Yes—Simultaneous Adrenal Crisis and Central Diabetes Insipidus Can Occur with a Suprasellar Mass
A patient with a suprasellar mass can absolutely develop both adrenal crisis (from secondary adrenal insufficiency) and central diabetes insipidus at the same time, and recognizing this dual presentation is critical because initiating glucocorticoid replacement will unmask the diabetes insipidus, potentially causing life-threatening hypernatremia if not anticipated. 1, 2, 3
Why Both Conditions Occur Together
Suprasellar masses commonly damage both the anterior pituitary (causing ACTH deficiency and secondary adrenal insufficiency) and the posterior pituitary or hypothalamic-neurohypophyseal axis (causing central diabetes insipidus). 4
Multiple pathologies can cause this dual presentation, including craniopharyngioma, meningioma, Rathke cleft cyst, germ-line tumors, lymphoma, leukemia, Langerhans cell histiocytosis, metastases, sarcoidosis, lymphocytic hypophysitis, and granulomatous infiltration. 4
In Langerhans cell histiocytosis specifically, 20–30% of patients develop diabetes insipidus, and among those with diabetes insipidus, 70–90% will develop anterior pituitary hormone deficits (including ACTH deficiency) within 5 years. 4
The Critical "Masking" Phenomenon
Secondary adrenal insufficiency masks the typical hypernatremia of diabetes insipidus because low cortisol impairs renal free-water clearance, leading to hyponatremia instead. 1, 2, 3
When you administer hydrocortisone to treat the adrenal crisis, you restore free-water clearance, which unmasks the underlying diabetes insipidus—the patient will then develop severe polyuria (often >6 L/day), hypernatremia (sodium can rise to 151 mmol/L or higher), and critical dehydration. 1, 2, 3
This unmasking can occur within hours to days of starting glucocorticoid replacement. 1, 3
Diagnostic Clues Before Treatment
Hyponatremia is present in approximately 90% of patients with secondary adrenal insufficiency, so a suprasellar mass patient presenting with hyponatremia should raise suspicion for ACTH deficiency. 5
Hyperkalemia is typically absent in secondary adrenal insufficiency (unlike primary adrenal failure) because aldosterone secretion remains intact; its absence should not exclude the diagnosis. 5
Low or inappropriately normal ACTH with low cortisol distinguishes secondary from primary adrenal insufficiency (where ACTH is markedly elevated). 5
MRI with high-resolution pituitary protocols is the gold standard for detecting suprasellar masses and abnormalities of the hypothalamic-neurohypophyseal axis that cause both conditions. 4
Loss of the normal T1 hyperintensity of the posterior pituitary ("bright spot") on MRI suggests diabetes insipidus, though this finding may be absent in long-standing disease. 4
Emergency Management Algorithm
Step 1: Immediate Treatment of Suspected Adrenal Crisis (Do Not Delay)
Administer hydrocortisone 100 mg IV bolus immediately upon clinical suspicion (hypotension, dehydration, nausea/vomiting, altered mental status, hyponatremia). 5
Begin aggressive fluid resuscitation with 0.9% isotonic saline 1 L over the first hour. 5
Draw blood for cortisol, ACTH, electrolytes (sodium, potassium), creatinine, glucose, and osmolality before treatment if feasible, but never delay therapy. 5
Step 2: Anticipate and Monitor for Unmasking of Diabetes Insipidus
Once hydrocortisone is started, monitor urine output hourly and serum sodium every 4–6 hours for the first 24–48 hours. 1, 2, 3
Watch for sudden onset of polyuria (>3 L/day, often >6 L/day), rising serum sodium, and dilute urine (urine osmolality <300 mOsm/kg despite hypernatremia). 1, 2, 3
If polyuria and hypernatremia develop, immediately perform a water deprivation test (if clinically stable) or empirically start desmopressin to prevent critical dehydration. 1, 2, 3
Step 3: Ongoing Glucocorticoid Management
Continue hydrocortisone 200 mg per 24 hours as continuous IV infusion (or 50 mg IV/IM every 6 hours) during the acute phase. 5
Provide a total of 3–4 L isotonic saline over 24–48 hours with frequent hemodynamic and electrolyte monitoring. 5
Do not add fludrocortisone during acute crisis—high-dose hydrocortisone provides adequate mineralocorticoid activity. 5
Step 4: Initiate Desmopressin if Diabetes Insipidus Unmasks
Start intranasal or subcutaneous desmopressin (typical dose 1–2 mcg SC or 10–20 mcg intranasal) to control polyuria and prevent hypernatremia. 1, 2, 3
Titrate desmopressin to maintain urine output 1–2 L/day and serum sodium 135–145 mmol/L. 1, 2
Step 5: Transition to Maintenance Therapy
Taper parenteral hydrocortisone over 1–3 days to oral maintenance (15–25 mg daily in divided doses) once the patient can tolerate oral intake. 5
Continue desmopressin indefinitely if diabetes insipidus persists—hormonal deficits from suprasellar masses are often permanent. 4
Arrange urgent endocrinology consultation for ongoing management, evaluation of other pituitary hormone deficiencies (TSH, LH, FSH, growth hormone, prolactin), and coordination with neurosurgery for definitive treatment of the mass. 5, 6
Critical Pitfalls to Avoid
Never assume hyponatremia rules out diabetes insipidus—the adrenal insufficiency masks it, and you will only see the diabetes insipidus after starting steroids. 1, 2, 3
Never start thyroid hormone replacement before glucocorticoid replacement in patients with suspected multiple pituitary deficiencies—this can precipitate fatal adrenal crisis. 5, 6
Never attribute rising sodium and polyuria after starting hydrocortisone to "appropriate diuresis"—this is unmasking of diabetes insipidus and requires immediate desmopressin. 1, 2, 3
Never delay glucocorticoid therapy to obtain diagnostic confirmation—mortality increases with treatment postponement. 5
Real-World Case Evidence
A 70-year-old man with lung adenocarcinoma metastatic to the pituitary presented with severe hyponatremia (122 mmol/L) and panhypopituitarism; hydrocortisone replacement unmasked diabetes insipidus with sodium rising to 151 mmol/L, requiring urgent desmopressin. 1
A 46-year-old man with metastatic lung adenocarcinoma on nivolumab developed severe hyponatremia (111 mmol/L) from secondary adrenal insufficiency; water restriction testing confirmed masked central diabetes insipidus, and desmopressin was required after steroid initiation. 2
A 45-year-old woman with neurosarcoidosis stopped prednisone abruptly and developed secondary adrenal insufficiency with hyponatremia; after starting IV hydrocortisone, she developed severe polyuria (>6 L/day) and hypernatremia from unmasked central diabetes insipidus. 3
Pituitary apoplexy after cardiac surgery presented as Addisonian crisis with a suprasellar mass on MRI, requiring both stress-dose cortisone and transsphenoidal decompression. 7