Hypokalaemic paresis, hypertension, alkalosis and adrenal-dependent hyperadrenocorticism in a dog

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Hypokalaemic paresis, hypertension, alkalosis and adrenal-dependent hyperadrenocorticism in a dog

SMALL ANIMALS

CASE REPORT

DR DAVIES,a SF FOSTER, BJ HOPPER, KL STAUDTE, AJ O’HARA and PJ IRWIN

Generalised paresis, severe hypokalaemia and kaliuresis, metabolic alkalosis and hypertension, characteristic of mineralocorticoid excess, were identified in a dog with hyperadrenocorticism due to a functional adrenocortical carcinoma. Aldosterone concentration was decreased and deoxycorticosterone concentration increased in the presence of hypokalaemia. These metabolic abnormalities resolved with resection of the carcinoma. Mineralocorticoid excess in dogs with hyperadrenocorticism is generally considered to be of little clinical significance but resulted in the acute presentation of this patient. The possible pathogenesis of mineralocorticoid excess in this case of canine hyperadrenocorticism is discussed. Aust Vet J 2008;86:139–146

11-β-HSD-2 ACTH ADH DOC HAC KTZ PDH

doi: 10.1111/j.1751-0813.2008.00276.x

11-β-hydroxysteroid dehydrogenase-2 Adrenocorticotropic hormone Adrenal-dependent hyperadrenocorticism 11-deoxycorticosterone Hyperadrenocorticism Ketoconazole Pituitary-dependent hyperadrenocorticism

H

yperadrenocorticism (HAC) is a common endocrinopathy of middle-aged to older dogs and approximately 15 to 20% of these dogs have adrenaldependent hyperadrenocorticism (ADH) with excessive production of cortisol from autonomously secreting adrenocortical tumours.1 The constellation of clinical and laboratory findings that occurs in canine HAC1 (canine Cushing’s syndrome) is well known to veterinary practitioners. Hypokalaemia and metabolic alkalosis are generally considered to be of little clinical significance in canine HAC.1 This is in contrast to the disease in humans, where some patients can develop severe and lifethreatening hypokalaemia.2 This case report describes severe hypokalaemia, paresis, systolic hypertension and alkalosis in a dog with HAC due to a functional adrenocortical carcinoma. These abnormalities resolved following surgical resection of the

a Division of Veterinary and Biomedical Sciences, Murdoch University, Murdoch, Western Australia, 6154 Current address: Adelaide Veterinary Specialist & Referral Centre, 102 Magill Road, Norwood, South Australia, 5067

© 2008 The Authors Journal compilation © 2008 Australian Veterinary Association

mass. The possible pathogenesis of these abnormalities, typical of mineralocorticoid excess, is discussed.

Case report A 10-year-old desexed female Maltese-Australian Silky Terrier cross presented to Murdoch University Veterinary Hospital for assessment of complications arising during treatment of HAC. HAC had been diagnosed one month previously with clinical signs of polyuria, polydipsia, polyphagia, abdominomegaly and cutaneous bruising, laboratory findings of increased alkaline phosphatase and alanine aminotransferase activity and supportive low-dose dexamethasone suppression test results (0-hour cortisol 147 nmol/L, 4-hour cortisol 124 nmol/L, 8-hour cortisol 122 nmol/L). Plasma potassium concentration was normal at this time. Testing to differentiate pituitary-dependent hyperadrenocorticism (PDH) from ADH had not been performed prior to treatment with mitotane. An ACTH stimulation test performed 5 days prior to referral, after 15 days of mitotane at approximately 50 mg/kg/day, showed a poststimulation cortisol concentration of 241 nmol/L, indicating inadequate control of HAC.3 Three days later, a gait abnormality with paresis developed. There was no improvement with cage rest and administration of prednisolone (5 mg orally) and carprofen (dose unknown) and the dog was referred for neurological assessment. Physical examination revealed a sparse hair coat with epidermal crusts (typical of superficial pyoderma), abdominomegaly and tachypnoea. The dog had a markedly abnormal gait, with generalised weakness and a shortened limb action. It was unable to walk for more than a few metres at a time and was unable to elevate its head. Neurological examination revealed no abnormalities in cranial nerves, spinal reflexes or nociception. Repeated Doppler sphygmomanometry was indicative of systolic hypertension, at 180 to 220 mmHg.4 Results of initial haematological examination, serum biochemical analysis, urinalysis and urine culture are presented in Table 1 and electrolytes and blood gas analysis in Table 2. Changes consistent with HAC were present, with marked increases in hepatic enzyme activities, marked hypokalaemia and a mild increase in creatine kinase also noted. Blood gas analysis showed metabolic Australian Veterinary Journal Volume 86, No 4, April 2008

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Table 1. Initial haematological, biochemical and urinalysis findings in a ten year-old female desexed Maltese-Australian Silky Terrier cross with adrenaldependent hyperadrenocorticism. Abnormal values are in bold Parameter

Patient Value

Reference Range

Haematology Haemoglobin (g/L)

190

Packed cell volume (L/L)

0.55

120–180 0.37–0.55

Red blood cells (× 1012/L)

8.1

5.5–8.5

Mean corpuscular haemoglobin concentration (g/L)

341

320–360

Mean corpuscular haemoglobin (pg)

23

20–25

Mean corpuscular volume (fL)

69

60–70

Total white blood cells (×109/L)

17.6

6.0–17.0

Neutrophils (×109/L)

14.08

3.0–11.5

Band neutrophils (×109/L)

0.0

0.0–0.3

Lymphocytes (×109/L)

1.41

1.0–4.8

Monocytes (×10 /L)

1.76

0.15–1.35

Eosinophils (×109/L)

0.35

0.15–1.25

Platelets (×1012/L)

Normal

200–900

Prothrombin time (sec)

6