited coagulation factor defect

such as Factor X or Factor II (Prothrombin).

Indications for Clotting Times

There are many congenital and acquired disease entities that can produce a

coagulopathy, either from dysfunctional endothelial cells, decreased platelet

number, platelet dysfunction or decreased clotting factors (See Table 1).Recommendations to establish baseline clotting times include:

• Pre-surgical blood work evaluation:

Evaluating clotting times as part of a rst

time pre-surgical (i.e. kitten/puppy) blood

screen can help identify patients with

hereditary disorders such as Hemophilia

A or B. Identication of these patients

prior to surgery is a necessity to prevent

prolonged surgical bleeding. Although

these diseases can affect any pure or

mixed breed canine or feline, veterinariansshould screen the following breeds closely

for hereditary coagulation disorders:

Hemophilia A: Beagles, Alaskan

Malamutes, Boxers, Miniature

Schnauzers, Bulldogs

Hemophilia B: Cairn Terriers,

Airedales, Coonhounds, St.

Bernards, American Cocker

Spaniels, French Bulldogs, Alaskan

Malamutes, Scottish Terriers,Shetland Sheepdogs, Labrador

Retrievers, Bichon Frise,

Old English Sheepdogs, British

Short Haired Cat

• Hospitalized and Ill Patients: Syndromes

that increase clotting times can include

diseases that affect liver function,

ingestion of toxins which affect Vitamin K

metabolism, and diseases that promote

Disseminated Intravascular Coagulopathy.

These entities can present subtly in an ill

patient and develop into a severe acute life

threatening syndrome. Baseline clotting times

are recommended for the following disease

conditions:

Sepsis/Infectious (Parvo Viral Infection

Pneumonia, Pyometra…)

Liver Disease

Heat Stroke

Anemia/Hemorrhage

Toxins or Poisonings

Severe Metabolic Disease (Diabetic

Ketoacidosis (DKA), Amyloidosis…)

Neoplasia

Patients requiring surgical procedure or

surgical biopsy should always have a

thorough coagulation prole completed prior

to the procedure.



Conclusion

The ability to evaluate and treat the at-risk patients withcoagulopathy is becoming a practical and necessary

solution to save patients’ lives.

2010 Apri l 09

References:

Clinical Pathology for the Veterinary Team. Rosenfeld, A. & Dial, S. Wiley, Ames Ia, 2010

Textbook of Veterinary Internal Medicine, 6th Edition. Ettinger, S. and Feldman, E., Elsevier, Baltimore, 2004.

Blackwell's Five-Minute Veterinary Consult – Canine and Feline, 4th Edition. Tilley, L. and Smith, F. Wiley, Ames, Ia, 2008.

Handbook of Small Animal Practice, 5th Edition. Morgan, R. Saunders, Baltimore, 2007.

Textbook of Medical Physiology, 11th Edition. Guyton, A. and Hall, J. Saunders. Baltimore, 2005.

Jergens, A.E., Turrentine, M.A., Kraus, K.H. and Johnson, G.S. (1987). Buccal mucosal bleeding time of healthy dogs and of dogs in variouspathological states, including thrombocytopenia, uremia and von Willebrand’s disease. American Journal of Veterinary Research 48 p 1337 - 1342.

From an emergency and general practice

perspective, the use of in-house clotting

analyzers or coagulation tests is an important

aspect of the standard of care. With the

tightening economy, clients are expecting

more from the general practitioner and are

less responsive to referring cases out to larger

secondary and tertiary care centers. The ability

to evaluate in-hospital clotting factors and

complete blood counts in ill patients allows the

veterinarian to treat the patient effectively before

severe bleeding occurs, and can save lives and

help maintain the patient’s quality of life.


