Episode 28 - EXTRA Bonus Episode! Endocrinopathies III - Addison’s disease and the Addisonian Crisis

1.The GP hook

Addison’s can look like everything and nothing: waxing-and-waning GI one day, proper crash the next. Here’s a clear, GP‑friendly route from first suspicion to stabilisation and long‑term management—plus the traps to dodge and the bits we check twice.

Addison’s can look like everything and nothing: vague, waxing-and-waning GI signs one week and a proper crash the next. This note walks you quickly from “could it be?” to stabilisation and long‑term follow‑up — the practical bits that matter in a busy GP clinic.

2.Why Addison’s keeps catching us out

Monday‑morning move

Add Addison’s to your differential when you see recurrent GI signs plus an absent stress leukogram — or a shocked dog with an inappropriately low heart rate.

• It’s uncommon in GP, so you might go years without a case.
• Two common presentations:
• The wax‑and‑wane patient: intermittent vomiting/diarrhoea, inappetence, lethargy that settles then returns.
• The crasher: hypovolaemic/vasodilatory shock, often with surprisingly slow heart rates and biochemical derangements.
• It mimics gastroenteritis, pancreatitis, renal disease, sepsis/SIRS and dietary indiscretion.
• Mostly a canine disease (young–middle‑aged females commonly reported). Very rare in cats.

3.Physiology reset you’ll actually use

• Think “salt, sugar, sex”:
• Salt = aldosterone (mineralocorticoid): keeps sodium — and therefore water — in the circulation; loss → hyponatraemia, dehydration, hyperkalaemia, acidosis.
• Sugar = cortisol (glucocorticoid): supports vascular tone, glucose homeostasis and dampens inflammation — loss → hypotension, hypoglycaemia, exaggerated inflammation.
• Sex = adrenal androgens (less clinically dominant here).
• Typical Addison’s = loss of both cortisol and aldosterone.
• Atypical Addison’s = cortisol deficiency without classic electrolyte changes.

4.The clinical pictures to expect

Clinical pearl: the absence of a stress leukogram (no neutrophilia/lymphopenia pattern) in a very sick dog should make you pause and consider hypoadrenocorticism.

• Wax‑and‑wane: vague GI signs, weight loss, episodic deterioration (often worse with stress such as travel, kennelling or heat).
• Crisis: pale or reddened mucous membranes, poor perfusion, hypotension, often profound bradycardia (eg. 30–60 bpm in some reported cases), dehydration, azotaemia. ECG often reflects the potassium story.
• Key red flag: “shocked but bradycardic” → check electrolytes and ECG urgently.

5.First hour with the crumpled patient

• Immediate priorities:
• IV access and bloods (haematology, biochemistry, electrolytes, glucose). Save serum for cortisol/ACTH‑stim samples if you suspect Addison’s.
• Monitoring: ECG and BP if possible.
• Point‑of‑care ultrasound (POCUS) for chest/abdomen/cardiac impression while labs run — rules in/out sepsis, uroabdomen, major cardiac disease.
• Fluids: resuscitate. Speakers typically use small crystalloid shock boluses and reassess frequently (speaker practice examples were discussed). Follow local protocols/SPCs for exact volumes and rates.

6.Proving (or parking) Addison’s

Common trap: don’t call Addison’s from a low Na:K ratio alone — interpret in the clinical context.

• Typical biochemical picture (classic Addison’s):
• Hyponatraemia, hyperkalaemia, often hypochloraemia, metabolic acidosis, azotaemia, possible hypoglycaemia and low albumin.
• Urine often less concentrated than expected for the degree of dehydration (medullary “washout” from chronic sodium loss).
• Sodium:potassium ratio:
• A low ratio (commonly cited thresholds discussed by the speakers) increases suspicion; a normal ratio does not exclude Addison’s. Many other conditions (GI disease, AKI, urinary obstruction, third‑space losses, hepatic disease, sepsis) can lower the ratio.
• Haematology:
• Look for absence of a stress leukogram in a clinically sick dog — that’s a clue.
• Basal cortisol:
• A reasonably high basal cortisol makes Addison’s unlikely (speakers discussed commonly used thresholds), but low values in sick dogs are nonspecific — follow with ACTH stimulation if suspicious.
• ACTH stimulation test:
• Basal cortisol sample, administer synthetic ACTH, re‑sample at the recommended interval. A flatline response confirms hypoadrenocorticism.
• Atypical Addison’s:
• Electrolytes may be normal. Use basal cortisol as a screening tool; ACTH‑stim if suspicion persists. Repeat electrolytes over time because some dogs progress to mineralocorticoid deficiency.

7.Crisis management — the practical route

Clinical pearl: recheck 30–60 minutes after initial resuscitation — you want to see the direction of travel (K+ trending down, glucose stabilising, renal values improving).

