Rapid Response

Hyponatremia signals acute adrenal insufficiency

Maryann Ward, age 56, is admitted to the chest pain unit. Sara, her nurse, finds her alert and oriented. Mrs. Ward tells Sara her chest pain started yesterday. When assessing her, Sara finds her heart rate (HR) is 60 beats/minute (bpm); blood pressure (BP), 142/58 mm Hg; respiratory rate (RR), 18 breaths/ minute; temperature, 97.7° F (36.5° C); and pulse oximetry, 98% on room air. As ordered, Sara inserts an I.V. line and begins an infusion of 0.9% normal saline solution at 50 mL/hour.

History and assessment hints

Sara notes that Mrs. Ward has a 40-year history of type 1 diabetes, as well as hypothyroidism, hypertension, and hyperlipidemia. She has experienced fatigue and nausea for the last 2 months.

Laboratory results show normal levels of cardiac enzymes, but her sodium and chloride values are below normal. A chest X-ray shows no infiltrates; an electrocardiogram reveals normal sinus rhythm with no ST- or T-wave changes. Mrs. Ward’s physician suspects her low sodium value is a lab error and orders repeat chemistries for the next morning.

On the scene

The next day, Mrs. Ward’s family calls Sara to the bedside to report the patient is feeling worse. Sara obtains a BP of 80/50 mm Hg; HR, 110 bpm; RR, 24 breaths/ minute; and pulse oximetry, 95% on room air. She notes Mrs. Ward is pale, confused, and restless and fails to follow instructions. She vomits her breakfast.

Sara obtains a point-of-care glucose reading, which is slightly elevated at 141 mg/dL. She recalls Mrs. Ward’s low sodium level and that an altered level of consciousness could signal hypothermia, so she calls the rapid response team (RRT).

The laboratory reports that Mrs. Ward’s sodium and chloride levels are again below normal and her glucose level is above normal. The RRT increases her I.V. to 125 mL/hour. Suspecting Mrs. Ward has adrenal insufficiency (AI), they administer dexamethasone I.V. 4 mg and transfer her to the intensive care unit.


There she undergoes a cosyntropin (synthetic ACTH) stimulation test. She experiences no increase in cortisol secretion in response to the cosyntropin injection. On the other hand, her ACTH level is extremely elevated at 1,654 pg/mL. Based on these findings, the physician diagnoses primary AI and prescribes dexamethasone 4 mg I.V. every 6 hours as corticosteroid replacement.

Outcome

About 6 hours after receiving two dexamethasone doses, Mrs. Ward’s mental status normalizes and her nausea resolves. She is transitioned from I.V. dexamethasone to oral hydrocortisone. The physician also prescribes oral fludrocortisone acetate daily as mineralocorticoid replacement. By 24 hours later, her sodium is within normal range. Two days after starting oral hydrocortisone, Mrs. Ward states she feels much better.

Education and follow-up

AI (formerly called Addison’s disease) results from impaired adrenal hormonal secretion. Stress, dehydration, and severe illness can precipitate AI. Common assessment findings include fatigue, hyponatremia, abdominal pain, nausea and vomiting, low blood pressure, and skin hyperpigmentation. AI risk increases in people with other autoimmune disorders. Ms. Ward had two such disorders—type 1 diabetes and hypothyroidism.

Patients with AI have little to no glucocorticoid and mineralocorticoid production and need lifelong replacement. Lacking the body’s normal increase in cortisol production in response to stress, they also need higher steroid doses during illness. To maintain fluid and electrolyte balance, they require mineralocorticoid replacement in the form of fludrocortisone.

Before Mrs. Ward is discharged, the nurse instructs her about her therapy and advises her to wear a medical alert bracelet. She also tells her that if she’s unable to take her hydrocortisone due to nausea or vomiting, she should call her healthcare provider or go to the nearest emergency department.

Katherine Pereira is an associate professor at Duke University School of Nursing in Durham, North Carolina.

Selected references

Betterle C, Morlin L. Autoimmune Addison’s disease. Endocr Dev. 2011;20:161-72.

Bornstein SR. Predisposing factors for adrenal insufficiency. N Engl J Med. 2009;360(22):2328-39.

Charmandari E, Nicolaides NC, Chrousos GP. Adrenal insufficiency. Lancet. 2014;383(9935):2152-67.

Husebye ES, Allolio B, Arlt W, et al. Consensus statement on the diagnosis, treatment and follow‐up of patients with primary adrenal insufficiency. J Intern Med. 2014;275(2):104-15.

 

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