Endothelial Dysfunction

Decreased platelet number

Decreased platelet function

Decreased Clotting Factors

• Hereditary Disease• Sepsis (i.e. Parvo, Pyometra, Pneumonia)• Endocrine Disease: Diabetes Miletus

• Immune Mediated Disease• Infectious Disease (i.e. Ehrlichia)• Consumption• Production Disorder (i.e. bone marrow)

• Congenital Disease(i.e. von Willebrand’s disease)

• Toxins / Drugs (i.e. Aspirin)

• Congenital Disease (i.e. Hemophilia A[deficiency of Factor VIII] & Hemophilia B[deficiency of Factor IX and deficiencyof Factor X])

• Hepatic Dysfunction: Infectious, Inflammatory,Toxin, Metabolic, Neoplastic

• Toxin – Coumadin / Anti-vitamin Kpoisons (Rodenticides)

• DIC: Sepsis, Heat Stroke, Neoplasia,Immune Mediated Disease, Shock, GDV,Advanced Heartworm Disease

• Neoplasia: Atraumatic Abdominal Bleeding• Chronic Bleeding Disorder

There are no specific tests for endotheliadysfunction. Diagnosis of this process isseen through elevation of clotting timesbased on prolonged bleeding.

Platelet Count

Buccal Mucosal Bleeding Time

Prothrombin Time (PT) and ActivatedPartial Thromboplastin Time (aPTT)

Pathology that disruptthe clotting process

Cause(Not intended to be a complete list)

In-House Clinical Diagnostics

Table 1

VetScan® VS pro





Date

4/8/10–4/10/10

4/9/10–4/10/10

4/10/10–4/11/10

4/10/10–4/12/10

4/15/10–4/17/10

4/16/10–4/18/10

4/17/10–4/18/10

4/18/10–4/21/10

4/24/10–4/25/10

6/10/10–6/13/10

6/10/10–6/12/10

6/17/10

6/24/10–6/27/10

6/26/10

Conference

Auburn University Vet Conference

Florida VMA

Special Species Symposium

CVC East

North American Veterinary

Dermatology Forum

ABVP

San Diego VMA

American Association forCancer Research

UC Davis Vet Tech Seminar

Alabama VMA

ACVIM

Utah VMA

Appalachian MountainVeterinary Conference

Arizona Veterinary Specialists

Location

Auburn, AL

Tampa, FL

Philadelphia, PA

Baltimore, MD

Portland, OR

Denver, CO

San Diego, CA

Washington, DC

Irvine, CA

Sandestin, FL

Anaheim, CA

Moab, UT

Asheville, NC

Tempe, AZ

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Send resumes to [email protected]



It is important to perform blood gases to differentiate

between metabolic and respiratory acidosis. Metabolic

acidosis typically results from poor tissue perfusion and

lactate accumulation while respiratory acidosis develops as

a result of hypoventilation caused by abdominal distention,

respiratory disease or pleural effusion. Differentiating

between these two is important in treatment. In treating

metabolic acidosis, rehydration often resolves the

problem. In dealing with respiratory acidosis, removing

the abdominal fluid and mechanical ventilation would be

utilized in treating this foal.

12 Apri l 2010

Physical examination was

performed and blood drawn

for a CBC and IgG levels at

approximately 24 hours of age.

All were found to be within

normal limits. The foal displayed

normal activity until the time

of examination.

Physical examination revealed

the foal to be in good body

condition, lethargic with

slightly enlarged abdominal

contours. The foal postured

to urinate during examination

and produced a small volume

of urine; posturing appeared

prolonged. She had an increased

body temperature (102.8°F),

was tachycardic (76 bpm), and

had normal respirations. Mucous

membranes and sclera were

within normal limits. Ballotmentof the abdomen was normal.

Blood was drawn for a CBC and

Equine Profile Plus. An arterial

sample was also obtained for

i-STAT® blood gas analysis. The

CBC showed a decreased WBC

compared to an initial CBC. The

Equine Profile Plus revealed

hyperkalemia, hyponatremia,

Terry C. Gerros,

DVM, MS, Diplomate,

ACVIM - Large Animal

and hypochloremia. The BUN

was normal, but the creatinine

levels were mildly elevated.

