Contributors: Carmel Mooney, Emma Roberts
Species: Feline | Classification: Diseases
- Rare endocrine disease in cats.
- Cause: insufficient mineralocorticoid and glucocorticoid production.
- Diagnosis: ACTH stimulation test ACTH stimulation test.
- Treatment: hormonal replacement therapy.
- Weight loss.
- Vomiting Vomiting.
- Muscle weakness.
- Young to middle-aged (mean 6 years).
- Impaired adrenocortical function.
- Thought to be immune-mediated.
- Other reported causes:
- Adrenal infiltration by lymphoma.
- 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.
- Bilateral adrenal excision (for treatment of hyperadrenocorticism Hyperadrenocorticism).
- Withdrawal of high-level, prolonged corticosteroid treatment.
- 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.
- 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.
- Circulatory collapse.
- Weight loss.
- Weakness (usually episodic).
- Waxing and waning clinical signs.
- Polyuria/polydipsia (adipsia also reported but rare).
- Dysphagia (rare).
- Hypothermia Hypothermia.
- Weak pulse/slow capillary refill time.
- Collapse/inability to rise.
- Abdominal pain.
- 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)
- Decreased [sodium] Blood biochemistry: sodium (130.6 mmol/L).
- Increased [potassium] Blood biochemistry: potassium (6.2 mmol/L).
- Na: K ratio (21.1).
- Decreased chloride Blood biochemistry: chloride (96.3 mmol/L).
- Increase in BUN Blood biochemistry: urea (19.8 mmol/L).
- Increase in creatinine Blood biochemistry: creatinine (282.9 µmol/L).
- Increased phosphate Blood biochemistry: phosphate (2.4 mmol/L).
- Increased creatine kinase Blood biochemistry: creatinine phosphokinase.
- Increased calcium Blood biochemistry: ionized calcium (2.18 mmol/L).
- SG Urinalysis: specific gravity: <1.030 (due to impaired concentrating mechanism) in the presence of azotemia.
Some cats retain the ability to concentrate urine.
- 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).
- Adrenocortical atrophy and destruction.
- Adrenocortical infiltration and destruction (lymphoma).
- 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.
- 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.
- Continue IV fluids until electrolytes are stabilized and animal eating again.
ChronicEither 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.
- 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.
- 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 3 (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.