Contributors: Carmel Mooney, Emma Roberts

 Species: Feline   |   Classification: Diseases

Introduction Pathogenesis Diagnosis Treatment Outcomes Further Reading


  • Rare endocrine disease in cats.
  • Cause: insufficient mineralocorticoid and glucocorticoid production.
  • Diagnosis: ACTH stimulation test ACTH stimulation test.
  • Treatment: hormonal replacement therapy.

Presenting Signs

  • Weight loss.
  • Anorexia.
  • Lethargy/depression.
  • Vomiting Vomiting.
  • Collapse.
  • Muscle weakness.
  • Polyuria.
  • Polydipsia.
  • Dysphagia.

Age Predisposition

  • Young to middle-aged (mean 6 years).



  • Impaired adrenocortical function.
  • Thought to be immune-mediated.
  • Other reported causes:
    • Adrenal infiltration by lymphoma.
    • Trauma-induced.
    • Secondary hypoadrenocorticism caused by lymphocytic panhypophysitis has been reported in one case.
    • Iatrogenic secondary hypoadrenocorticism can occur following cessation of chronic corticosteroid treatment.
    • Atyical hypoadrenocorticism (lack of glucocorticoid production but not mineralocorticoids) reported in one case BUT aldosterone levels were not checked.

Predisposing Factors


  • Iatrogenic:
    • Bilateral adrenal excision (for treatment of hyperadrenocorticism Hyperadrenocorticism).
    • Withdrawal of high-level, prolonged corticosteroid treatment.


Aldosterone deficiency

  • Reduced ability to conserve sodium and chloride and excrete potassium and hydrogen ions.
  • Sodium loss may be further increased by vomiting/diarrhea and intake reduced by anorexia.  
  • Depletion of total body salt stores leads to volume depletion.
  • Reduced renal perfusion  → further increase in hyperkalemia  →  reduced myocardial excitability.

Glucocorticoid deficiency

  • Reduced gluconeogenesis + fat metabolism may  →  hypoglycemia  Hypoglycemia.
  • Reduced cortisol to the CNS may lead to lethargy and depression.
  • Cortisol also required for intestinal integrity and reduction contributes to vomiting, diarrhea and inappetence.
  • Cortisol stimulates appetite and red blood cell production, therefore deficiency can result in inappetence and anemia.
  • In 1° adrenal insufficiency →  increased ACTH secretion from pituitary →  impaired tolerance to stress.


  • Days to months.


Presenting Problems

  • Depression.
  • Weakness.
  • Anorexia.
  • Circulatory collapse.

Client History

  • Lethargy/depression.
  • Anorexia.
  • Weight loss.
  • Vomiting.
  • Weakness (usually episodic).
  • Waxing and waning clinical signs.
  • Polyuria/polydipsia (adipsia also reported but rare).
  • Dysphagia (rare).

Clinical Signs

  • Depression.
  • Weakness.
  • Weak pulse/slow capillary refill time.
  • Collapse/inability to rise.
  • Bradycardia.
  • Abdominal pain.

Diagnostic Investigation


  • Mild anemia (but may be masked by hemoconcentration): mean PCV 29.5% Hematology: packed cell volume.
  • Lymphocytosis and eosinophilia can be seen (rare).


(the mean value of biochemical parameters from a study that assessed 10 cats with hypoadrenocorticism are shown in brackets)


  • SG Urinalysis: specific gravity: <1.030 (due to impaired concentrating mechanism) in the presence of azotemia.
    Some cats retain the ability to concentrate urine.

Hormonal assay

  • ACTH stimulation test ACTH stimulation test (definitive).
  • Plasma [cortisol] undetectable or low normal initially with a minimal to no response to ACTH.
  • Normal levels:
    • Pre-ACTH 10-140 nmol/L.
    • Post-ACTH 140-415 nmol/L.
  • Endogenous [ACTH] will be elevated in primary hypoadrenocorticism due to lack of negative feedback.


  • Microcardia - due to dehydration and hypovolemia.
  • Hypoperfusion of lungs


  • Sinus bradycardia (not common) ECG: overview .
  • Atrial premature complexes (not common).

Histopathology Findings

  • Adrenocortical atrophy and destruction.
  • Adrenocortical infiltration and destruction (lymphoma).

Differential Diagnosis

  • Hemolysis of sample may falsely elevate [potassium] with some automated analyzers.
  • Urinary disease including acute renal failure Kidney: acute renal failure and urethral outflow obstruction.
  • Gastrointestinal disease.
  • Ascites/pleural effusion.
  • Endocrine disease (including diabetes mellitus).