The GGT and ALP were

elevated, but this is a normal

finding in newborn foals. The

arterial blood sample showed

a mild metabolic acidosis.

Based on the physical

examination and supported by

laboratory data, the working

diagnosis was uroperitoneum

due to ruptured bladder. Similar

abnormalities may also be

observed in foals which are

septic, suffering from renal

or gastrointestinal disease,

or urinary obstruction. All

of these problems may

occur simultaneously.

Paracentesis was then

performed and yielded >500 ml

of a clear fluid, which had a

protein concentration <2.5 g/dl

that had an odor similar to

urine and confirmed our

working diagnosis.

Initial treatment consisted of

glucose, calcium gluconate,

sodium bicarbonate followed

by saline, which was aimed

at stabilizing the foal and

correcting the electrolyte and

acid-base abnormalities. A Foley

catheter was then placed in the

abdomen to remove the excess

peritoneal fluid; another 3 liters

were drained.

After the metabolic

abnormalities were corrected,

the foal became much more

alert and active. The foal was

then anesthetized, placed

in dorsal recumbency, and

underwent celiotomy to

repair the suspected bladder

defect. A 5 cm rent was found

on the dorsal aspect of the

urinary bladder. Recovery was

uneventful and the foal made a

complete recovery.

In this case, the ability to

perform both field and

in-house testing with the

i-STAT and the VetScan

allowed prompt medical and

surgical intervention resulting in

complete recovery of this foal.

A 3-day-old filly was

presented for lethargy.

Foaling was uneventful

and the foal was observed

nursing shortly after birth.

Full Recovery for This Foal



Renal Failure in

a Green Iguana:

Avian/ReptilianProfile Plus Rotor

Mark A. Mitchell DVM, MS, PhD

A 2.3 kg intact male greeniguana (Iguana iguana) was

presented with a history of

anorexia and weakness of

7 days duration.

The animal was allowed

free-roam of the house,

but was offered a basking

spot that maintained a

temperature of 90°F (32°C).

The only type of articiallight provided to the iguana

was the incandescent lamp

used at the basking site and

the uorescent lights used

to light the house. The oors

of the house were covered

in tile and wood. The iguana

was offered a diet of mixed

greens, based on availability.

In general, dark leafy greens

were offered, but the iguana

would refuse collared greens.

The iguana received no other

supplementation. A largewater bowl was provided for

the iguana (approximately

30.5 cm). The animal did

not have access to a water

source that it could climb into,

nor was it ever bathed. The

owners did have 2 cats in the

house. They did not bother the

iguana, although the owner did

mention that the cats almost

seemed to “enjoy” watchingthe iguana eat their food.

On physical examination the

iguana was found to be quiet

and depressed. His skin color

had a bronze hue. The iguana’s

eyes had a sunken appearance.

The mucous membranes in

the oral cavity were tacky and

pale. The skin elasticity over

the lateral body wall was poor.The only abnormal nding on

coelomic palpation was two

rm masses cranial to the pelvis.

The iguana was missing two

digits on his right front foot. The

iguana had a body temperature

of 75°F (24°C). A Doppler unit

was used to determine the heart

rate, which was 52 beats per

minute. Respirations were

12/minute.

The problem list for this animal

included: anorexia, lethargy,

eating carnivore (cat) food,

no supplemental ultraviolet

B radiation, a lack of a large

bathing/drinking source,

dehydration, and abnormal

masses in the coelomic cavity.

Based on this problem list, the

initial diagnostic tests ordered

for this animal included: a

complete blood count (CBC),

plasma biochemistry prole,and radiographs. The blood

sample was collected from

the jugular vein using a 25

gauge needle fastened to a

3-ml syringe (Figure 1). The

CBC included a packed cell

volume (PCV), white blood

cell estimate, and a differential.

