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Sarra Borne UID: 000493586VETE 405: Pharmacology and Pharmacy

Hypoadrenocorticism

The Great Pretender

Sarra Borne VETE 405: Pharmacology and PharmacyUID: 000493586 November 30, 2013Assignment: FINAL EXAM CASE STUDY

Hypoadrenocorticism the Great Pretender

Finnegan is a 9 year-old, normally 77- 79 lb, MN, Labradoodle who was initially referred

to the internal medicine department of Veterinary Specialists of North Texas (VSNT) for

increased renal values, and hyperphosphatemia. Finnegan was originally from the Washington

D.C. area, and had only moved to Texas recently. Shortly after his arrival in the Dallas area, he

had an episode of hind end collapse while going upstairs. This was his first such episode. His

owners took him to the emergency clinic where he was examined and diagnosed with lower back

pain and neuritis. At that time Finnegan was placed on Rimadyl ® (carprofen) at a dose of 75

mg PO q 24h (twice daily).

The following day October 23rd 2013, Finnegan had another episode of apparent hind end

weakness, so his owners took him to a local day practice. While there he was sedated and

radiographs of his spine, shoulders, pelvis and coxofemoral joints were done. The cervical spine

was overall normal, with no signs of degeneration or collapse. The lumbar spine, pelvis and

coxofemoral joints were all within normal limits. Radiographically his shoulders showed the

formation of osteophytes (bone spurs), and joint mice (small, loose pieces of bone in the synovial

space) bilaterally on the caudal points of the humerus and his scapular rim showed some

remodeling. He was assessed to have detectable pain in the right shoulder region, and

osteoarthritis bilaterally, with the left being greater than the right.

Osteoarthritis, also known as degenerative joint disease is a chronic degenerative disease

that affects one or more joints in the body. It is caused by a deterioration of joint cartilage.

Cartilage is a smooth, resilient tissue that lines the joints, allowing nearly frictionless joint

movement and providing shock absorption. The deterioration of cartilage leads to increased

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friction and inflammation of the joints. This erodes the bone and can cause formation of new

bone, called osteophyte (bone spur) formation, which interferes with normal movement and can

cause pain. (Lennon & Marcellin-Little, 2005)

Figure 1: The x-ray on the left is an abnormal glenohumeral or shoulder joint. Image on the right is a normal glenohumeral joint. (Fairfield Veterinary Centre, n.d.)

Finnegan’s owners were instructed to continue the Rimadyl ® as previously prescribed,

and to return if there was no improvement or if there was another flare up of symptoms.

On October 24th, Finnegan returned to the day practice with a complaint of vomiting,

lethargy and inappetence. Finnegan was mildly dehydrated as evidenced by a decreased skin

turgor and slightly tacky mucous membranes. His rectal temperature (T) was 99.4 and his

weight was 68 lb. At this time a complete blood count and serum chemistry panel were run. The

CBC was within normal limits other than a few changes related to dehydration, the serum

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chemistry panel showed signs of moderate to marked azotemia, hyperphosphatemia, and a slight

increase in plasma proteins. Blood values on 10/24/2013 from the day practice

Normal Range (Heska)

WBC 13.0 6.0 -17.0 103/ul

HCT 55.7 37-55 %

RBC 8.94 5.50 – 8.50 106/ul

BUN 127.7 9 – 29 mg/dl

CREA 3.8 0.4 – 1.4 mg/dl

Phos 13.7 1.9 – 5.0 mg/dl

TP 7.9 5.5 – 7.6 g/dl

Albumin 4.0 2.5 – 4.0 g/dl

Globulin 3.9 2.0 – 3.6 g/dl

ALT 87 0 – 120 U/L

ALP 44 0 – 140 U/L

GGT 15 0 – 14 U/L

K 8.1 3.8 – 5.3 mEq/L

Na 133 141 – 152 mEq/L

Cl 108 102 – 120 mEq/L

The assessment was renal insufficiency of undetermined cause. The differential included

occult infection, leptospirosis, toxin exposure or neoplasia. At this point, Finnegan was referred

to VSNT for monitored overnight hospitalization with intravenous fluids, and an ultrasound

examination of the abdomen. The referring veterinarian was concerned that Finnegan might

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have leptospirosis. The referring veterinarian sent leptospirosis titers to a reference lab, and they

were not available at the time of his initial exam with the internists at VSNT. All seven of the

tested serovars eventually came back negative effectively eliminating infection with leptospirosis

as part of the differential.

On Finnegan’s arrival at VSNT a complete history was taken. There was no history of

toxic exposure, and no travel history other than the family move from the East Coast. The

owners noted that Finnegan is a couch potato indoor dog. The owners commented that Finnegan

had not recovered well from the anesthetic event the previous day, and was lethargic, had

vomited several times, and wouldn’t eat.

