Management of LVAD in Cerebral Salt-Wasting Syndrome

The use of left ventricular assist devices (LVADs) is now commonplace in the management of nonischemic cardiomyopathy. LVADs are preload-dependent and afterload-sensitive, meaning rapid changes in a patient's volume status can significantly impact device function. Cerebral salt-wasting syndrome (CSWS), a rare cause of hyponatremia, is characterized by an acute increase in urine output and low serum sodium. Here, we present the case of a 43-year-old man with end-stage heart failure supported by an LVAD, who experienced refractory low-flow alarms due to CSWS. The patient initially presented with a new-onset headache. Brain computed tomography (CT) scan revealed an acute subdural hematoma with midline shift, requiring emergency craniotomy, which was performed without complications. After discharge from the intensive care unit (ICU), he returned with multiple low-flow alarms on his LVAD (flow less than 1.5 L/h), despite high mean arterial pressures and normal perfusion indexes. Laboratory evaluation showed a serum sodium of 130 mmol/L, a urine osmolality of 522 mmol/kg, a serum osmolality of 282 mmol/kg, and a urine sodium of 147 mEq/day. His urine output was 4 L/day. A diagnosis of CSWS was made. Treatment included normal saline drip for 1:1 volume replacement, daily fludrocortisone, low-dose desmopressin, and intermittent 3% hypertonic saline boluses. Salt tablets were prescribed to maintain a serum sodium goal of 135-140 mmol/L and a urine output of 2.5-3.5 L/day. Over time, the frequency of low-flow alarms decreased significantly, and the patient was discharged. CSWS is an unlikely cause of hyponatremia in the ICU. Aggressive fluid hydration and sodium supplementation are necessary for positive clinical outcomes. This is especially true in patients with LVADs, who are both preload-dependent and afterload-sensitive. Failure to rapidly treat CSWS can lead to respiratory arrest, brainstem herniation, and even death.