Causes of hypovolemia or shock can include

  • Gastrointestinal disease.
  • Acute and chronic blood loss.
  • Repeated drainage of chylous and non-chylous pleural effusions Pleural effusion.


Standard Treatment

Acute crisis

  • Rapid infusion of 0.9% saline over 2-4 hours to restore blood pressure and replace fluid deficits.
  • Intravenous glucocorticoids: Perform ACTH stimulation test before administering glucocorticoids.
    • Hydrocortisone sodium succinate (2-4 mg/kg q4-8 h extrapolated from dogs) Hydrocortisone.
    • Dexamethasone sodium phosphate (0.1-2 mg/kg IV or IM q12 h) Dexamethasone.
  • Continue IV fluids until electrolytes are stabilized and animal eating again.


Either Fludrocortisone acetate (0.05 - 0.1 mg/cat/day PO BID) Fludrocortisone.
Or Desoxycorticosterone acetate (mineralocorticoid) (reported doses include 10-12.5 mg IM or 2.2 mg/kg IM every 25 days) combined with prednisolone (reported starting doses 1.15-5 mg/day) tapered to the minimal dose that controls clinical signs). Glucocorticoid supplementation can also be provided in cats that are difficult to handle with methylprednisolone acetate at 10 mg/month IM.
  • Additional prednisolone may be needed at times of stress Prednisolone.
  • If truly an atypical case, then glucocortocoids supplementation needed only.
  • Water ad lib.


  • Usually show rapid response to therapy (within 1-2 hours).
    Lethargy, weakness and anorexia may persist for 3-5 days after treatment started.
  • [Sodium] and [potassium]: normalizing.
  • Azotemia resolving.

Subsequent Management


  • Lifelong therapy.
  • Regular monitoring of Na: K ratio.
  • Increased dose of glucocorticoid during periods of stress.



  • Excellent once adrenal crisis is controlled and not caused by lymphoma.
  • If induced by trauma, hypoadrenocorticism may be transient.

Expected Response to Treatment

Reasons for Treatment Failure

  • Initial therapy and monitoring not sufficiently aggressive.
  • Owner not realizing importance of:
    • Lifelong therapy.
    • Regular monitoring.
    • Need to increase glucocorticoid dose during stress.

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Rudinsky A J, Clark E S, Russell D S et al (2015) Adrenal insufficiency secondary to lymphocytic panhypophysitis in a cat. Aus Vet J 93 (9), 327-331 PubMed.
  • Woolcock A D & Ward C (2015) Successful treatment of a cat with primary hypoadrenocorticism and severe hyponatremia with desoxycorticosterone pivalate (DOCP). Can Vet J 56 (11), 1158-1160 PubMed
  • Sicken J & Neiger R (2013) Addisonian crisis and severe acidosis in a cat: a case of feline hypoadrenocorticism. J Fel Med Surg 15 (10), 941-944 PubMed.
  • Hock C E (2011) Atypical hypoadrenocorticism in a Birman cat. Can Vet J 52 (8), 893-896 PubMed.
  • Bell R, Mellor D J, Ramsey I et al (2005) Decreased sodium:potassium ratio in cats: 49 cases. Vet Clin Pathol 34 (2), 110-114 PubMed.
  • Gunn-Moore D (2005) Feline endocrinopathies. Vet Clin North Am Sm Anim Pract 35 (1), 171-210 PubMed.
  • Smith S A, Freeman L C & Bagladi-Swanson M (2002) Hypercalcemia due to iatrogenic secondary hypoadrenocorticism and diabetes mellitus in a cat. JAAHA 38 (1), 41-44 PubMed.
  • Stonehewer J & Tasker S (2001) Hypoadrenocorticism in a cat. JSAP 42 (4), 186-190 PubMed.
  • Parnell N K, Powell L L, Hohenhaus A E et al (1999) Hypoadrenocorticism as the primary manifestation of lymphoma in two cats. JAVMA 214 (8), 1200, 1208-1211 PubMed.
  • Peterson M E, Greco D S, Orth D N (1989) Primary hypoadrenocorticism in ten cats. JVIM (2), 55-58 PubMed.

Other sources of information

  • Scott-Moncrieff J C (2015) Hypoadrenocorticism. In: Canine and Feline Endocrinology. 4th edn. Feldman E C, Nelson R W, Reusch C R & Scott-Moncrieff J C (eds). St Louis, Missouri. Elsevier Saunders. pp 514-516.
  • Scott-Moncrieff J C (2010) Hypoadrenocorticism. In: Textbook of Veterinary Internal Medicine. 7th edn. Ettinger S J & Feldman E C (eds). St Louis, Missouri. Elsevier Saunders. p 1857.

Other Sources of Information