Adrenal Insufficiency (Adrenal Crisis)
The constellation of hypotension, bradycardia, hyponatremia, hyperkalemia, hyperchloremia, and elevated urea in an ICU patient is most consistent with adrenal insufficiency (adrenal crisis), making none of the listed options A-D the primary "cause" but rather all are manifestations of the underlying adrenal crisis. 1
Clinical Reasoning
This patient presents with the classic triad of adrenal crisis:
Hyponatremia occurs in 90% of newly presenting cases of primary adrenal insufficiency, resulting from sodium loss in urine combined with impaired free water clearance due to elevated vasopressin and angiotensin II 1
Hyperkalemia is present in approximately 50% of patients at diagnosis, resulting from aldosterone deficiency, impaired glomerular filtration, and acidosis 1
Hypotension and bradycardia are cardinal features of adrenal crisis, resulting from volume depletion, loss of cortisol's vascular effects, and electrolyte disturbances 1
Elevated urea reflects prerenal renal failure from hypovolemia and hypotension 1
Hyperchloremia occurs as part of the metabolic acidosis pattern seen with aldosterone deficiency 1
Why the Listed Options Are Manifestations, Not Causes
The question asks for the "cause" of these changes, but options A-D (hyperkalemia, hyponatremia, hyperchloremia, uremia) are all consequences of the same underlying pathophysiology—adrenal insufficiency. These electrolyte and metabolic derangements do not cause each other; they co-occur due to cortisol and aldosterone deficiency 1, 2.
Distinguishing From Other Syndromes
BRASH Syndrome
While BRASH syndrome (Bradycardia, Renal failure, AV blockade, Shock, Hyperkalemia) can present similarly, it requires the presence of AV-nodal blocking medications (beta-blockers, calcium channel blockers, digoxin) in a patient with underlying renal insufficiency 3, 4. The synergistic effect between hyperkalemia and these medications creates the bradycardia 4. Without a history of these medications, BRASH is less likely.
Relative Adrenal Insufficiency in Critical Illness
Importantly, the "classic" teaching about adrenal insufficiency laboratory findings does not reliably predict relative adrenal insufficiency in critically ill patients. A study of 212 ICU patients found that 75% with relative adrenal insufficiency had hypernatremia (not hyponatremia), 90% had hypokalemia (not hyperkalemia), and 97% had hyperglycemia 5. However, this patient's presentation is more consistent with primary adrenal insufficiency (Addison's disease) rather than relative adrenal insufficiency.
Immediate Management Required
Do not wait for confirmatory testing before initiating treatment in a patient with suspected adrenal crisis:
Draw blood immediately for serum cortisol, plasma ACTH, sodium, potassium, creatinine, and glucose before initiating treatment 1
Administer 100 mg hydrocortisone IV bolus immediately, followed by continuous infusion or repeated boluses every 6 hours (100-300 mg/day total) 1
Simultaneously infuse 1 liter of 0.9% saline over the first hour, then continue at slower rates for 24-48 hours (total 3-4 liters in first 24 hours) 1
High-dose hydrocortisone saturates 11β-hydroxysteroid dehydrogenase type 2, providing mineralocorticoid effects and eliminating the need for separate fludrocortisone during acute crisis 1
Critical Pitfalls to Avoid
Do not assume normal cortisol rules out adrenal insufficiency in acute illness—cortisol levels within the normal range may be inappropriately low for the stress state 1
Do not wait for the "classic" combination of hyponatremia and hyperkalemia—sodium levels are often only marginally reduced, and potassium is elevated in only about 50% of cases at diagnosis 1
Monitor for hypoglycemia, especially as this can occur with adrenal insufficiency 1, 2
Diagnostic Confirmation
Serum cortisol <250 nmol/L (<9 µg/dL) with elevated ACTH in acute illness is diagnostic of primary adrenal insufficiency 1
Serum cortisol <400 nmol/L (<14.5 µg/dL) with elevated ACTH raises strong suspicion and warrants immediate treatment 1
Primary adrenal insufficiency is typically characterized by low morning cortisol levels (<5 µg/dL), high corticotropin levels, and low DHEAS levels 2
If forced to choose from the given options, the answer would be D (Uremia), as elevated urea is the marker that best reflects the hemodynamic compromise and prerenal failure driving the entire clinical picture 1. However, this is misleading because uremia itself is a consequence, not the root cause—the true underlying diagnosis is adrenal crisis.