On physical examination it was noted that Finnegan was bright and alert. He had a rectal

temperature (T) of 98.6 F, heart rate (HR) 132 bpm, respiratory rate (RR) 36 bpm, and weighed

70.4 lb on our scale. The abdominal palpation elicited discomfort on palpation of the kidney

area. An abdominal ultrasound was done where it was discovered that Finnegan had a normal

left kidney, and an absent right kidney.

The radiologist had the following comments: Absent right kidney. Considerations are

given to renal agenesis (one or both fetal kidneys fail to develop) or possibly a severe renal

hypoplasia (an abnormally small kidney that has a reduced number of or smaller nephrons)

resulting in unrecognizable renal tissue. The mild pelvic renal dilation on the left could be due to

mild pyelonephritis (a urinary tract infection affecting the kidneys), renal insufficiency or fluid

therapy. Otherwise a sonographically normal abdomen. A radiographic or CT intravenous

pyelogram could be considered to evaluate the expected location of the right kidney. The

ultrasound images are of Finnegan’s left kidney, and the area where his right kidney should be.

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A urinalysis via cystocentesis demonstrated the following values:

Appearance Clear

Color Dark Yellow

Specific Gravity 1.076

Bacteria, WBC, Casts, Crystals, Epithelial

Cells

None Seen

pH 6.5

RBC Occasional

Finnegan was admitted to the hospital for aggressive fluid diuresis. He was prescribed

ampicillin at 22 mg/kg IV q 6 h to treat for the potential leptospirosis. Finnegan was maintained

in the quarantine area, and the staff was instructed to treat him as potentially infectious.

Finnegan did well overnight, and the azotemia was almost completely resolved by the

following morning.

10/25/13 6 AM Normal (Catalyst Analyzer)

BUN 6am 33 7-27 mg/dl

CREA 1.4 0.5 – 1.8 mg/dl

Phos 4.5 2.5 – 6.8 mg/dl

TP 6.3 5.2 – 8.2 %

Globulin 3.2 2.5 – 4.5 g/dl

Albumin 3.1 2.3 – 4.0 g/dl

T. Bili 0.2 0.0 – 0.9 mg/dl

Na 143 144 – 160 mmol/L

K 7.6 3.5 – 5.8 mmol/L

Cl 114 109 – 122 mmol/L

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The fluid rate was decreased throughout the day, and his BUN remained within normal

limits.

10/25/13 3 PM Normal

BUN 24 7-27 mg/dl

Na 144 144 – 160 mmol/L

K 6.8 3.5 – 5.8 mmol/L

Cl 113 109 – 122 mmol/L

He was released that afternoon on oral doxycycline at 5 mg/kg q 12h, pending the

leptospirosis results. It was recommended that Finnegan be fed a low protein diet such as Hill’s

Prescription k/d or Purina Veterinary Diet NF, and that he be allowed free access to water. A

recheck was scheduled with his primary vet for the following week.

On 10/28/2013 Finnegan had another episode of collapse and was taken to the emergency

clinic. His vital signs were 71.8 lb, rectal temperature 100.5 F, heart rate 76 bpm, respiratory

rate 28 bpm. Alert. A CBC and serum chemistry were run, and the results showed a mild

azotemia, hyperphosphatemia, hyperkalemia, hyponatremia, and a mildly increased hematocrit.

10/28/2013 9:25 PM Normal (Heska analyzer)

HCT 57.5 37 – 55%

BUN 63.1 9.0 – 29.0 mg/dl

CREA 2.2 0.4 – 1.4 ,g/dl

Phos 6.0 1.9 – 5.0 mg/dl

Na 134 3.8 – 5.3 mEq/L

K 8.5 141 – 152 mEq/L

CL 108 102 – 120 mEq/L

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Finnegan was hospitalized overnight on intravenous fluids, and referred back to VSNT

for follow-up in the morning. A cardiac arrhythmia was noted by the emergency clinic possibly

related to the elevated potassium. The differential diagnosis was still acute renal failure,

leptospirosis, or other renal disease.

On the morning of 10/29/13 Finnegan transferred back to VSNT for further care. His

vital signs were 70.7 lb, rectal temperature 101.3, HR 90, RR panting. His owners related the

following: “After coming home on 10/25 and sleeping for most of the day, he was steadily

improving, ate some canned dog food. The following day he was more alert and ate hungrily

and drank water, more like himself. Yesterday 10/28 Finny wanted to chase his ball, we went for

a walk and he was himself, ate and drank normally, had a normal bowel movement, on evening

walk around 8pm he would not get up so we took him next door (emergency hospital).