The white blood cell estimate

was done using the eosinophil

unopette system (Becton,Dickinson, and Co., Franklin

Lakes, NJ USA), and the

differential slide prepared

using a modied Wright-

Giemsa stain.1 The plasma

biochemistry was performed

using the Abaxis VetScan VS2

(Union City, CA USA) and the

Avian/Reptilian Prole Plus

rotor. Survey radiographs were

taken without sedation.

Once the diagnostic tests

were collected, the iguana

was placed into an incubator

with a thermostatically set

temperature of 88°F (31°C).

After allowing the animal’s

body temperature to rise

for one hour, an intraosseus

(IO) catheter was placed

in the proximal tibia. Theprocedure was performed

using a local anesthetic. A 20

gauge hypodermic needle

was used as the catheter.

The author prefers these

over spinal needles because

of their shorter length. If

the needle cores during

penetration into the bone

RENAL fAILURE IN A GREEN LGUANA



marrow, a replacement needle

can be placed directly into

the insertion site. Survey

radiographs can be used

to ensure the catheter isplaced correctly (Figure 2).

Normosol-R uids (Abbott

Laboratories, North Chicago,

IL USA) were used to correct

the animal’s uid decit and

provide maintenance uids.

The decit was estimated to

be 10% (pending bloodwork),

which meant that the animal

required 230 ml of lost uid.

Maintenance was determinedto be 15 ml/kg/day. The

decit was to be corrected

over 72 hours, while the

maintenance level would be

provided daily. The uids were

delivered continuously via

a syringe pump. The animal

was returned to the incubator

pending the diagnostic

test results.

The results of the CBC

suggested that the iguana

had a chronic inammatory

response (14.6 x 103 cells/µL),

characterized by a monocytosis

(2.6 x 103 cells/µL), and was

dehydrated (PCV: 40%)

(Mitchell, unpublished data).

The results of the plasma

biochemistry panel can be found

in Table 1. The iguana was foundto be severely hypocalcemic,

severely hyperphosphatemic,

hypernatremic, hyperuricemic,

and had elevated AST and

CK levels. The inverse calcium:

phosphorus ratio is a strong

indicator of renal disease.

Under normal conditions, the

kidneys should conserve calcium

and excrete phosphorus. The

elevated sodium and uric

acid were considered to be

associated with dehydration.

Elevated CK and AST areconsistent with muscle

degradation, likely associated

with the catabolic state of

the patient. The total protein

values suggest an elevation

in the globulins, as there is

an inverse albumin: globulin

ratio. It is possible that albumin

was not being retained at

the level of the kidneys, but

the dehydration could alsofalsely elevate the value. It is

important to consider that

some patient values may fall

within a minimum-maximum,

but still be abnormal. Many

parameter ranges are quite

large, and depending on where

the patient’s value started can

have a large impact on where

it is at the time of testing.

The radiographs revealed

that the two coelomic masses

originated from the pelvis

(Figure 3). The primary

structures found in the caudal

coelomic cavity in a green iguana

include the two fat pads, the

rectum, urinary bladder and

kidneys. The kidneys are actually

lobulated structures located

within the pelvic canal. Thendings on the radiographs

and the bloodwork suggested

that the animal had chronic

renal disease.

Based on these ndings, the

owners were given a grave

prognosis. Renal biopsies were

recommended to conrm a

diagnosis, but were declined.

A decision was made to

institute additional therapies

to manage the chronic renal

failure and continue the uidtherapy over 72 hours. At that

time, the blood work and the

animal would be re-assessed.

Over the next 72 hours the

iguana was started on calcium

gluconate (400 mg/kg/day)

IO to correct decits and

ensure rapid availability to

cells, aluminum hydroxide

(25 mg/kg twice daily) to

serve as a phosphate binder,

and enrooxacin (10 mg/

kg once daily) as a broad

spectrum antibiotic with good

penetration to the kidneys.

