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Tag: ACTH

  • Handling an Addisonian crisis – part 2

    Handling an Addisonian crisis – part 2

    Managing an Addisonian crisis can be daunting, especially when the patient looks like it is about to check out and its baseline bloods show a sodium of 110mmol/L, a potassium of 8mmol/L and a glucose of 2.3mmol/L. That is enough to make anyone’s brain explode.

    The patient can be treated in many ways, but I find it useful to try to simplify and prioritise. I have outlined my thought process in the hope some of you will find it helpful.

    First 10 minutes: protect heart and manage hypoglycaemia

    • Protect the heart – calcium gluconate 10% 0.5mL/kg to 1.5mL/kg slow IV over 10 minutes to counter the effects of hyperkalaemia on cardiac electrical activity. This buys about 20 minutes of time.
    • Treat the hypoglycaemia – the dose depends on the severity, but 0.5ml/kg of 50% dextrose IV diluted 50:50 with Hartmann’s is a good place to start. This dose of dextrose will also help correct hyperkalaemia by stimulating endogenous insulin release.

    First 20 minutes: start addressing perfusion deficits

    • Create a custom IV fluid – I do not aim to increase sodium concentration at all at this stage. I am a big fan of creating custom IV fluids. I create a fluid with a same sodium concentration as the patient then use boluses of this fluid to correct signs of shock without concerns of increasing the sodium. I use Hartmann’s as my base fluid – it has the lowest sodium concentration – and add 5% dextrose to reduce the sodium concentration (you may need to remove 100ml to 200ml from the bag first). I usually run the new fluid through the electrolyte machine to check the final sodium concentration.
    • Hartmann’s contains buffers that help address metabolic acidosis (and hyperkalaemia). It also contains potassium; however, if this concentration is less than that of serum it will still help to dilute serum potassium.
    • The formula I use to create a custom sodium IV fluid bag is beyond the scope of this blog and is detailed in the fluid therapy chapter of my book, The MiniVet Guide, under hyponatraemia.

    First hour: address hyperkalaemia

    • Image © mintra / Adobe Stock
      The author warns not to rush the sodium increase in patients. Image © mintra / Adobe Stock

      If the hyperkalaemia is severe enough to warrant more aggressive management than alkalinising IV fluids, improving renal perfusion and providing a dextrose bolus (such as potassium of more than 7mmol/L to 8mmol/L) then I would use regular short acting insulin at 0.25U/kg to 0.5U/kg IV. This should always be used in combination with a bolus of dextrose at 2g of dextrose per unit of insulin or 4ml of 50% dextrose for each unit of insulin, followed by a CRI of 2.5% to 5% glucose until insulin wears off (this could be up to six hours). This should prevent hypoglycaemia.

    • I administer dexamethasone up to 0.5mg/kg IV while running the adrenocorticotropic hormone (ACTH) stimulation test. This is the only corticosteroid that can be given as it does not cross react with the ACTH stimulation test.

    Next 2 to 24 hours: correct hydration and correct hyponatraemia

    • After I have corrected perfusion deficits with my custom IV fluid, I will address hydration deficits with an appropriate fluid plan over the next 24 hours. I usually replace 50% of the hydration deficit over the first 6 hours then the remaining 50% over the following 18 hours.
    • Correction of hyponatraemia can take a couple days as sodium should only be increased by 0.5mmol/L/hr (max 12mmol/L/day). If the sodium has not increased from the initial fluids given, I would create another custom IV fluid bag with a sodium concentration 10mmol/L above that of the patient’s. I would monitor electrolytes every one to four hours, depending on response.

    Supply mineralocorticoids and glucocorticoids

    • Options for steroid supplementation include dexamethasone 0.5mg/kg IV then 0.1mg/kg IV q12hrs or IV hydrocortisone sodium succinate at 0.5mg/kg/hr. Personally I use hydrocortisone CRI, asit has equal mineralocorticoid and glucocorticoid activity. Oral steroids can be used once the patient starts eating and drinking.
    • I only use a mineralocorticoid if I see no increase in sodium after starting hydrocortisone, despite using a fluid with a higher sodium concentration than the patient.

    Addressing patients this way will generally gets them out of the crisis. One thing that I don’t do is rush the sodium increase, it can take time and I am good with that. I have seen patients develop neurological signs from sodium levels that have increased too quickly. As for the long term management; well, I will leave that to you.

  • SNAP cortisol test

    SNAP cortisol test

    While hyperadrenocorticism is not an uncommon incidental finding in patients presenting to our emergency clinic, hypoadrenocorticism is a lot less common. Or, possibly, more frequently underdiagnosed.

    Textbook clinical presentations combined with haematology and biochemicial changes can make diagnosis straightforward, but not all patients will present with all the classic signs.

    SNAP cortisol test
    The SNAP cortisol test is a quantitative ELISA test that measures the level of serum cortisol in dogs.

    To complicate things further, hypoadrenocorticism is the great mimicker of diseases; it is often impossible to arrive at a definitive diagnosis without knowing the cortisol levels.

    The SNAP cortisol test allows clinicians to determine cortisol levels in-house – a blessing to those of us who work out-of-hours – but is not without its limitations.

    Suspicious signs

    Patients with hypoadrenocorticism often present with vague and non-specific clinical signs, but certain clinicopathological changes help raise the suspicion:

    • a decrease in sodium-to-potassium ratio (below 1:27)
    • azotaemia
    • an inappropriately low urinary specific gravity, despite evidence of dehydration or hypovolaemia
    • a leukogram unfitting to the degree of illness of the patient (a “reverse stress leukogram”- neutropenia, lymphocytosis, eosinophilia)
    • anaemia
    • hypoglycaemia
    • hypercalcaemia

    Although most Addisonian patients will not present with all these signs – especially those in the early stages of disease or those with atypical Addisonian disease (glucocorticoid insufficiency only) – any patients showing any of these haematology and biochemicial changes should have hypoadrenocorticism ruled out as part of the diagnostic plan.

    Imperfect ELISA

    The SNAP cortisol test has been advertised as an in-house assay to aid the diagnosis, treatment and management of both hyperadrenocorticism and hypoadrenocorticism, although the quality of the result is not perfect. This quantitative ELISA test measures the level of serum cortisol in dogs.

    In one study1, the SNAP cortisol test appears to have a good correlation with an external laboratory chemiluminescent assay test; however, in 12.8% of cases (5 of 39 patients), the SNAP test result could have led to a different clinical decision regarding the management of the patient.

    Since long-term Cushing’s management relies on reliable, repeatable cortisol level detection, this high level of discrepancy is unacceptable, especially when more accurate alternatives are available at external laboratories.

    Still useful

    Despite this, it is still very useful helping to assess for the presence or absence of hypoadrenocorticism, especially in an emergency setting.

    I use the SNAP cortisol to measure the resting cortisol level. If it is below 2ug/dL or in inconclusive range (between 2ug/L and 6ug/L), but the clinical picture suggests hypoadrenocorticism, I would perform an adrenocorticotropic hormone (ACTH) stimulation test and send samples to an external laboratory. If it is well above the inconclusive range, I would not perform an ACTH stimulation test.

    In summary, I think the SNAP cortisol test can be useful in helping assess for hypoadrenocorticism, but would still recommend performing an ACTH stimulation test and running the samples externally.

    However, use it with caution for hyperadrenocorticism diagnosis and its long-term management – especially when more accurate and economical alternatives are available.