It was again noted that Finnegan had an irregular heartbeat, so the doctor ordered an

ECG. The results were consistent with

hyperkalemia. Tall, peaked T-waves, shortened

QT interval, and a depressed ST segment. This

particular pattern was the result of atrial standstill

which is the lack of atrial activity resulting from a failure of atrial depolarization. The ventricles

still function normally. This can be caused by electrolyte abnormalities especially hyperkalemia

(which can develop secondary to a number of conditions including Addison’s disease, oliguric

renal failure and urethral obstruction), cardiomyopathy, muscular dystrophy and drug toxicity.

(WikiVet, 2013)

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The atrial standstill and the hyperkalemia, and the hyponatremia, plus the faxed copy of

the negative leptospirosis titers were highly suspicious for hypoadrenocorticism or Addison’s

disease. An ACTH stimulation test was ordered. A baseline serum cortisol sample was drawn, a

dose of cosyntropin at 5mcg/kg was given IV and a post ACTH serum cortisol sample was

drawn an hour later. The results were conclusive.

PRE ACTH CORTISOL <0.2 ug/dl

POST ACTH CORTISOL <0.2 ug/dl

ACTH reference range:

<2 Post-ACTH cortisol consistent with hypoadrenocorticism.

Finnegan was again hospitalized overnight and given a loading dose of dexamethasone

sodium phosphate at 0.15 mg/kg IV, and then a second dose 12 hours later at 0.075 mg/kg IV.

He was maintained on 5% Dextrose in 0.9 % NaCl intravenous fluids, and did remarkably well

overnight. The following day he was treated with the mineralocorticoid Percorten-V ® (DOCP

or desoxycorticosterone pivalate) at 2.2 mg/kg IM, which is to be repeated every 25 days.

DOCP is a long-acting mineralocorticoid agent which is indicated for the parenteral treatment

of adrenocortical insufficiency in dogs (Plumb, 2011). That afternoon Finnegan was released

with a prescription for Prednisone 30 mg PO q 24 hr for 3 day, then 20 mg PO q 24 hr for 7 day,

then 10 mg PO q 24 hr until otherwise directed. The owners were instructed to continue the low

protein diet, and return in 10 days for a recheck examination. They were also given several

handouts on Addison’s disease.

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We saw Finnegan back on 11/11/13 and he looked remarkable. His energy and appetite

were back. He had no further episodes of collapse, and his blood work was all within normal

limits. A recheck was scheduled for two weeks for another DOCP injection and electrolytes.

11/11/13 Normal (Catalyst)

BUN 22 7-27 mg/dl

Creat 1.3 0.5-1.8 mg/dl

Phos 3.7 2.5-6.8 mg/dl

Na 154 144-160 mmol/L

K 3.9 3.5-5.8 mmol/L

Cl 118 109-122 mmol/L

The owners had some concerns about the cost involved in the DOCP injections, as

Finnegan is a rather large dog, and DOCP is not inexpensive. The discussed it with the internist

and the decision was made to switch to fludrocortisone (Florinef ®) which is an oral

mineralocorticoid at a dose of 0.01 mg/kg q 12 hr. Finnegan’s dose came out to 0.3 mg.

Commercially available fludrocortisone is only available in 0.1 mg tablets, so his prescription

was called into a compounding pharmacy.

Fludrocortisone has some glucocorticoid activity as well as mineralocorticoid, so it may

have more side effects than DOCP. These may include polyuria, polydipsia, polyphagia,

and poor skin and coat. If Finnegan receives an overdose it could lead to hypotension,

hypernatremia, edema, and hypokalemia. Monitoring is crucial, especially during his

first few months of therapy (Brooks, 2012).

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Finnegan returned for another follow-up visit on 11/26/2013. His owners are very

pleased with his progress. He is eating and drinking normally, has a normal activity level, and

takes his medications well. Their only complaint is that Finnegan is having some soft stool with

occasional mucus, but no blood.

His vital signs were good. T 99.1 F, HR 140, RR 50. He is back to his normal weight of

76.9 lb. An electrolyte panel was ordered and all values were within normal limits.

11/26/13 Normal (Catalyst)

Na 159 144-160 mmol/L

K 3.6 3.5-5.8 mmol/L

Cl 44 109-122 mmol/L

A rectal exam was done and it was normal. There were no parasites found on a fecal flotation. It

was suggested that the owners try adding some fiber to Finnegan’s diet, which currently consists

mostly of canned Hill’s Prescription Diet k/d. Some methods of doing this are adding green

beans, carrots and/or canned pumpkin. Also ¾ tsp. of Benefiber or Metamucil may be of benefit.

Finnegan’s next recheck is scheduled for a month. His fludrocortisone is to be refilled as

needed.

