A54-30 Triple Trouble: Subarachnoid Hemorrhage Complicated by Takotsubo Cardiomyopathy and Cerebral Salt Wasting

Introduction Acute neurologic injury can provoke systemic dysfunction through autonomic dysregulation. Two hallmark manifestations are (1) neurogenic Takotsubo cardiomyopathy (catecholamine-mediated, reversible myocardial stunning) and (2) cerebral salt wasting (CSW), marked by renal sodium loss, hypovolemia, and dehydration from hypothalamic and sympathetic disruption. Both exemplify the intricate brain-heart-kidney axis frequently seen after subarachnoid hemorrhage (SAH). Early recognition is essential as unnecessary anticoagulation, coronary angiography, or fluid restriction may exacerbate morbidity or mortality. Case Report A 66-year-old woman with hypertension presented with abrupt headache, nausea, vomiting, and lethargy. She was hypoxic with mild left-sided weakness and was intubated for airway protection. ECG showed mild ST-segment elevation in lead II; high-sensitivity troponin rose from 1,548 ng/L to 4,364 ng/L. Head CT revealed right frontal intraparenchymal hematoma with diffuse subarachnoid and intraventricular extension and prominent blood in the basal cisterns. Cerebral angiography identified and coil-embolized a ruptured right MCA bifurcation aneurysm. Transthoracic echocardiography demonstrated mid-to-apical hypokinesis with an ejection fraction of 35%, consistent with Takotsubo cardiomyopathy. Coronary angiography and anticoagulation were deferred. The patient was extubated the following day. She later developed polyuria, negative fluid balance, and dry mucous membranes. Serum sodium declined despite 3% saline infusion, while urine sodium increased from 88 mmol/L to 188 mmol/L within 24 hours, consistent with CSW. She received sodium and volume repletion with improvement in hemodynamics and serum sodium. Cardiac function normalized within three weeks without cardiac-specific therapy. Conclusion This case underscores the interplay between the central nervous system, cardiovascular system, and renal physiology following aneurysmal SAH. Hemorrhage involving the basal cisterns likely disrupted hypothalamic and medullary autonomic centers, triggering catecholamine surges that produced transient myocardial stunning and natriuretic peptide-mediated renal salt loss. The neurogenic Takotsubo cardiomyopathy and CSW represent downstream expressions of a shared neurohumoral cascade. Distinguishing these reversible complications is vital. Takotsubo cardiomyopathy may mimic acute coronary syndrome, while CSW is often misdiagnosed as syndrome of inappropriate ADH secretion (SIADH). Diagnostic clues include modest but disproportionate troponin elevation relative to wall-motion abnormalities, absence of coronary occlusion, polyuria with high urine sodium, and persistent hypovolemia despite hypertonic therapy. Misinterpretation can lead to inappropriate and sometimes harmful interventions. This case highlights that multidisciplinary awareness within neurocritical care teams is crucial for timely identification and management of these interconnected syndromes. Recognition of the brain-heart-kidney axis not only guides appropriate therapy but also reinforces the reversibility and excellent prognosis achievable with supportive, physiology-based care. This abstract is funded by: None