• Fluids first:
• Isotonic balanced crystalloids are the practical first choice; they help circulation and commonly improve potassium. The speakers favoured Hartmann’s in many cases for initial resuscitation. Reassess frequently.
• Avoid hypertonic saline if Addison’s is suspected; rapid large increases in sodium can cause harm. If sodium is very low, involve a referral/intensivist for bespoke correction plans.
• Sodium correction:
• Recheck sodium after initial resuscitation. If it’s rising quickly, seek advice on tailored correction to avoid central nervous system complications.
• Potassium:
• Initial fluid therapy often reduces K+. Speakers commonly used dextrose CRIs (described as low‑percentage solutions at maintenance‑type rates in their practice) to support potassium shifts; they advised caution with insulin because hypoglycaemia can be hard to manage afterwards. Always monitor glucose closely.
• Calcium gluconate is used to stabilise the myocardium when K+ is high — the speakers use slow IV administration with ECG monitoring (this is speaker practice; check your local guidance on dose, rate and monitoring).
• Glucose:
• Hypoglycaemia is common; bolus appropriately and consider a CRI if needed. Again, follow local protocols for concentrations and rates — the speakers described pragmatic approaches used in clinic.
• Steroids in crisis:
• If practical, take ACTH‑stim samples before giving steroids. Dexamethasone does not interfere with the ACTH‑stim test and many clinicians give IV dex early; others prefer to obtain samples first and then give steroids. Hydrocortisone (if available) provides glucocorticoid and some mineralocorticoid activity and may be run as a CRI — check availability and local protocols.
• If you give steroids before sampling, document timing and remember this may affect interpretation depending on the steroid chosen.
• If persistent hypotension after fluids: consider vasopressors. The speakers referenced noradrenaline CRIs in more severe cases (speaker practice ranges were mentioned) — this requires ICU‑level monitoring and verification of local protocols.
• Supportive care:
• Antiemetics (maropitant; add ondansetron if severe nausea), prokinetics for ileus, analgesia as needed, gastric protection if clinically indicated.
• Repeat electrolytes and glucose early (30–60 minutes) to check direction of travel.

8.Long‑term management that works in GP

Practice move: create a one‑page Addison’s protocol for the whole team — consistency saves rechecks, confusion and client anxiety.

• Replace what’s missing:
• Mineralocorticoid replacement with monthly injectable therapy (trade name discussed in the episode).
• Daily physiologic glucocorticoid replacement with oral prednisolone. Speakers discussed different maintenance regimens and stress‑dosing recommendations — individualise and verify against local guidance/SPCs.
• Stress dosing:
• Owners need clear instructions about increasing glucocorticoids during illness, surgery, heat, travel or boarding.
• Check and tweak the injectable mineralocorticoid:
• Monitor at the peak period after injection and later in the dosing interval to ensure dose and interval are appropriate for that dog — adjust based on electrolytes and clinical signs.
• Build a team protocol:
• Agree a practice protocol (initial doses/schedules, day‑10 and day‑25 checks or equivalents, owner handouts) so management is consistent across clinicians and continuity is maintained.

9.Atypical Addison’s — don’t miss the quiet ones

• Normal electrolytes do not exclude Addison’s.
• Basal cortisol is a useful screening test; confirm suspicion with ACTH‑stimulation.
• Watch for low albumin/cholesterol, occasional hypoglycaemia and that absent stress leukogram. Periodic electrolyte monitoring is sensible as some dogs later develop mineralocorticoid deficiency.

10.Quick clinical scenarios

Patient conversation tip: teach owners stress‑dosing early — when to increase pred, when to call, and why kennelling/boarding and heat can unmask Addison’s.

Takeaway

Think Addison’s when recurrent GI signs combine with an absent stress leukogram, odd electrolytes, or a shocked dog with an inappropriately low heart rate. Basal cortisol is a good rule‑out; ACTH‑stimulation confirms. In crisis, prioritise bloods, balanced crystalloids, ECG/BP monitoring, and manage potassium and glucose while securing samples for definitive testing. Long‑term therapy needs both mineralocorticoid and glucocorticoid replacement plus clear owner education and a consistent practice protocol.

Note on doses and rates: the episode speakers discussed specific fluid boluses, steroid and drug doses, CRI concentrations and infusion rates as examples of their practice. Treat those numbers as clinician experience rather than universal guidance — always verify exact doses, concentrations and infusion rates against your local protocols, SPCs and current clinical governance before use.

• Recurrent vague GI in a young dog with normal lytes but low albumin and absent stress leukogram: use basal cortisol as a screen; ACTH‑stim to confirm if low.
• Collapsed dog with azotaemia, low Na, high K and low urine concentration: classic crisis — IV access, balanced crystalloids, ECG/BP monitoring, save ACTH‑stim samples, consider IV dexamethasone once samples taken, serial lytes/glucose, cardioprotection if K+ high, glucose support if needed, and consider vasopressors if refractory hypotension.
• Known Addisonian who can’t keep oral pred down: treat the cortisol gap (antiemetics, consider IV dexamethasone or give parenteral glucocorticoid dose per your clinic protocol) and rule out other GI differentials.