Recurrent Cerebral Salt Wasting in Subarachnoid Hemorrhage

Introduction: Hyponatremia occurs in over 50% of patients with subarachnoid hemorrhage (SAH) due to various etiologies such as diuretic therapy, SIADH, and cerebral salt wasting (CSWS) (Nakajami,2017). Differentiating between SIADH and CSWS is challenging due to similar diagnostic results. SIADH and CSWS present with increased urinary sodium and volume but differ in management. This case highlights the diagnostic difficulties and management of CSWS. Case Description: 49-year-old male presented with a severe headache. Imaging showed a SAH. A ventricular drain was placed, and the patient was put on a sodium goal, nimodipine, and intra-arterial verapamil for vasospasm. During admission, the patient developed high urinary output and hyponatremia. Initial treatment with fluids and desmopressin failed. Hypertonic fluids and fludrocortisone were started. Despite this, sodium levels dropped, necessitating increased hypertonic fluid rates and NaCl tablets. Recurrence of high urinary output with hyponatremia called for monitoring of hypertonic fluids and overall fluid balance until complete resolution. Discussion: Hyponatremia in CNS disease is often due to SIADH; however, CSWS can be on the differentials, especially in SAH. Proposed CSWS mechanisms include impaired sympathetic input to the kidneys and elevated levels of brain natriuretic peptide (BNP). Disruption of neural input and BNP release decreases sodium reabsorption and inhibits renin release, leading to hyponatremia without potassium wasting(Sherlock,2006). CSWS is uncommon but significant in acute brain injuries like SAH. Characterized by renal sodium excretion leading to hyponatremia, CSWS poses diagnostic challenges due to its overlap with SIADH. Prompt differentiation is critical as CSWS requires salt replacement and volume repletion, whereas SIADH is managed with fluid restriction(Luo &Wang,2022).