After 24 hours of treatment

and rehydration, the iguana

was more alert and active.

Nutritional support was

initiated at that time using

Repta-Aid Herbivore (Fluker

Farms, Port Allen, LA USA).

After 72 hours of treatment,

the plasma biochemistries

were re-tested using an Abaxis

VetScan Avian/Reptilian

Prole Plus. Because the

changes to the calcium (3.9

mg/dL) and phosphorus (25.6

mg/dL) were minimal, and the

iguana had a grave prognosis,

the owner elected euthanasia.

Renal failure is a common

problem identied in adult

captive green iguanas. There

are several theories as to why

this occurs, including chronic

dehydration, high protein diets,

and toxic exposure. In this

case, and with many others,



the author nds that iguanas

with free roam in a house and

exposure to carnivore diets

(e.g., cat diet) tend to develop

this disease. Green iguanasare herbivores, and their

gastrointestinal system is not

built for the high protein and

fat-soluble vitamins found in

carnivore diets.

A biopsy in this case would

have been helpful for

conrming the diagnosis and

determining if there were

more specic treatments that

could be used to manage the

patient, but it was declined by

the owner. A necropsy was

also declined, but the author

has seen similar cases where

the post-mortem diagnosis

is glomerulonephrosis. A

prognostic indicator that can

be used to predict the potential

success with these cases is the

calcium and phosphorus levels.

Under normal conditions the

ratio of calcium: phosphorus

should be 1.5–2.0:1. When the

inverse ratio is slight (1:1–1.5),

it is often possible to manage

the patient by correcting

husbandry deciencies (e.g.,

no carnivore diets, access to

water in an appropriately

sized container), providing

uids and oral calcium, andbinding phosphate. When the

ratio gets as large as was seen in

this case (1:7.9), it is not possible

to stabilize these patients short

of renal transplant.

References:

1. Raskin RE. 2000. Reptilian complete blood count. In Laboratory Medicine: Avian and Exotic Pets. Fudge, A.WB Saunders CO., Philadelphia, PA, 193-197.

2. Grant KR, Thode HP, Connor S, Johnston M. 2009. Establishment of plasma biochemical reference values for captivegreen iguanas, Iguana iguana, using a point-of-care biochemistry analyzer. J Herp Med Surg 19 (1).

Parameter Green Iguana patient Reference2

Mean Minimum–Maximum

Albumin (g/dL) 1.6 2.02 0.91–3.01

AST (IU/L) 248 19.80* 11.2–41.08

Bile Acids (µmol/L) <35 3.97* 0.51–18.16Calcium (mg/dL) 3.4 13.61 9.20–25.68

Phosphorus (mg/dL) 26.8 1.51 0.88–2.27

Creatine kinase (IU/L) 4712 495.17* 74.23–4912.18

Total protein (g/dL) 5.6 6.22 4.66–8.79

Globulin (g/dL) 4.0 4.21 2.99–6.08

Glucose (mg/dL) 187 165.29 86.76–269.95

Potassium (mEq/L) 4.7 5.42 3.74–7.34

Sodium (mEq/L) 167 157.11 144.23–175.00

Uric acid (mg/dL) 16.7 2.54 0.6–5.48

*median

Table 1. Green iguana plasma biochemistry test results (pre-treatment).

Figure 1. Jugular venipuncture is an

excellent site for collecting a blood

sample from a green iguana that is

hypothermic and dehydrated.

Figure 2. Dorsovental radiograph being used to

assess the placement of an IO catheter in the tibia

of an iguana. A second lateral survey radiograph

is also necessary to confirm placement.

Figure 3. Lateral survey radiograph of the

green iguana patient. Note (arrows) the large

caudal masses originating from the pelvic inle

RENAL fAILURE IN A GREEN LGUANA



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VetCom April 2010