Introduction: Cushing’s syndrome is a multisystem disorder with significant cardiovascular morbidity, yet presentation as acute heart failure is uncommon. When driven by adrenocortical carcinoma (ACC), the clinical course is often aggressive and rapidly fatal, with particularly poor out-comes in resourcelimited settings where access to therapy is constrained. Case: A 39-year-old previously well female presented with acute decompensated heart failure, newly diagnosed hypertension, type 2 diabetes mellitus, and obesity, preceded by a 3-year history of secondary amenorrhea and progressive weight gain. On admission, she exhibited florid Cushingoid features. Biochemical evaluation confirmed severe adrenocorticotropic hormone (ACTH)-independent hypercortisolism: morning serum cortisol 1,950 nmol/L, failure of suppression on overnight dexamethasone suppression test (post-ODST cortisol 2022.9 nmol/L), and elevated 24-hour urinary free cortisol (2,069 nmol/24 hours, 2.56 × upper limit of normal). Androgen excess was evident, with elevated dehydroepiandrosterone sulfate (DHEAS more than 27 µmol/L) and testosterone (9.91 nmol/L). ACTH was suppressed, supporting an adrenal source, while aldosterone was normal. Contrast-enhanced computed tomography demonstrated a large left adrenal mass (12 cm) with tumor thrombus extending into the inferior vena cava and renal veins, with extensive hepatic and pulmonary metastases, consistent with advanced ACC. Management was limited by disease severity and resource constraints. Ketoconazole was contraindicated due to transaminitis, and alternative steroidogenesis inhibitors were unavailable, leaving metyrapone as the only feasible option. Oncological therapy was deferred due to sepsis and clinical instability. Her course was fulminant, complicated by recurrent heart failure, sepsis, and metabolic derangements, culminating in refractory cardiopulmonary failure. She died within 1 month of diagnosis, prior to definitive oncological intervention. Conclusion Fulminant cortisol-secreting ACC may present catastrophically as acute heart failure and progress rapidly. Early recognition and timely access to multimodal cortisollowering therapy are critical, particularly in resourcelimited settings. In fulminant hypercortisolism, the challenge is not diagnosis—but timing.
Adrenocortical Carcinoma ; Hydrocortisone ; Heart Failure