Everything the nurse needs to know about Addison’s disease
Hypoadrenocorticism or Addison’s disease is characterized by low circulating steroid levels. In most cases, this is caused by immune-mediated adrenalitis, but in rare cases can be caused by necrosis or amyloidosis. It is also seen in patients on excessive doses of Cushing’s treatment (trilostane).
When we talk steroids, we are focussing on two main types:
1) Glucocorticoids, e.g. cortisol, produced by the zona fasciculata in the adrenal cortex, and
2) Mineralocorticoids, e.g. aldosterone, produced by the zona glomerulosa in the adrenal cortex.
The clinical signs we see in our Addisonian patient depend on whether cortisol, aldosterone or both hormones are deficient.
Clinical Signs
Addisons disease is termed 'The Great Pretender' as many clinical signs are initially non-specific and easily mistaken for gastrointestinal disease. These include diarrhoea, lethargy, anorexia, dehydration and vomiting, and are associated with cortisol loss. Other signs include PU/PD, abdominal pain and signs of shock. Classically, the Addisonian crisis patient presents with lethargy and dehydration/hypovolaemia, and signs of hyperkalaemia/hyponatraemia may be apparent, such as bradycardia and cardiac arrhythmias. This is associated with the loss of aldosterone, as this hormone is responsible for retaining sodium and excreting potassium in the kidney. The loss of aldosterone, therefore, causes increased sodium loss, and reduced potassium excretion, causing hyponatraemia and hyperkalaemia.
Diagnosis
There are several tests performed in a patient with suspected Hypoadrenocorticism, including:
Basal cortisol levels: These can be used as an initial 'screening' test. A low result (<55mmol/L) should be followed up with confirmatory testing such as an ACTH stimulation test.
ACTH stimulation test: This is the collection of a baseline serum cortisol sample, followed by a 5mcg/kg injection of synthetic ACTH, and a repeat cortisol sample collected 1-hour post-injection. A failure to stimulate will be seen in an Addisonian patient.
Serum electrolyte levels: These may be within normal limits or hyponatraemia and hyperkalaemia may be seen, depending on the degree of aldosterone loss. The ratio of sodium to potassium should also be evaluated even if the electrolyte results are within the reference range. A Na:K ratio of <27:1 (27mmol sodium for every 1mmol potassium) is seen in 95% of Addisonian dogs.
Haematology: these patients may have mild non-regenerative anaemia and lack a stress leukogram (neutrophilia, monocytosis, lymphopenia and eosinopenia).
Serum biochemistry: Addisonian patients may have any of the following biochemical changes: hypoglycaemia, hypercalcaemia, hyperphosphataemia, hypoalbuminaemia and increased liver enzymes.
Abdominal imaging may show small adrenal glands.
Stabilising the Crisis Patient
Stabilisation of the Addisonian crisis patient includes some or all of the following, depending on the patient's presentation:
Protection of the heart from high potassium levels (calcium gluconate administration)
Fluid resuscitation to correct fluid deficits and metabolic acidosis with an appropriate crystalloid solution
Administration of glucose to correct hypoglycaemia
Collection of samples to confirm the diagnosis (before steroids are given as most of these will cross-react with cortisol testing - dexamethasone can be given in an emergency and will not cross-react with an ACTH stimulation test)
Slow correction of hyponatraemia with fluid therapy (rate of sodium correction should not exceed 0.5mmol/kg/hour)
Administration of steroids
Treatment
Treatment of the Addisonian patient includes the administration of exogenous glucocorticoid (prednisolone) and mineralocorticoid (desoxycorticosterone pivilate or DOCP) to replace those deficient hormones. Response to treatment is monitored with regular blood samples for serum electrolyte (Na:K) levels, alongside clinical examination and client history collection. Dosages may need to be adjusted long-term during periods of increased stress, such as during illness, injury or planned anaesthesia/surgery.
Nursing Considerations
Patients in Addisonian crisis should be intensively monitored including continuous ECG and regular blood pressure assessment. All patients should receive a regular clinical examination, assessment of hydration and perfusion parameters, regular toileting opportunities in case of PU/PD, grooming and coat care in case of gastrointestinal signs, and other appropriate symptomatic treatment and nursing care depending on the individual patient.
Steps should be taken to minimise stress during hospitalisation as Addisonian patients cannot surmount an appropriate stress response. Anaesthesia should be avoided wherever possible, especially in an unstable or crisis patient. Where anaesthesia is required in a stable or previously diagnosed patient, they should be appropriately fluid resuscitated and have appropriate electrolyte derangement correction, and premedicated with steroid in addition to analgesic/sedative medications as prescribed by the veterinary surgeon.
References
Lotatti, M. 2014. Canine hypoadrenocorticism: overview, diagnosis and treatment. Today's Veterinary Practice, [Online], Available from: https://todaysveterinarypractice.com/canine-hypoadrenocorticism-overview-diagnosis-treatment/
Merrill, L. 2012. Small Animal Internal Medicine for Veterinary Technicians and Nurses. Iowa: Wiley-Blackwell.
Nelson, R W. and Couto, C G. Small Animal Internal Medicine. 5th ed. Missouri: Elsevier Mosby, 2014.
