24. Hypoadrenocorticism Flashcards

1
Q

Signalment?

A

Signalment:
Uncommon In the dog and rare in the cat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pathophysiology?

A

canine hypoadrenocorticism:
Pathophysiology:
Primary hypoadrenocorticism (Addison’s disease):
- Destruction of the adrenal cortex, most commonly Immune-mediated
- Leads to mineralocorticoid and glucocorticoid deficiencies
- Isolated hypocortisolism (Atypical Hypoadrenocorticism):
>Hypocortisolaemia without mineralocorticoid deficiency:
Isolated destruction of the zona fasciculate
Secondary: Reduced ACTH secretion due to pituitary gland pathology
Iatrogenic: Post corticosteroid therapy or treatment of hyperadrenocorticism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clinical signs?

A

Clinical signs:
- Acute presentation = Addisonian crisis
- Vomiting and diarrhoea,
lethargy and weakness,
anorexia and PU/PD
- Chronic Intermittent gastrointestinal signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Diagnosis?

A

Diagnosis:
- Biochemistry, haematology, electrolytes and urinalysis
- No stress leukogram (No eosinopenia, lymphopenia and neutrophilia} and mild anaemia (possibly masked by dehydration}
> Azotaemia (pre-renal}, hypochotesterolaemia, hypoalbumlnaemia
> Hypoglycaemia, +/- hypercalcaemia
Electrolyte abnormalities:
Due to aldosterone deficiency
» Hyponatraemia (Na+ <140mmoVL}
;., Hyperkalaemia (K+ >5.6mmol/L)
» Sodium: potassium, ratio (Na+:K+):
Ratio less than 25:1 is considered suggestive
* Ratio less than 15:1 virtually diagnostic
Differentials for low Na+:K+ ratio Include whipworm, acute kidney injury, effusions,
gastrointestinal Inflammation
;> NOTE:
*
Electrolyte abnormalities are due to mineralocorticoid deficiency, in “isolated
hypoadrenocorticism* the electrolytes are normal or may get hyponatraemia
Dehydration: May mask the hyponatraemia and hypochloraemia
* Blood results may appear like renal failure
» USG: <1.030 due to medullary washout from Na+ loss
ACTH stimulation test:
> Definitive diagnostic test
» Hypoadrenocorticism = No response In cortisol concentration to simulation = pre and· post-ACTH
cortisol measurements < 5nmol/L
> Normal cortisol response to ACTH testing = Extremely unlikely to be hypoadrenocorticism
: Does not distinguish between primary and secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Treatment?

A

Treatment:
Emergency therapy of acute adrenal crisis;
- Correct perfusion and dehydration deficits
- Correct electrolyte and acid-base imbalances
- Supply mineralocorticoids and glucocorticoids
Protocol:
- Collect blood for baseline diagnostics
- Haematology, biochemistry, electrolytes and resting cortisol levers
- IV catheter and select/create IV fluid with Na+ concentration within 10 mmol of the patient’s Na+
-Severe hyponatraemia:
-aim for gradual increase less than 1mmol/hr if less than 130mmol/L
-Correct perfusion deficits with a low sodium fluid
- Correct dehydration deficits, half of the fluid deficits over the following 6 hours, then the rest over next 24 hours
- Perform an ACTH stimulation test and avoid glucocorticoid therapy until completion
- Steroid supplementation:
- Dexamethasone phosphate 0.5mg/kg IV, then reduce to 0.1mg/kg IV BID
- Hydrocortisone sodium succinate CRI 0.5mg/kg/hr
-Commence oral therapy once eating and no vomiting
- Mineralocorticoid supplement - to correct electrolyte derangement:
- Single injection of desoxycortisone pivalate 2.2mg/kg IM/SC q25days OR Fludrocortisone (Florinef®) 0.01mg/kg) day PO BID
- Not required In less common cases of glucocorticoid-dependent (secondary) hypoadrenocorticism
- Severe hyperkalaemia
- Metabolic acidosis
- Once stabilised and eating, transition to maintenance therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Monitoring?

A

Monitoring:
-Reassessment of vitals, CRT and pulse pressure and hydration status every 4 hours
- ECG: Monitored every two hours until hyperkalaemia changes subside
-Electrolytes: Every four to eight hours
- Others: PCV/TP, CVP, urine output, and renal function, blood gases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Maintenance therapy?

A

Maintenance therapy:
Mineralocorticoids: lifelong therapy may be required
- Fludrocortisone [Florinef ®]
- Given orally at 0.01mg/kg/day BID
- Dosage adjusted by measuring serum electrolytes
- Re-evaluated every week until stabilised, then every 3 to 4 months
- May need to increase dose over the first 12 to 18 months, until fully stable
Desoxycortisone pivalate (DOCP):
- Pure mineralocorticoid, long-acting IM injection every 25 days
- Starting dose of 2.2mg/kg every 25 days
- Electrolytes are re-evaluated every week until stabilised, then every 3 to 4 months
- Can try to extend dosing interval with DOCP:
If normal electrolytes Increase dose Interval by 1 to 2 days each time up to 30 day dosing If stable
* If levels are abnormal, reduce the Interval
Glucocortlcolds:
- May need In conjunction with mineralocorticoid supplementation
- Prednisolone: Prednisolone 0.1-0.3mg/kg PO BID, In times of stress, Increase dose to 1-2mg/kg PO
./ Cortisone acetate: 0.5mg/kg PO SID to BID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly