⚠ Addisonian Crisis — This is an Emergency

An Addisonian crisis (acute hypoadrenocorticism) is a life-threatening emergency. Collapsed, weak dogs with bradycardia and poor pulses need immediate IV fluid therapy and glucocorticoid injection. Do not delay. Mortality rises rapidly without treatment. If you suspect Addisonian crisis in a collapsed dog with weak pulses and bradycardia — treat first, test second.

Overview

Addison's disease results from deficient adrenal hormone production. Primary hypoadrenocorticism — immune-mediated destruction of the adrenal cortex (most common, ~95% of cases) — causes deficiency of both cortisol and aldosterone. Secondary hypoadrenocorticism — pituitary ACTH deficiency from long-term glucocorticoid use or pituitary disease — causes cortisol deficiency only, with normal aldosterone (electrolytes normal). Aldosterone deficiency causes sodium wasting and potassium retention → hyponatremia, hyperkalemia, and hypovolemia. Cortisol deficiency causes anorexia, vomiting, lethargy, and poor stress response. The clinical signs are caused by the combined loss of both hormones. Most dogs present in crisis, but some show milder chronic signs for months. The classic presentation: a young-to-middle-aged female dog with chronic GI signs, weakness, and bradycardia.

Common Clinical Signs

Lethargy and weakness Vomiting Diarrhea Anorexia Bradycardia (unusually slow heart rate for the dog's size) Weak peripheral pulses Hypothermia Collapse (Addisonian crisis) Weight loss Polyuria / polydipsia (less prominent than in Cushing's or renal disease)

Diagnostic Approach

Diagnostic Test Findings in Addison's Disease
Serum Electrolytes (Critical First Step) Hyponatremia (Na <135 mEq/L) — from aldosterone deficiency (sodium wasting). Hyperkalemia (K >5.5 mEq/L) — from aldosterone deficiency (reduced renal K excretion). Na:K ratio <27:1 — classic Addisonian marker. Not all Addisonian dogs show this pattern (atypical Addison's with normal electrolytes from partial aldosterone preservation).
ACTH Stimulation Test (Gold Standard) No cortisol response to cosyntropin. Baseline cortisol drawn, then cosyntropin (5 µg/kg IV/IM) given, cortisol re-measured at 60 minutes. Post-ACTH cortisol <2 µg/dL in both samples confirms hypoadrenocorticism. Can be done on a single sample if baseline is very low. Perform before starting steroids if possible — steroids will invalidate the test.
Endogenous ACTH Level Markedly elevated in primary Addison's (pituitary trying to stimulate destroyed adrenals). Normal in secondary Addison's. Run on EDTA plasma, transported cold. Differentiates primary from secondary — important for prognosis and workup of underlying cause.
Complete Blood Count (CBC) Lack of stress leukogram — Addisonian dogs are too ill to mount a stress response, so despite severe illness they have normal or low WBC. Eosinophilia and lymphocytosis may be present (normally suppressed by cortisol). Normocytic, normochromic anemia (likely from dilutional effect of hypovolemia).
Serum Chemistry Panel Azotemia (pre-renal from hypovolemia). Hypoglycaemia (common in Addisonian crisis — cortisol is gluconeogenic). Hypoalbuminemia and hypocholesterolemia. Elevated CK (muscle damage from hypovolemia). Hypocalcaemia occasionally.
ECG (Electrocardiogram) Hyperkalemia changes: peaked T waves, prolonged PR interval, widened QRS complex, bradycardia. If ECG changes are present with hyperkalaemia — this is an emergency requiring immediate IV calcium (cardiac membrane stabilizer) and insulin/dextrose therapy.

Differential Diagnoses

  • Gastrointestinal disease (pancreatitis, IBD) — Shares vomiting, diarrhea, weakness. No electrolyte abnormalities of Addison's pattern. Abdominal ultrasound differentiates. Lipase and specPL differentiate pancreatitis.
  • Chronic kidney disease — Azotemia and isosthenuria present. No hyperkalemia in CKD unless advanced. BUN:creatinine ratio may be high in Addison's (prerenal). USG is dilute in CKD but may also be dilute in Addison's. Electrolytes and ACTH stimulation differentiate.
  • GDV (bloat) — Acute abdominal emergency with weakness, collapse. Usually large, deep-chested breeds. Abdominal distension and tympany. Radiographs confirm — stomach distended, possibly with compartmentalization in volvulus.
  • Sepsis / endotoxemia — Weakness, vomiting, collapse. Hypothermia + fever are possible. Often hyperdynamic (tachycardic) rather than bradycardic. May have pyrexia. Leukogram may show left shift or toxemia rather than lack of stress response.
  • Hyperkalemia from other causes — Acute kidney injury, urinary obstruction. These also cause hyperkalaemia. History, urinalysis, and ACTH stimulation differentiate.

Treatment

Addisonian crisis (emergency): Immediate IV fluid therapy (0.9% NaCl bolus of 20-30 mL/kg over 20 min, repeat as needed). IV methylprednisolone or hydrocortisone (10-20 mg/kg loading dose). If ECG changes from hyperkalemia: IV calcium gluconate (50 mg/kg slowly) — cardiac membrane stabilizer. Followed by insulin (0.1 U/kg regular insulin IM) + dextrose (2 mL/kg of 50% dextrose diluted, IV) or 10% dextrose CRI. Long-term management: Prednisolone (0.2-0.5 mg/kg/day PO) for glucocorticoid replacement + DOCP (desoxycorticosterone pivalate/Percorten-V, 2.2 mg/kg IM q25 days) or fludrocortisone acetate (0.02-0.05 mg/kg/day PO) for mineralocorticoid replacement. Dogs on DOCP still need glucocorticoid supplementation — they lack both hormones.