Addisonian Crisis: A Summary of Emergency Presentation, Diagnosis, and Stabilization

Addison's disease in patients can present in many different ways. Learn from Staff Veterinarian Meghan Carlton, DVM about presentation symptoms and emergency stabilization.

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AS “THE GREAT PRETENDER,” Addison's disease (hypoadrenocorticism) can look like just about anything. Thought to be most commonly secondary to immune-mediated adrenalitis, primary Addison's usually results in deficiency of both glucocorticoids (primarily cortisol) and mineralocorticoids (primarily aldosterone). Atypical Addison's is only the deficiency of glucocortoicoids and the patient has normal mineralocorticoid status and electrolyte values. In a crisis, most of the patients you see will be typical Addisonians due to their mineralocorticoid deficiency contributing to their clinical signs of shock and electrolyte derangements.

As a sometimes slippery diagnosis, it is always important to keep on your differential list, however stabilization in the emergency room requires quick recognition of concerning signs and immediate steps towards stabilization and definitive diagnosis. Provided below is a summary of information provided in The Textbook of Veterinary Internal Medicine, 7th Edition, by Stephen J. Ettinger and Edward C. Feldman.

 

PRESENTATION

  • Symptoms can be acute or can be chronic and wax and wane
  • GI signs such as anorexia, vomiting, weakness, lethargy, weight loss, and diarrhea are common, and sometimes polyuria, polydipsia, and abdominal pain can be seen
  • With mineralocorticoid deficiency, you can more commonly see polyuria, polydipsia, hypovolemic shock, collapse, and severe dehydration
  • Less commonly you can see hypoglycemia and even seizures, episodic muscle cramping, and gastrointestinal hemorrhage

 

DIAGNOSTIC FINDINGS

  • CBC changes: many patients will have a nonregenerative anemia (27% of confirmed Addisonian patients), eosinophilia (20%), neutrophilia (32%), lymphocytosis (10%), and almost all will lack a stress leukogram (92%)
  • Chemistry changes: hyperkalemia (95%), hyponatremia (81%), hypochloremia (42%), hypercalcemia (31%), azotemia (88%), hyperphosphatemia (68%), hypoglycemia (17%), increased liver enzymes (30-50%), metabolic acidosis (40%), hypoalbuminemia (6-39%), hypocholesterolemia (7%), USG <1.030 (60%)
    • The Na:K ratio is usually low in dogs with typical Addison's, however this ratio can be normal, especially in dogs with atypical Addison’s disease. Other disorders can also cause changes to the Na:K ratio, including renal and urinary tract disease, GI diseases and cardiorespiratory disease, so it is important to consider other causes of hyponatremia and hyperkalemia when interpreting the Na:K ratio.
  • Thoracic / abdominal radiographs: changes secondary to hypovolemic shock including microcardia, small cranial lobar pulmonary artery, narrow posterior vena cava, microhepatica. There can also be megaesophagus or esophageal dilation though to be secondary to muscle weakness due to cortisol deficiency
  • Abdominal ultrasound: a measurable reduction in the size of the adrenal glands can be observed, however normal sized adrenal glands does not preclude a diagnosis of Addison's
  • ECG: changes secondary to hyperkalemia including peaking of T wave, widening of QRS complex, decreased QRS amplitude, increased duration of P wave, increased PR interval and as values increase there can be loss of P waves, ventricular fibrillation, and asystole

 

DEFINITIVE DIAGNOSIS

  • ACTH stimulation test is the gold standard of definitive diagnosis and should be performed in an emergency situation
    • This test result CANNOT be interpreted if patient recently or currently treated with glucocorticoids (however, in an emergency shock situation dexamethasone SP can be administered prior to or during an ACTH stimulation test)
  • Basal cortisol is a screening test in non-emergency settings: if greater than 2ug/dL then this is diagnostic for the patient NOT having Addison's, if it is less than 2ug/dL then this should prompt you to run an ACTH stimulation test

 

EMERGENCY STABILIZATION

  • Place IVC (cephalic or jugular vein ideal)
  • Replacement crystalloid fluid therapy: correct for hypovolemic shock by titrating 10-20ml/kg IV boluses for a maximum total of 90ml/kg shock bolus; then continue at a 30-80ml/kg/24 hour fluid rate pending clinical response to therapy. Although 0.9% NaCl is often the replacement crystalloid of choice, care must be taken with severely hyponatremic patients not to correct the sodium level too quickly. When hyponatremia is severe, a crystalloid containing a sodium concentration similar to the patient’s sodium, such as Lactated Ringer’s Solution, which contains 130mEq sodium/L2 should be clean.
  • Collect blood and urine samples for CBC, Chemistry with electrolytes, Urinalysis and Baseline cortisol. (Please note a single dose of dexamethasone SP is okay to give prior to collecting baseline cortisol / ACTH stimulation samples if patient is in shock and you feel this is clinically indicated.)
  • If in shock and your suspicion for Addison's is high, administer single dose of dexamethasone SP 0.25mg/kg IV once.
    • Please note that this is lower than Plumb's recommendation!
  • Administer cosyntropin 5mcg/kg (max 250mcg/dog) IV.
  • Collect post sample 1 hour after administration of cosyntropin.
  • Add dexamethasone SP 0.05mg/kg IV q12 until able to switch to oral prednisone.
    • Please note this dose will be lowered for longer-term management and high doses are only necessary in shock scenario.
  • If hyperkalemia present: consider IV glucose (2g / unit of insulin administered) and regular insulin (0.5U / kg) to lower potassium quickly if hyperkalemia is > 6.5 mEq/L or ECG shows changes such as bradycardia, loss of P waves, or prolonged P-R interval. Additionally, consider giving 10% calcium gluconate IV over 10 to 15 minutes (2-10 ml/dog) to protect myocardium from effects of hyperkalemia
    • Clinically, I have seen profound bradycardia result from administration of calcium gluconate, so this should always be given slowly while on ECG monitoring. I always start with the low end of the dosage.
    • If insulin is given, I also always start the patient on 2.5-5% dextrose in the IV fluids and recheck a BG in 1-2 hours for a total of at least 4-6 hours to ensure not seeing hypoglycemia
  • If hypoglycemia present: you can perform an IV bolus of 25% dextrose with BG monitoring q2-4, or you can add 2.5-5% dextrose in IV fluid with glucose monitoring.
  • If acidosis present: consider correction of acidosis (if serum bicarbonate <12 mEq/L). Administer 25% to 50% of calculated dose IV over 6 hours.
    • However, in most cases the acidosis will resolve with fluid support and I personally have not needed to perform this treatment.
  • If anemia due to blood loss present: blood products and colloid support if needed
  • Consider administration of one dose of injectable mineralocorticoid (Percorten V) 2.2mg/kg IM while waiting for diagnosis to be confirmed if suspicion of Addison's is high.
  • Monitor serum electrolytes, blood glucose, acidbase status, blood pressure, UOP if severe azotemia present, ECG if hyperkalemia present.

 

Following these interventions, most patients will respond well with correction of their hypovolemia and electrolyte changes. For longer-term management once the ACTH stimulation test confirms the diagnosis of Addison’s, there are recommendations to find the lowest possible prednisone and DOCP doses and frequencies provided in most internal medicine textbooks. These patients can be managed in primary care clinics, or it is also appropriate to refer them to internal medicine specialists as they can sometimes prove difficult to manage, develop secondary Cushingoid signs, or develop concurrent endocrinopathies.

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