Hypoadrenocorticism or Addison’s disease is a deficiency of adrenocortical hormones

that is most commonly seen in young to middle-aged dogs. It may be familial in Standard

Poodles, so Finnegan may have inherited the genetic disposition from his Poodle ancestors.

Clinical signs of Addison’s disease are often indistinct. They may be acute or chronic, appear

episodic for weeks or even months and intensify in stressful situations

(Labor fur Klinische Diagnostik, 2009). This is one of the reasons that Addison’s disease is

known as “the great pretender”, it has the ability to mimic other common canine diseases. The

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differential diagnosis list is long and includes primary GI disease (especially infection with

Trichuris vulpis or whipworm), renal failure, liver failure, uroabdomen, pleural effusion, acute

pancreatitis, toxin ingestion, leptospirosis, neurologic disease and many others. History, physical

exam findings, and other diagnostics should help whittle down this list. There are no

pathognomonic clinical signs for hypoadrenocorticism and naturally occurring

hypoadrenocorticism is an uncommon canine disease with estimates of its incidence ranging

from 0.36% to 0.5 % (Klein & Peterson, 2010). Naturally occurring primary adrenocortical

failure occurs from atrophy or destruction of all three adrenal cortical layers, which results in

inadequate secretion of both mineralocorticoids and glucocorticoids (Kintzer & Peterson, 1997).

Immune mediated destruction of the adrenal cortex appears to cause this form of primary

hypoadrenocorticism, and is the most common reason for primary hypoadrenocorticism in

humans (Feldman & Nelson, 2004).

Hyperkalemia, hyponatremia, hypochloremia, and decreased sodium to potassium ratios

represent the classic electrolyte changes in Addisonian dogs, and hypoadrenocorticism should be

on the differential list anytime this pattern of electrolyte imbalance is seen. A definitive

diagnosis of Addison’s disease can be made with the ACTH stimulation test. Dogs with

Addison’s disease do not possess adequate reserves of cortisol to adequately respond.

The prognosis is fairly good. Finnegan will require lifelong mineralocorticoid and

glucocorticoid supplementation. His serum electrolytes will need to be monitored on a regular

basis, every few weeks until he stabilizes, and then quarterly. However, with drug therapy he

can return to being a clinically normal and healthy animal with normal blood parameters. A

study evaluating long-term treatment of 205 dogs with hypoadrenocorticism (1979-1993)

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reported that there was a good to excellent response to treatment in more than 80% of the dogs,

and a fair response tin 12.5% (Kintzer & Peterson, 1997) The median survival time for dogs in

this study was 4.7 years and many of the dogs were still alive at the end of the study period.

There was no difference in survival time between dogs treated with fludrocortisone versus

DOCP. Of the 124 dogs that died, 120 expired for reasons unrelated to hypoadrenocorticism

(Kintzer & Peterson, 1997)

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References

Brooks, W. (2012, March 6). Fludrocortisone acetate. Retrieved from VeterinaryPartner.com: http://www.veterinarypartner.com/Content.plx?A=536

Feldman, E., & Nelson, R. (2004). Canine and feline endocrinology and reproduction (3 ed.). St. Louis, Missouri: WB Saunders.

Kintzer P.P., P. M. (1997, March). Primary and secondary canine hypoadrenocorticism. Veterinary Clinics of North America Small Animal Practice, 27(2), 349-357.

Kintzer, P., & Peterson, M. (1997, Mar-Apr). Treatment and long-term follow-up of 205 dogs with hypoadrenocorticism. Journal of Veterinary Internal Medicine, 11(2), 43-49.

Klein, S., & Peterson, M. (2010, January). Canine hypoadrenocorticism: Part 1. The Canadian Veterinary Journal, 51(1), 63-69. Retrieved from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2797351/

Labor fur Klinische Diagnostik. (2009, June). Addison's disease in dogs: What do lab results tell us. Retrieved from Laboklin Aktuell: http://www.laboklin.de/pdf/en/aktuell/lab_akt_0906_en.pdf

Lennon, E., & Marcellin-Little, D. (2005). Canine Osteoarthritis. Retrieved from Arthritis M.D.: http://www.arthritismd.com/canine-osteoarthritis.html

Normal Shoulder Joint. Fairfield Veterinary Centre, Leicestershire, UK. Retrieved from http://www.fairfieldvets.co.uk/ic/dog/erin-1.htm

Plumb, D. (2011). Plumb's Veterinary Drug Handbook (Vol. 7). Ames, Iowa: Wiley-Blackwell.

WikiVet. (2013, October 15). Atrial Standstill. Retrieved from http://en.wikivet.net/Atrial_Standstill

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